Acute myocardial infarction (AMI) is one of the leading causes of death in the world, demands early and complete reperfusion in therapy strategy. Reperfusion is the definitive treatment to salvage ischaemic myocardium from infarction. A primary determinant of infarct size is the duration of ischaemia. In myocardium that has not been irreversibly injured by ischaemia, reperfusion induces additional injury in the area at risk. Ischaemic postconditioning (IPO), brief intermittent ischaemia during the onset of reperfusion, both are known as endogenous protective mechanism, which could markedly limit myocardial infarction and render the myocardium more resistant to the subsequent I/R injury. Endoplasmic reticulum (ER) is the most important organelle in eukaryocyte, serving for macromolecules biosynthesis, stress action and calcium homeostasis adjusting. Recently study show that ischaemia/reperfusion injury (I/R) can affect ER function, namely ER stress (ERs). ERs induces ER molecular chaperones such ...

The aim of the present study was to determine whether curculigoside protects against myocardial ischemia‑reperfusion injury (MIRI) and to investigate the underlying mechanisms. An in vitro model of hypoxia/reoxygenation (H/R) was established by culturing H9c2 cells under hypoxic conditions for 12 h, followed by reoxygenation for 1 h. Cell Counting kit‑8 and lactate dehydrogenase (LDH) assays were subsequently used to examine cell viability and the degree of cell injury. In addition, isolated rat hearts were subjected to 30 min of ischemia followed by 1 h of reperfusion to establish a MIRI model. Triphenyltetrazolium chloride (TTC) staining was performed to measure the infarct size. Furthermore, TUNEL staining and flow cytometry were employed to evaluate cell apoptosis. The opening of the mitochondrial permeability transition pore (MPTP) and changes in the mitochondrial membrane potential (ΔΨm) were assessed. Reverse transcription‑quantitative PCR and western blot analysis were performed ...

TY - JOUR. T1 - Sodium nitroprusside exacerbates myocardial ischemia-reperfusion injury. AU - Cope, Jeffrey T.. AU - Banks, David. AU - Laubach, Victor E.. AU - Binns, Oliver A.R.. AU - King, R. Christopher. AU - Richardson, R. Mark. AU - Shockey, Kimberly S.. AU - Tribble, Curtis G.. AU - Kron, Irving L.. PY - 1997/12/1. Y1 - 1997/12/1. N2 - Background. The role of nitric oxide in myocardial ischemia-reperfusion is controversial. Although many studies claim that nitric oxide ameliorates reperfusion injury, others suggest that it exacerbates such injury, possibly through peroxynitrite production. These discordant results may be attributable to a dose-dependent phenomenon. Methods. Isolated rabbit hearts sustained sequential periods of blood perfusion (20 minutes), warm ischemia (30 minutes), and reperfusion (20 minutes). During reperfusion, four groups underwent intracoronary infusion of saline solution (n = 6), or the nitric oxide donor sodium nitroprusside (100 nm/min [SNP100, n = 6], 1 nmol ...

b,Background,/b, Norepinephrine (NE)-derived free radicals may contribute to myocyte injury after ischemia -reperfusion, so the influence of sympathetic denervation on myocardial ischemia - reperfusion injury was investigated in the present study. ,b,Methods and Results,/b, Cardiac sympathetic denervation was produced in Wistar rats by a solution of 10% phenol 1 week before ischemia. Atenolol (0.5 mg/kg) was intravenously administered 10 min before the coronary occlusion. The left coronary artery was occluded for 30 min and thereafter reperfused. Cardiac interstitial fluid was collected by a microdialysis probe and free radicals in dialysate were determined by electron paramagnetic resonance (EPR) spin trapping, using 5,5-dimethyl-1-pyrroline-N-oxide as a spin trap. The ratio of infarct size to the ischemic area at risk (I/R) was decreased in both the phenol and atenolol groups compared with control (28.5±11.3, 31.8±10.7 vs 50.6±14.7%, p,0.05). During the coronary occlusion, concentrations of ...

Limited microRNAs (miRNAs, miRs) have been reported to be necessary for exercise-induced cardiac growth and essential for protection against pathological cardiac remodeling. Here we determined members of the miR-17-92 cluster and their passenger miRNAs expressions in two distinct murine exercise models and found that miR-17-3p was increased in both. miR-17-3p ... read more promoted cardiomyocyte hypertrophy, proliferation, and survival. TIMP-3 was identified as a direct target gene of miR-17-3p whereas PTEN was indirectly inhibited by miR-17-3p. Inhibition of miR-17-3p in vivo attenuated exercise-induced cardiac growth including cardiomyocyte hypertrophy and expression of markers of myocyte proliferation. Importantly, mice injected with miR-17-3p agomir were protected from adverse remodeling after cardiac ischemia/reperfusion injury. Collectively, these data suggest that miR-17-3p contributes to exercise-induced cardiac growth and protects against adverse ventricular remodeling. miR-17-3p may ...

TY - JOUR. T1 - (−)-Phenserine inhibits neuronal apoptosis following ischemia/reperfusion injury. AU - Chang, Cheng Fu. AU - Lai, Jing Huei. AU - Wu, John Chung Che. AU - Greig, Nigel H.. AU - Becker, Robert E.. AU - Luo, Yu. AU - Chen, Yen Hua. AU - Kang, Shuo Jhen. AU - Chiang, Yung Hsiao. AU - Chen, Kai Yun. PY - 2017/12/15. Y1 - 2017/12/15. N2 - Stroke commonly leads to adult disability and death worldwide. Its major symptoms are spastic hemiplegia and discordant motion, consequent to neuronal cell death induced by brain vessel occlusion. Acetylcholinesterase (AChE) is upregulated and allied with inflammation and apoptosis after stroke. Recent studies suggest that AChE inhibition ameliorates ischemia-reperfusion injury and has neuroprotective properties. (−)-Phenserine, a reversible AChE inhibitor, has a broad range of actions independent of its AChE properties, including neuroprotective ones. However, its protective effects and detailed mechanism of action in the rat middle cerebral ...

Rationale: There is a special role for estrogens in preventing and curing cardiovascular disease in women. Soy isoflavone (SI), a soy-derived phytoestrogen, is a group of biologically active plant substances with chemical structures which are similar to that of an endogenous estrogen-estradiol.. Objective: We ought to elucidate possible mechanism of SI to improve myocardial ischemia/reperfusion (MI/R) injury in ovariectomized rats.. Methods and Results: Female SD rats were underwent bilateral ovariectomy or sham ovariectomy. One week later, rats were randomly divided into several groups and began to feed soy-free chow: sham ovariectomy operation (control group), ovariectomy with MI/R or ovariectomy with sham MI/R. Other ovariectomy rats were given different doses of SI dissolved in 0.5% carboxymethycellulose (CMC-Na) by gavage. Additional ovariectomy rats were administrated with the same volume of CMC-Na by gavage or 50 μg/kg·d of 17β-estradiol (E2) by subcutaneous injection. After four-week ...

article: Dexmedetomidine reduces myocardial ischemia-reperfusion injury in rats through PI3K/AKT/GSK-3β signaling pathway - Minerva Cardioangiologica 2020 February;68(1):58-9 - Minerva Medica - Journals

In this study, we have demonstrated that SIRT1 is a powerful regulator in diabetic MI/R injury. This conclusion is based on several novel findings. First, we have provided evidences that SIRT1 expression was decreased in diabetic heart, and overexpression of SIRT1 alleviated MI/R injury and improved cardiac function in diabetic rats. Second, SIRT1-mediated cardioprotection involved inhibition of oxidative stress. Third, the mechanisms of the cardioprotection were mediated by modulation of eNOS activity.. Overwhelming epidemiological and clinical data have demonstrated that the diabetic heart is more sensitive to I/R injury [6, 29, 30]. It has been demonstrated that diabetes mellitus can exacerbate MIR injury and blunt the protective effect of various therapeutic agents [31, 32]. Thus, novel strategies and targets are urgently needed to reduce myocardial susceptibility to I/R injury in diabetic state. To address this issue, high-fat diet-fed and streptozotocin-induced (HFD-STZ) type 2 diabetic ...

Fingerprint Dive into the research topics of Effect of brief hypoxia on reperfusion arrhythmias and release of Ca,sup,2+,/sup, by rat heart homogenate blocked by ryanodine. Together they form a unique fingerprint. ...

Coronary artery disease is the single largest cause of mortality worldwide, with myocardial infarction being the most serious manifestation. Timely and effective myocardial reperfusion using primary PCI in acute ST elevation myocardial infarction (STEMI) has substantially improved clinical outcomes of patients. Following reopening of the blocked artery, reperfusion itself can cause myocardial injury and cell death (myocardial ischaemia/reperfusion injury). Studies in animal MI models and human therapeutic interventions indicate that ischemia/reperfusion injury is responsible for up to 50% of final infarct size. While CD4 T-lymphocytes (T-cells) have been shown to promote myocardial ischemia/reperfusion injury in the mouse model, their role during STEMI in humans is by large unknown. A low number of lymphocytes following myocardial infarction is a negative predictor of survival, and we have previously shown (PLoS One 2012) that CD4 and CD8 T-cells drop by up to 50% in the peripheral blood during ...

Methods and Results-Twenty-one rabbits were randomly assigned to 3 groups: (1) vehicle control, (2) SAHA pretreatment (1 day before and at surgery), and (3) SAHA treatment at the time of reperfusion only. Each arm was subjected to ischemia/reperfusion surgery (30 minutes coronary ligation, 24 hours reperfusion). In addition, cultured neonatal and adult rat ventricular cardiomyocytes were subjected to simulated ischemia/reperfusion to probe mechanism. SAHA reduced infarct size and partially rescued systolic function when administered either before surgery (pretreatment) or solely at the time of reperfusion. SAHA plasma concentrations were similar to those achieved in patients with cancer. In the infarct border zone, SAHA increased autophagic flux, assayed in both rabbit myocardium and in mice harboring an RFP-GFP-LC3 transgene. In cultured myocytes subjected to simulated ischemia/reperfusion, SAHA pretreatment reduced cell death by 40%. This reduction in cell death correlated with increased ...

Our group demonstrated previously that postconditioning by angioplasty reduces infarct size, as assessed by early CK release, in the human heart.16 This was the first study demonstrating that postconditioning can reduce lethal reperfusion injury in the human heart. In a retrospective study, Darling et al23 similarly reported a reduced release of CK in ST-segment-elevation MI patients who underwent ,4 inflations of the angioplasty balloon at the time of reperfusion compared with those who received ,3 inflations. The present study is in agreement with the initial results of the Staat study, further reporting a mean reduction of 47% of the area under the curve of TnI in postconditioned versus control groups. This infarct size reduction was observed with the control and postconditioned groups having similar duration of ischemia and size of the area at risk, ie, 2 major determinants of infarct size. Area at risk was assessed by measurement of the percentage of abnormally contracting segments on ...

Restoration of blood flow after myocardial infarction (MI), surgery or fibrinolytic therapy is necessary, but can lead to cardiomyocyte dysfunction within a generalised condition commonly known as reperfusion injury. The role of cyclophilins, heat shock proteins (HSP), and the mitochondrial chaperone complex (MCC), was studied in this pathological condition. In vitro and in vivo models were used to replicate conditions of ischaemia/reperfusion (IR) injury. H9c2 and COS-7 cell lines were employed in nitric oxide (NO) donor and transfection applications. Experimental protocols were used to determine mitochondrial membrane potential (MMP), mitochondrial morphology, protein expression, enzyme activity and cell damage in these models. No difference was observed in activity or expression in cyclophilin or expression of the MCC in any of the models. It was noted that in the in vitro model, cell death was predominantly necrotic with only a minority of cells undergoing apoptosis, and as the degree of ...

TY - JOUR. T1 - Changes of endothelin-1 and big endothelin-1 levels and action potential duration during myocardial ischemia-reperfusion in dogs with and without ventricular fibrillation. AU - Vágó, Hajnalka. AU - Soós, Pál. AU - Zima, Endre. AU - Gellér, László. AU - Keltai, Katalin. AU - Róka, Attila. AU - Kékesi, Violetta. AU - Juhász-Nagy, Alexander. AU - Merkely, Béla. PY - 2004/11. Y1 - 2004/11. N2 - Myocardial ischemia-reperfusion is associated with increased production of endothelin-1 (ET-1). Moreover, exogenous ET-1 has arrhythmogenic properties. Our aim was to investigate the correlation between endogenous ET-1, big ET-1 levels and epicardial monophasic action potential duration during myocardial ischemia-reperfusion in anesthetized dogs. Thirty-minute myocardial ischemia was followed by a 90-minute reperfusion period in 18 mongrel dogs. The total incidence of ventricular fibrillation (VF) during ischemia and reperfusion was 11.1% and 33.3%, respectively. During ischemia, ...

TY - JOUR. T1 - Delayed onset of apoptosis following ischemia/reperfusion in rat liver. T2 - Downregulation of BAX gene. AU - Lai, W. Y.. AU - Chien, C. T.. AU - Cheng, C. L.. AU - Yang, B. C.. AU - Hsu, S. M.. AU - Lee, P. H.. PY - 1999/11/1. Y1 - 1999/11/1. UR - http://www.scopus.com/inward/record.url?scp=0032720663&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0032720663&partnerID=8YFLogxK. U2 - 10.1016/S0041-1345(99)00616-8. DO - 10.1016/S0041-1345(99)00616-8. M3 - Article. C2 - 10578340. AN - SCOPUS:0032720663. VL - 31. SP - 2924. EP - 2925. JO - Transplantation Proceedings. JF - Transplantation Proceedings. SN - 0041-1345. IS - 7. ER - ...

Myocardial infarction (MI) is one of the leading causes of death. Wilms' tumor 1-associating protein (WTAP), one of the components of the m6A methyltransferase complex, has been shown to affect gene expression via regulating mRNA modification. Although WTAP has been implicated in various diseases, its role in MI is unclear. In this study, we found that hypoxia/reoxygenation (H/R) time-dependently increased WTAP expression, which in turn promoted endoplasmic reticulum (ER) stress and apoptosis, in human cardiomyocytes (AC16). H/R effects on ER stress and apoptosis were all blocked by silencing of WTAP, promoted by WTAP overexpression, and ameliorated by administration of ER stress inhibitor, 4-PBA. We then investigated the underlying molecular mechanism and found that WTAP affected m6A methylation of ATF4 mRNA to regulate its expression, and that the inhibitory effects of WTAP on ER stress and apoptosis were ATF4 dependent. Finally, WTAP’s effects on myocardial I/R

There is vast literature on the topic of ischemia-reperfusion injury. A summative discussion of the complex pathogenicity will aid practicing physicians in diagnosis and management. We offer a review of this literature as well as a discussion on a rare case of tense edematous bullae as a presentation of ischemia-reperfusion injury. A 65-year-old male underwent a right femoropopliteal bypass for rest pain that had not improved after iliac stent placement. He presented three days after discharge with blistering lesions on the reperfused limb that resembled bullous pemphigoid. This case describes the variability in the presentation of reperfusion injury, as well as the necessity to educate those managing atypical presentations of reperfusion injury.

OBJECTIVE Ischemia reperfusion injury is partly responsible for the high mortality associated with induced myocardial injury and the reduction in the full benefit of myocardial reperfusion. Remote ischemic preconditioning, perconditioning, and postconditioning have all been shown to be cardioprotective. However, it is still unknown which one is the most beneficial. To examine this issue, we used adult male Wistar rat ischemia reperfusion models to compare the cardioprotective effect of these three approaches applied on double-sided hind limbs. METHODS The rats were randomly distributed to the following five groups: sham, ischemia reperfusion, remote preconditioning, remote perconditioning, and remote post-conditioning. The ischemia/reperfusion model was established by sternotomy followed by a 30-min ligation of the left coronary artery and a subsequent 3-h reperfusion. Remote conditioning was induced with three 5-min ischemia/5-min reperfusion cycles of the double-sided hind limbs using a tourniquet.

CCD-WT mice exhibited heightened nociception than pain free mice and nociception tightly correlated with circulating aldehyde (4-HNE) accumulation and cardiac protein carbonylation. CCD induced 4-HNE overload provoked cardiac SIRT1 carbonylative inactivation and impairment the cardioprotection of LKB1-mediated AMPK activation during MI/R, which resulting in enhanced MI/R injury and higher mortality compare with pain free WT mice. In comparison to WT, chronic neuropathic pain enhanced susceptibility to MI/R injury was further exacerbated by ALDH2 deficiency in which associated with more impaired SIRT1-LKB1-AMPK signaling. Further, peripheral injection of 4-HNE induced a sustained allodynia, and increased circulating aldehyde load to the same degree as that seen in CCD-WT mice. The 4-HNE exposure can simulate cardiac SIRT1 carbonylative inactivation and sensitization to MI/R injury, which was observed in CCD-WT mice. However, treatment of CCD-WT mice with ALDH2-selective activator (Alda-1) ...

A rat model of MIRI was established by 30 min of ligation of the left anterior descending coronary artery followed by 120 min of reperfusion; this method has been widely used to research the underlying mechanisms of cardiomyocyte apoptosis (36). Several studies have reported that rats are prone to death after ligation of the left anterior descending coronary artery due to arrhythmia; the mortality rate of this model can be as high as 60% (32,37). In the present study, 27 rats died and the mortality rate was ~30%; five rats died during the operation due to excess blood loss, 18 rats were euthanized due to reaching humane endpoints and four rats were deeply anesthetized and died of respiratory depression. It has been reported that the safety range of sodium pentobarbital is too narrow, which causes poor control of anesthesia depth, and some rats may die of respiratory depression even at the recommended anesthetic dose (38,39). This rat model of MIRI was used to evaluate the cardioprotective effect ...

Mitochondria-mediated cardiomyocyte apoptosis is involved in myocardial ischemia/reperfusion (MI/R) injury. Clematichinenoside (AR) is a triterpenoid saponin isolated from the roots of Clematis chinensis with antioxidant and anti-inflammatory cardioprotection effects against MI/R injury, yet the anti-apoptotic effect and underlying mechanisms of AR in MI/R injury remain unclear. We hypothesize that AR may improve mitochondrial function to inhibit MI/R-induced cardiomyocyte apoptosis. In this study, we replicated an in vitro H9c2 cardiomyocyte MI/R model by hypoxia/reoxygenation (H/R) treatment. The viability of H9c2 cardiomyocytes was determined by MTT assay; apoptosis was evaluated by flow cytometry and TUNEL experiments; mitochondrial permeability transition pore (mPTP) opening was analyzed by a calcein-cobalt quenching method; and mitochondrial membrane potential (ΔΨm) was detected by JC-1. Moreover, we used western blots to determine the mitochondrial cytochrome c translocation to cytosolic and

TY - JOUR. T1 - The harmful effects of ventricular distention during postischemic reperfusion. AU - Lucas, S. K.. AU - Schaff, H. V.. AU - Flaherty, J. T.. AU - Gott, Vincent L. AU - Gardner, T. J.. PY - 1981. Y1 - 1981. N2 - To assess the effects of left ventricular distention during the early reperfusion period following ischemic arrest, 16 canine heart preparations were subjected to 45 minutes of hypothermic (27°C) cardioplegic arrest and normothermic reperfusion. Isovolumic left ventricular developed pressure and rate of rise of left ventricular pressure (dP/dt) were measured with an intraventricular balloon; endocardial/epicardial flow ratios were determined with microspheres; and myocardial gas tensions were monitored with mass spectrometry. During early reperfusion, Group 1 hearts (n=8) were not distended (end-diastolic pressure = 0). Group 2 hearts (n = 8) were subjected to an enddiastolic pressure of 20 mm Hg for the initial 15 minutes of reperfusion. Group 2 hearts demonstrated ...

Objectives. Pharmacological treatment of reperfusion injury using insulin and GSK3β inhibition has been shown to be cardioprotective, however, their interaction with the endogenous cardioprotective strategy, ischemic postconditioning, is not known. Design. Langendorff perfused ex vivo rat hearts were subjected to 30 min of regional ischemia and 120 min of reperfusion. For the first 15 min of reperfusion hearts received either vehicle (Ctr), insulin (Ins) or a GSK3β inhibitor (SB415286; SB41), with or without interruption of ischemic postconditioning (IPost; 3 × 30 s of global ischemia). In addition, the combination of insulin and SB41 for 15 min was assessed. Results. Insulin, SB41 or IPost significantly reduced infarct size versus vehicle treated controls (IPost 33.5 ± 3.3%, Ins 33.5 ± 3.4%, SB41 30.5 ± 3.0% vs. Ctr 54.7 ± 6.8%, p , 0.01). Combining insulin and SB415286 did not confer additional cardioprotection compared to the treatments given alone (SB41 + Ins 26.7 ± 3.5%, ns). ...

The antioxidant properties of flavonols in vivo and their potential benefits in myocardial ischaemia/reperfusion (I/R) injury have been little investigated. We evaluated the ability of a synthetic flavonol, 3,4-dihydroxyflavonol (DiOHF) to scavenge superoxide in post-I/R myocardium and to prevent myocardial I/R injury. 2 Anaesthetized sheep were studied in four groups (n = 5-6): control, ischaemic preconditioning (IPC), vehicle and DiOHF (before reperfusion, 5 mg kg-1, i.v.). The left anterior descending coronary artery was occluded distal to the second diagonal branch for 1 h followed by 2 h of reperfusion. Infarct size, myocardial function, NADPH-activated superoxide generation and biochemical markers of injury were measured. 3 DiOHF (10-8-10-4 M) incubated in vitro with post-I/R myocardium from the vehicle group suppressed superoxide production dose-dependently. DiOHF administered in vivo also significantly reduced superoxide generation in vitro. 4 DiOHF and IPC markedly reduced infarct ...

Experimental and clinical studies have demonstrated that myocardial ischemia induces activation of various components of the renin-angiotensin system (RAS), including angiotensinogen, renin, angiotensin-converting enzyme (ACE), angiotensins, and angi

Early myocardial reperfusion is an effective therapy but ischemia/reperfusion (I/R) causes lethal myocardial injury. The aging heart was reported to show greater cardiac damage after I/R injury than that observed in young hearts. Senescence marker protein 30 (SMP30), whose expression decreases with age, plays a role in reducing oxidative stress and apoptosis. However, the impact of SMP30 on myocardial I/R injury remains to be determined. In this study, the left anterior descending coronary artery was occluded for 30 min, followed by reperfusion in wild-type (WT) and SMP30 knockout (KO) mice. After I/R, cardiomyocyte apoptosis and the ratio of infarct area/area at risk were higher, left ventricular fractional shortening was lower, and reactive oxygen species (ROS) generation was enhanced in SMP30 KO mice. Moreover, the previously increased phosphorylation of GSK-3β and Akt was lower in SMP30 KO mice than in WT mice. In cardiomyocytes, silencing of SMP30 expression attenuated Akt and GSK-3β

Weve investigated the consequences of hypoxia and myocardial ischemia/reperfusion for the framework and function of cytochrome oxidase (CcO). immunoprecipitated CcO complicated. Most oddly enough, both H89 and MPI put into the perfusion moderate dramatically decreased the ischemia/reperfusion problems for the myocardial cells. Our results directed to a thrilling chance for using CcO activity modulators for managing myocardial damage connected with ischemia and oxidative tension circumstances. 404950-80-7 Cytochrome oxidase (CcO)3 may be the terminal oxidase from the mitochondrial 404950-80-7 electron transportation string, whose activity is normally modulated in response to O2 stress and the task load from the tissues (1-6). This rate-limiting enzyme can be an essential site of legislation of mitochondrial respiration and oxidative phosphorylation (7). In the 404950-80-7 SCA12 fungus, changed CcO activity in response to aerobic and anaerobic circumstances is from the differential appearance of ...

TY - JOUR. T1 - Impact of a novel cardioprotective agent on the ischaemia-reperfusion- induced Akt kinase activation. AU - Toth, Ambrus. AU - Kovacs, Krisztina. AU - Deres, Peter. AU - Halmosi, Robert. AU - Czopf, Laszlo. AU - Hanto, Katalin. AU - Kalai, Tamas. AU - Hideg, Kalman. AU - Sumegi, Balazs. AU - Toth, Kalman. PY - 2003/12/1. Y1 - 2003/12/1. N2 - Cardioprotective effect of a free radical-scavenging compound (HO-3073) was examined during ischaemia-reperfusion (IR) in isolated heart perfusion system and its influence on the pro-survival Akt signalling pathway was addressed. Rat hearts were perfused according to the Langendorff method and subjected to a global 25-min ischaemia and 15, 45 and 90-min reperfusion either untreated or treated with HO-3073 (2, 5 and 10μM) and/or wortmannin (100nM, inhibitor of phosphatidylinositol-3-kinase). HO-3073 facilitated the recovery of myocardial energy metabolism as assessed by 31P NMR spectroscopy (creatine phosphate recovery in reperfusion was ...

Ischaemic preconditioning is the most powerful endogenous mechanism for limiting myocardial infarct size in the experimental setting. Its clinical application is limited to scenarios in which the index episode of ischaemia and reperfusion can be anticipated such as in the setting of cardiac surgery • Ischaemic postconditioning represents an endogenous cardioprotective strategy which is applied at the onset of myocardial reperfusion, thereby allowing its use as an adjunct to reperfusion in patients presenting with an acute myocardial infarction • Both ischaemic preconditioning and postconditioning recruit a common signal transduction pathway at the time of myocardial reperfusion, which can be targeted by pharmacological agents administered as adjuncts to reperfusion. ...

TY - JOUR. T1 - S1P 3-mediated cardiac fibrosis in sphingosine kinase 1 transgenic mice involves reactive oxygen species. AU - Takuwa, Noriko. AU - Ohkura, Sei Ichiro. AU - Takashima, Shin Ichiro. AU - Ohtani, Keisuke. AU - Okamoto, Yasuo. AU - Tanaka, Tamotsu. AU - Hirano, Kaoru. AU - Usui, Soichiro. AU - Wang, Fei. AU - Du, Wa. AU - Yoshioka, Kazuaki. AU - Banno, Yoshiko. AU - Sasaki, Motoko. AU - Ichi, Ikuyo. AU - Okamura, Miwa. AU - Sugimoto, Naotoshi. AU - Mizugishi, Kiyomi. AU - Nakanuma, Yasuni. AU - Ishii, Isao. AU - Takamura, Masayuki. AU - Kaneko, Shuichi. AU - Kojo, Shosuke. AU - Satouchi, Kiyoshi. AU - Mitumori, Kunitoshi. AU - Chun, Jerold. AU - Takuwa, Yoh. PY - 2010/2. Y1 - 2010/2. N2 - Aims Sphingosine kinase 1 (SPHK1), its product sphingosine-1-phosphate (S1P), and S1P receptor subtypes have been suggested to play protective roles for cardiomyocytes in animal models of ischaemic preconditioning and cardiac ischaemia/reperfusion injury. To get more insight into roles for SPHK1 in ...

Cardiovascular drugs attenuated myocardial resistance against ischaemia-induced and reperfusion-induced injury in a rat model of repetitive occlusion ...

BACKGROUND: Acute myocardial infarction is one of the leading causes of death. It is caused by a blockage of a coronary artery leading to reduced blood flow to the myocardium and hence ischemic damage. In addition, a second wave of damage after the flow has been restored, named reperfusion injury greatly exacerbate the damage. For the latter, no medical treatment exist. In this study the aim was to characterize Ca(2+) sensitivity in coronary arteries following experimental ischemia/reperfusion injury.. METHODS: Arteries were isolated from hearts exposed to a well-established rat ischemia/reperfusion model. Wire myograph combined with FURA2-AM measurements was applied to study the Ca(2+) dependency of the vasoconstriction.. RESULTS: The results presented herein show that ETB receptors (R) have much weaker Ca(2+)-sensitizing effect than ETA-R and that ETB-R appear to be more dependent on Ca(2+) influx presumably through voltage-gated Ca(2+) channels (VGCC). In addition, we show that there is an ...

Ticlopidin is a well-known antithrombocytic drug used in the prophylaxis of arteriosclerotic diseases. Ticlopidin is supposed to reduce ischemia reperfusion injury with its effects against platelet aggregation which play important roles in ischemia reperfusion injury by means of different mediators. 32 female Sprague-Dawley rats were randomised to four groups one being as control in the study design. Only anesthesia was performed to group 1 (n=8). The right hind limb ischemia was induced by tourniquets applied at the hip level group 2 (n=8). After 4 hours the samples were collected before tourniquets were removed. Group 3 (n=8) and group 4 (n=8) rats were randomised to 2 hours of reperfusion after 4 hours of ischemia. Ticlopidin (50 mg/day) were given five days before the experiment day twice daily to the animals in the group 4. Tissue malondialdehyde levels were recorded by thiobarbutiric acid method as a marker for lipid peroxidation. According to the lung levels of malondialdehide, ticlopidin ...

Our data clearly demonstrate significant cardioprotective activities of the novel small molecule C1 inhibitor (C1s-INH-248) in myocardial ischemia and reperfusion. The cardioprotection exerted by C1s-INH-248 was characterized by a reduction of necrosis and decreased serum CK activity compared with rabbits given the vehicle only. The cardioprotective effect of C1s-INH-248 was dose dependent when administrated as a 0.1-1 mg/kg body weight bolus injection. Even compared with the treatment with the C1 esterase inhibitor (C1-INH) C1s-INH-248 demonstrated superior potency. The protection of C1s-INH-248 also resulted in inhibition of PMN accumulation in the reperfused myocardium. Further, the protective effect could be attributed to decreased deposition of C5b-9 on ischemic reperfused myocardium or vascular endothelial cells. To our knowledge, this is the first study demonstrating cardioprotection with a highly specific synthetic C1 inhibitor following myocardial ischemia and reperfusion.. To date, ...

Background: Cardiac autophagic flux is impaired during myocardial ischemia/reperfusion (MI/R). Impaired autophagic flux may exacerbate MI/R injury. Charged multivesicular body protein 2B (CHMP2B) is a subunit of the endosomal sorting complex required for transport (ESCRT-III) complex that is required for autophagy. However, the reverse role of CHMP2B accumulation in autophagy and MI/R injury has not been established. The objective of this article is to elucidate the roles of AMP-activated protein kinase (AMPK)/atrogin-1 pathways in inhibiting CHMP2B accumulation in ischemia-reperfusion injury. Methods: Male C57BL/6 mice (3-4 months) and H9c2 cardiomyocytes were used to evaluate MI/R and hypoxia/reoxygenation (H/R) injury in vivo and in vitro, respectively. MI/R was built by a left lateral thoracotomy and occluded the left anterior descending artery. H9c2 cells were firstly treated in 95% N2 and 5% CO2 for 15 h and reoxygenation for 1 h. Metformin (100 mg/kg/d) and CHMP2B (Ad-CHMP2B) transfected ...

As progressive organ shortage in cardiac transplantation demands extension of donor criteria, effort is needed to optimize graft survival. Reactive oxygen and nitrogen species, generated during organ procurement, transplantation, and reperfusion, contribute to acute and late graft dysfunction. The combined application of diverse substances acting via different molecular pathways appears to be a reasonable approach to face the complex mechanism of ischemia reperfusion injury. Thus, an antioxidant solution containing |i|α|/i|-ketoglutaric acid, 5-hydroxymethylfurfural, |i|N|/i|-acetyl-L-methionine, and |i|N|/i|-acetyl-selenium-L-methionine was combined with endogenous angiotensin-(1-7). Its capacity of myocardial protection was investigated in isolated Langendorff-perfused rat hearts subjected to warm and cold ischemia. The physiological cardiac parameters were assessed throughout the experiments. Effects were evaluated via determination of the oxidative stress parameters malondialdehyde and carbonyl

TY - JOUR. T1 - Hydrogen Flush After Cold Storage as a New End-Ischemic Ex Vivo Treatment for Liver Grafts Against Ischemia/Reperfusion Injury. AU - Tamaki, Ichiro. AU - Hata, Koichiro. AU - Okamura, Yusuke. AU - Nigmet, Yermek. AU - Hirao, Hirofumi. AU - Kubota, Toyonari. AU - Inamoto, Osamu. AU - Kusakabe, Jiro. AU - Goto, Toru. AU - Tajima, Tetsuya. AU - Yoshikawa, Junichi. AU - Tanaka, Hirokazu. AU - Tsuruyama, Tatsuaki. AU - Tolba, Rene H.. AU - Uemoto, Shinji. PY - 2018/11. Y1 - 2018/11. N2 - Cold storage (CS) remains the gold standard for organ preservation worldwide, although it is inevitably associated with ischemia/reperfusion injury (IRI). Molecular hydrogen (H2) is well known to have antioxidative properties. However, its unfavorable features, ie, inflammability, low solubility, and high tissue/substance permeability, have hampered its clinical application. To overcome such obstacles, we developed a novel reconditioning method for donor organs named hydrogen flush after cold storage ...

TY - JOUR. T1 - Anticoagulant therapy in critical organ ischaemia/reperfusion injury. AU - Loubele, Sarah T. B. G.. AU - ten Cate, Hugo. AU - Spronk, Henri M. H.. PY - 2010/7. Y1 - 2010/7. KW - Ischaemia/reperfusion injury. KW - anti-coagulant therapy. KW - animal models. KW - inflammation. KW - apoptosis. U2 - 10.1160/TH09-08-0582. DO - 10.1160/TH09-08-0582. M3 - Article. VL - 104. SP - 136. EP - 142. JO - Thrombosis and Haemostasis. JF - Thrombosis and Haemostasis. SN - 0340-6245. IS - 1. ER - ...

ABCC6 is expressed mainly in liver and kidney, and phenotypes associated with PXE appear to be complemented by a circulating factor11; thus, restoration of the natural substrate of ABCC6 may be of clinical benefit in the setting of PXE.23 Although Abcc6-deficient mice do not develop myocardial infarction, as noted in some patients with PXE, the data herein demonstrates a significant increase in infarct size using the mouse model subjected to cardiac I/R. This was accompanied by an increased inflammatory infiltrate but no change in cardiac calcification or perfusion, reflected by a similar region at risk following I/R, and no change in baseline cardiac function as determined by echocardiography. Our results suggest that the substrate of ABCC6 may have a wider therapeutic value, including broader use in the setting of myocardial infarction. Importantly, the consequences of Abcc6 deficiency on adverse outcomes following cardiac I/R may occur at the level of the cardiac myocyte, which is a novel ...

Keywords: Ethanol, ischemia-reperfusion injury, preconditioning, heart. Abstract: Epidemiological studies demonstrate that excessive drinking is associated with hypertension, cerebral bleeding and loss of cardiac contractility. Conversely, studies have shown that mortality rates for people who regularly drink ethanol in moderation are lower than in abstainers, primarily due to decreased fatal ischemic heart disease. Further, moderate ethanol consumers have lower rates of myocardial infarction compared with abstainers. These beneficial cardiac effects may be due to pleiotropic effects of ethanol on lipids, platelets, and fibrinolytic activity. During the past decade, studies conducted in several animal models have revealed that light to moderate regular ethanol consumption renders hearts more tolerant to myocardial ischemia-reperfusion injury; to a degree similar to cardiac ischemic preconditioning (brief episodes of ischemia dramatically limit infarct size following prolonged ischemia). Recent ...

Normal myocardium can derive energy for contraction and relaxation from oxidative metabolism of a variety of substrates. This investigation examined the influence of substrate availability early during reperfusion on the substrate pattern of oxidative metabolism and recovery of contractile function. For this purpose, isovolumically beating isolated rat hearts, perfused retrogradely with erythrocyte-supplemented buffer containing 0.4 mmol/L palmitate and 11 mmol/L glucose, were subjected to 40 minutes of no-flow ischemia. Hearts were reperfused with medium containing selected concentrations of palmitate and glucose. The substrate pattern for oxidative metabolism was determined on the basis of myocardial release of 14CO2 after equilibration of the hearts during the initial 15 minutes of reperfusion with either [1-14C]palmitate or [U-14C]glucose. In continuously perfused control hearts, glucose oxidation was largely inhibited by palmitate. During postischemic reperfusion, oxidation of glucose was ...

Abstract. Objective: To investigate the effect of ischemic postconditioning on protein aggregation caused by transient ischemia and reperfusion and to clarify its underlying mechanism.. Methods: Two-vessel-occluded transient global ischemia rat model was used. The rats in ischemic postconditioning group were subjected to three cycles of 30-s/30-s reperfusion/clamping after 15min of ischemia. Neuronal death in the CA1 region was observed by hematoxylin-eosin staining, and number of live neurons was assessed by cell counting under a light microscope. Succinyl-LLVY-AMC was used as substrate to assay proteasome activity in vitro. Protein carbonyl content was spectrophotometrically measured to analyze protein oxidization. Immunochemistry and laser scanning confocal microscopy were used to observe the distribution of ubiquitin in the CA1 neurons. Western blotting was used to analyze the quantitative alterations of protein aggregates, proteasome, hsp70 and hsp40 in cellular fractions under different ...

In the present study, dogs were pretreated with intravenous digoxin, 0.0125 mg/kg/day, for 6 to 7 consecutive days to achieve clinically relevant serum concentrations; untreated animals were used as control subjects. After pretreatment, nine digoxin-

TY - JOUR. T1 - Acute inflammatory reaction after myocardial ischemic injury and reperfusion. Development and use of a neutrophil-specific antibody. AU - Hawkins, Hal K.. AU - Entman, Mark L.. AU - Zhu, Jessica Y.. AU - Youker, Keith A.. AU - Berens, Kurt. AU - Doré, Monique. AU - Smith, C. Wayne. PY - 1996/6. Y1 - 1996/6. N2 - Reperfusion of the infarcted canine myocardium after 1 hour of ischemia is associated with an acute inflammatory infiltrate at the border of the infarct. In this paper, we demonstrate that early margination and emigration of neutrophils originate in thin-walled (∼5-μm) venous cisterns that average 200 μm in length and vary from 10 to 70 μm in width and show strong constitutive expression of both ICAM-1 and P-selectin; this class of vessels (venous cisterns) appears to be a unique feature in heart. A monoclonal antibody (SG8H6) with specificity for canine neutrophils was developed that allowed much more sensitive immunohistochemical detection of neutrophils in tissue ...

Despite prompt reperfusion by primary percutaneous coronary intervention (PPCI), the mortality and morbidity of patients presenting with an acute ST-segment elevation myocardial infarction (STEMI) remain significant with 9% death and 10% heart failure at 1 year. In these patients, one important neglected therapeutic target is myocardial reperfusion injury, a term given to the cardiomyocyte death and microvascular dysfunction which occurs on reperfusing ischaemic myocardium. A number of cardioprotective therapies (both mechanical and pharmacological), which are known to target myocardial reperfusion injury, have been shown to reduce myocardial infarct (MI) size in small proof-of-concept clinical studies-however, being able to demonstrate improved clinical outcomes has been elusive ...

Reperfusion of ischemic tissue leads to the generation of oxygen derived free radicals which plays an important role in cellular damage. Objective of the current study is to evaluate the cardio-protective and antioxidant effect of diosmin on ischemia-reperfusion related cardiac dysfunction, oxidative stress and apoptosis. Diosmin (50 and 100 mg/kg body weight (bw)) was given every day to the rats orally throughout the experimental period. Ischemia/reperfusion protocol was carried out ex vivo using langendorff perfusion method and the cardiac functional recovery was assessed in terms of percentage rate pressure product ...

Introduction: Ischemia/Reperfusion (IR) injury mainly causes the increase of enzymes involved in myocytes injury including CK-MB (creatine kinase-MB) isoenzyme and LDH (lactate dehydrogenase). Leakage of CK-MB isoenzyme and LDH from myocardial tissues to blood is indicator of acute myocardial infarction. The aim of this study was to assess the effect of HEMADO on IR injury and its relationship with mitochondrial ATP-sensitive K+ channels (mitoKATP) in rat heart. Methods: Twenty eight male Wistar rats (250-300g) were divided into four groups (seven members in each group): control (without ischemia), I/R (with ischemia+without HEMADO), ischemia received HEMADO (HEMADO), ischemia received HEMADO and 5-HD (5-hydroxydecanoate, specific mitoKATP channel blocker) (HEMADO+5-HD). The animals were anesthetized and the hearts were quickly removed and mounted on Langendorff apparatus and perfused by Krebs-Henseleit solution under constant pressure and temperature of 37ºC. After 20 minutes of stabilization,

TY - JOUR. T1 - Retrograde continuous warm blood cardioplegia. T2 - A new concept in myocardial protection. AU - Salerno, Tomas A.. AU - Houck, James P.. AU - Barrozo, Carlos A.M.. AU - Panos, Anthony. AU - Christakis, George T.. AU - Abel, James G.. AU - Lichtenstein, Samuel V.. PY - 1991/2. Y1 - 1991/2. N2 - This report presents the results in our first clinical series of patients receiving continuous warm blood cardioplegia through the coronary sinus. Warm oxygenated blood cardioplegia has certain theoretical advantages, such as continuously supplying oxygen and substrates to the arrested heart while avoiding the side effects of hypothermia. Retrograde infusion of cardioplegia also offers certain advantages (eg, in valve operations and in patients with severe coronary artery disease) that are complementary to warm blood cardioplegia. Retrograde warm blood cardioplegia was used in 113 consecutive patients (85 men and 28 women with a mean age of 61 years) undergoing various procedures. Three ...

TY - JOUR. T1 - Long-term treatment with eicosapentaenoic acid ameliorates myocardial ischemia-reperfusion injury in pigs in vivo. T2 - Involvement of rho-kinase pathway inhibition. AU - Gao, Jun Yi. AU - Yasuda, Satoshi. AU - Tsuburaya, Ryuji. AU - Ito, Yoshitaka. AU - Shiroto, Takashi. AU - Hao, Kiyotaka. AU - Aizawa, Kentaro. AU - Kikuchi, Yoku. AU - Ito, Kenta. AU - Shimokawa, Hiroaki. N1 - Copyright: Copyright 2012 Elsevier B.V., All rights reserved.. PY - 2011/8. Y1 - 2011/8. N2 - Background: Eicosapentaenoic acid (EPA), the major n-3 fatty acid in fish oil, exerts cardioprotective effects against ischemic heart disease; however, the detailed mechanisms remain to be elucidated. Rho-kinase plays an important role in the pathogenesis of cardiovascular diseases including ischemia-reperfusion (I/R) injury. Thus, the hypothesis that long-term EPA treatment ameliorates myocardial I/R injury through Rho-kinase pathway inhibition in pigs in vivo was investigated. Methods and Results: Male pigs ...

Cardioprotection against ischemia/reperfusion injury by QiShenYiQi Pill® via ameliorate of multiple mitochondrial dysfunctions Jing Rui Chen,1-3 Jing Wei,1-3 Ling Yan Wang,1-3 Yan Zhu,1-3 Lan Li,1-3 Mary Akinyi Olunga,1-3 Xiu Mei Gao,1-3 Guan Wei Fan1-31Tianjin State Key Laboratory of Modern Chinese Medicine, Tianjin, Peoples Republic of China; 2Key Laboratory of Pharmacology of Traditional Chinese Medicine Formulae, Ministry of Education, 3Institute of Traditional Chinese Medicine, Tianjin University of Traditional Chinese Medicine, Tianjin, Peoples Republic of ChinaAim: To investigate the potential cardioprotective effects of QiShenYiQi Pill® (QSYQ) on myocardial ischemia/reperfusion (I/R) injury through antioxidative stress and mitochondrial protection.Methods and results: Sprague Dawley rats were pretreated with QSYQ or saline for 7 days and subjected to ischemia (30 minutes occlusion of the left anterior descending coronary artery) and reperfusion (120 minutes). Cardiac functions were evaluated

TY - JOUR. T1 - Profound cardioprotection with chloramphenicol succinate in the swine model of myocardial ischemia-reperfusion injury. AU - Sala-Mercado, Javier A.. AU - Wider, Joseph. AU - Reddy Undyala, Vishnu Vardhan. AU - Jahania, Salik. AU - Yoo, Wonsuk. AU - Mentzer, Robert M.. AU - Gottlieb, Roberta A.. AU - Przyklenk, Karin. N1 - Copyright: Copyright 2010 Elsevier B.V., All rights reserved.. PY - 2010/9/14. Y1 - 2010/9/14. N2 - Background-: Emerging evidence suggests that adaptive induction of autophagy (the cellular process responsible for the degradation and recycling of proteins and organelles) may confer a cardioprotective phenotype and represent a novel strategy to limit ischemia-reperfusion injury. Our aim was to test this paradigm in a clinically relevant, large animal model of acute myocardial infarction. Methods and results-: Anesthetized pigs underwent 45 minutes of coronary artery occlusion and 3 hours of reperfusion. In the first component of the study, pigs received ...

Context: Panax ginseng C. A. Mey (Araliaceae) has been widely used in clinic for treatment of cardiovascular diseases in China. Ginsenoside Rb3 is the main chemical component of Panax ginseng. Objective: The aim of this study was to evaluate the effect of ginsenoside Rb3 on myocardial ischemia-reperfusion injury in rats. Methods: Sprague−Dawley rats were orally treated with Rb3 (5, 10 or 20 mg/kg) daily for 3 days followed by subjecting to left anterior descending coronary artery ligation for 30 min and reperfusion for 24 h. Results: This study showed that ginsenoside Rb3 treatment resulted in a reduction in myocardial infarct size. Ginsenoside Rb3 significantly attenuated the changes of creatine kinase activity and lactate dehydrogenase activity. The cardioprotective effect of ginsenoside Rb3 was further confirmed by histopathological examination. Ginsenoside Rb3 alleviated the increase of malondialdehyde content and the decrease of superoxide dismutase activity in left ventricle. Treatment ...

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The present study determined the dynamic change of adiponectin (APN, a cardioprotective adipokine), its receptor expression, and their impact upon myocardial ischemia/reperfusion (MI/R) injury during type 1 diabetes mellitus (T1DM) progression, and involved underlying mechanisms. Diabetic state was induced in mice via multiple intraperitoneal injections of low-dose streptozotocin. The dynamic change of plasma APN concentration and cardiac APN receptor-1 and -2 (AdipoR1/2) expression were assessed immediately after diabetes onset (0 wk) and 1, 3, 5, and 7 wk thereafter. Indicators of MI/R injury (infarct size, apoptosis, and LDH release) were determined at 0, 1, and 7 wk of DM duration. The effect of APN on MI/R injury was determined in mice subjected to different diabetic durations. Plasma APN levels (total and HMW form) increased, whereas cardiac AdipoR1 expression decreased early after T1DM onset. With T1DM progression, APN levels were reduced and cardiac AdipoR1 expression increased. MI/R injury was

Introduction/Aim Ischemia Reperfusion injury is a poorly understood entity with wide-ranging clinical implications touching on most fields of clinical medicine. Using skin flap and hind limb models of injury in the mouse we attempt to reduce ischemia reperfusion injury by targeting different parts of the ischemia reperfusion injury pathway. Methods Dorsal lateral thoracic artery island skin flaps (3.5x1.5 cm) were elevated in C57BL/6 mice and rendered ischemic for 10 hours by placing a 7 mm microclamp on the vascular pedicle followed by 7 days of reperfusion. Hind-limb ischemia (was achieved with orthodontic rubber bands applied above the greater trochanter of male C57BL/6 mice using a McGivney Haemorrhoid Ligator. Limbs underwent ischemia for two hours followed by 24 hours reperfusion prior to euthanasia. Animals were treated with intravenous Poloxamer 188 and P8 IgM-binding protein to assess their effect on ischemiareperfusion injury. Results Administration of P188 prior to ischemia gave an ...

1. Hausenloy DJ, Yellon DM. Ischaemic conditioning and reperfusion injury. Nat Rev Cardiol. 2016;13:193-209 2. Chen L, Zhang D, Yu L, Dong H. Targeting MIAT reduces apoptosis of cardiomyocytes after ischemia/reperfusion injury. Bioengineered. 2019;10:121-32 3. Liu T, Song D, Dong J, Zhu P, Liu J, Liu W. et al. Current understanding of the pathophysiology of myocardial fibrosis and its quantitative assessment in heart failure. Front Physiol. 2017;8:238 4. Yang X, Fu J, Wan H, Liu Z, Yu L, Yu B. et al. Protective roles and mechanisms of taurine on myocardial hypoxia/reoxygenation-induced apoptosis. Acta Cardiol Sin. 2019;35:415-24 5. Lal H, Ahmad F, Zhou J, Yu JE, Vagnozzi RJ, Guo Y. et al. Cardiac fibroblast glycogen synthase kinase-3β regulates ventricular remodeling and dysfunction in ischemic heart. Circulation. 2014;130:419-30 6. Hao G, Han Z, Meng Z, Wei J, Gao D, Zhang H. et al. Ets-1 upregulation mediates angiotensin II-related cardiac fibrosis. Int J Clin Exp Pathol. 2015;8:10216-27 7. ...

AIM To investigate the protective effects of metallothionein induced by Zn 2+ on ischemia/reperfusion myocardium in isolated rat heart. METHODS 32 Sprague-Dawley rats were randomly divided into 4 groups (n=8, respectively): control group, ischemia/reperfusion (I/R) group, Zn 2+ pretreated group (ZPC), PD98059 (inhibitor of extracellular signal regulated protein kinase)+Zn 2+ pretreated group (PZPC). The levels of creatime kinase (CK), lacatate dehydrogenase (LDH) and adenosine triphosphate (ATP), which indicated myocardium injury, and the cardiac function(LVSP and±dp/dt max), were observed in this study. The expression levels of MT were valued by the 109Cd/hemoglobin affinity assays. RESULTS The expression level of MT was higher in ZPC group than in control group and I/R group. Compared with I/R group, the level of LDH and CK was reduced, ATP content was increased, and cardiac function (LVSP and±dp/dt max) was improved (P0.01) in ZPC group. The correspond data between

TY - JOUR. T1 - Remifentanil protects myocardium through activation of anti-apoptotic pathways of survival in ischemia-reperfused rat heart. AU - Kim, H. S.. AU - Cho, J. E.. AU - Hong, S. W.. AU - Kim, S. O.. AU - Shim, J. K.. AU - Kwak, Y. L.. PY - 2010. Y1 - 2010. N2 - Remifentanil is a commonly used opioid in anesthesia with cardioprotective effect in ischemia-reperfused (I/R) heart. We evaluated the influence of remifentanil on myocardial infarct size and expressions of proteins involved in apoptosis in I/R rat heart following various time protocols of remifentanil administration. Artificially ventilated anesthetized Sprague-Dawley rats were subjected to a 30 min of left anterior descending coronary artery occlusion followed by 2 h of reperfusion. Rats were randomly assigned to one of five groups; Sham, I/R only, remifentanil preconditioning, postconditioning and continuous infusion group. Myocardial infarct size, the phosphorylation of ERK1/2, Bcl2, Bax and cytochrome c and the expression ...

Xuesaitong injection (XST), which mainly consists of Panax notoginseng saponins, has been widely used for treating cardio-cerebral vascular diseases. However, the underlying mechanisms of XST associated with its cardioprotective effects are still unclear. To identify the potential target proteins of XST, two

TY - JOUR. T1 - Exogenous high-mobility group box 1 improves myocardial recovery after acute global ischemia/reperfusion injury. AU - Abarbanell, Aaron M.. AU - Hartley, Jacob A.. AU - Herrmann, Jeremy L.. AU - Weil, Brent R.. AU - Wang, Yue. AU - Manukyan, Mariuxi C.. AU - Poynter, Jeffrey A.. AU - Meldrum, Daniel R.. PY - 2011/3/1. Y1 - 2011/3/1. N2 - Background: High-mobility group box 1 (HMGB1) is a mediator of inflammation with dose-dependent effects. In the setting of regional myocardial infarction, a high-dose HMGB1 treatment decreases myocardial function, whereas low-dose HMGB1 improves function; however, it is unknown what role HMGB1 has in the setting of global ischemia/reperfusion (I/R) injury. We hypothesized that a low-dose HMGB1 treatment would improve myocardial functional recovery and decrease infarct size after global I/R injury in association with increased levels of cardioprotective paracrine factors and decreased inflammation. Methods: Adult rat hearts were isolated and ...

Evidence-Based Complementary and Alternative Medicine (eCAM) is an international peer-reviewed, Open Access journal that seeks to understand the sources and to encourage rigorous research in this new, yet ancient world of complementary and alternative medicine.

An increasing number of preclinical and clinical studies show that high-dose i. v. vitamin C can mitigate systemic, cerebral and myocardial ischemia/reperfusion injury. Vitamin C administration has been associated with reduced oxidative stress, myocardial injury and arrhythmias and improved microcirculation, neurological outcome and survival, although not all studies showed benefit. Because of the common pathophysiological pathway of sepsis and ischemia/reperfusion injury, the potential role of vitamin C for ischemia/reperfusion injury is further supported by the results of preliminary sepsis studies, showing earlier recovery from organ failure and higher survival rates. Therefore, early, high-dose i. v. vitamin C is a promising therapeutic intervention after cardiac arrest to diminish the systemic ischemia/reperfusion injury due to overwhelming oxidative stress. The supportive evidence from preclinical and clinical studies is too large to continue considering early high-dose i. v. vitamin C as ...

Aging and skeletal muscle ischemia/reperfusion (I/R) injury both lead to skeletal\r\nmuscle dysfunction, evidenced by decreased contractile force generation, particularly in\r\nglycolytic muscle. The deficits in I/R are more severe and persistent in aged animals.\r\nPrevious studies in our lab led us to hypothesize that the expression of the glycolytic\r\nenzyme glyceraldehyde-3-phosphate dehydrogenase may be altered following I/R. We\r\nfurther hypothesized that aging would enhance the oxidative stress and oxidative damage\r\nexperienced by the muscle. GAPDH protein levels were measured by Western blotting.\r\nWe observed that the enzyme is significantly decreased at 3 and 5 days of reperfusion in\r\nthe young muscle, while the enzyme was significantly decreased in the aged muscle at 1,\r\n3, 5, and 7 days. Using PCR, we compared GAPDH mRNA levels at 5 days reperfusion\r\nand found that the I/R tissue from both young and old have significant increases in\r\nGAPDH transcript at this time point ...

Transient cerebral ischemia often results in secondary ischemic/reperfusion injury, the pathogenesis of which remains unclear. This study provides a comprehensive, temporal description of the molecular events contributing to neuronal injury after transient cerebral ischemia. Intraluminal middle cerebral artery occlusion (MCAO) was performed to induce a 2-h ischemia with reperfusion. Microarray analysis was then performed on the infarct cortex of wild-type (WT) and glutathione peroxidase-1 (a major antioxidant enzyme) knockout (Gpx1(-/-)) mice at 8 and 24h postreperfusion to identify differential gene expression profile patterns and potential alternative injury cascades in the absence of Gpx1, a crucial antioxidant enzyme, in cerebral ischemia. Genes with at least ±1.5-fold change in expression at either time point were considered significant. Global transcriptomic analyses demonstrated that 70% of the WT-MCAO profile overlapped with that of Gpx1(-/-)-MCAO, and 28% vice versa. Critical analysis ...

BACKGROUND: New evidence shows that high density lipoproteins (HDL) have protective effects beyond their role in reverse cholesterol transport. Reconstituted HDL (rHDL) offer an attractive means of clinically exploiting these novel effects including cardioprotection against ischemia reperfusion injury (IRI). However, basic rHDL composition is limited to apolipoprotein AI (apoAI) and phospholipids; addition of bioactive compound may enhance its beneficial effects. OBJECTIVE: The aim of this study was to investigate the role of rHDL in post-ischemic model, and to analyze the potential impact of sphingosine-1-phosphate (S1P) in rHDL formulations. METHODS AND RESULTS: The impact of HDL on IRI was investigated using complementary in vivo, ex vivo and in vitro IRI models. Acute post-ischemic treatment with native HDL significantly reduced infarct size and cell death in the ex vivo, isolated heart (Langendorff) model and the in vivo model (-48%, p<0.01). Treatment with rHDL of basic formulation ...

TY - JOUR. T1 - S1P lyase. T2 - A novel therapeutic target for ischemia reperfusion injury of the heart. AU - Bandhuvula, Padmavathi. AU - Honbo, Norman. AU - Wang, Guan Ying. AU - Jin, Zhu Qiu. AU - Fyrst, Henrik. AU - Zhang, Meng. AU - Borowsky, Alexander D. AU - Dillard, Lisa. AU - Karliner, Joel S.. AU - Saba, Julie D.. PY - 2011/5. Y1 - 2011/5. N2 - Sphingosine-1-phosphate (S1P) is a bioactive sphingolipid that promotes cardiomyocyte survival and contributes to ischemic preconditioning. S1P lyase (SPL) is a stress-activated enzyme responsible for irreversible S1P catabolism. We hypothesized that SPL contributes to oxidative stress by depleting S1P pools available for cardioprotective signaling. Accordingly, we evaluated SPL inhibition as a strategy for reducing cardiac ischemia-reperfusion (I/R) injury. We measured SPL expression and enzyme activity in murine hearts. Basal SPL activity was low in wild-type cardiac tissue but was activated in response to 50 min of ischemia (n = 5, P , 0.01). ...

Madecassoside (MA), one of the principle terpenoids in Centella asiatica, has shown protect effect on isolated rat hearts and isolated cardiomyocytes against reperfusion injury in our previous studies. The aim of this study is to investigate if MA also protected against myocardial ischemia-reperfusion injury in vivo. The ischemia infarction model was established in rats. Left ventricular function was monitored during the ischemia-reperfusion period by a multi-channel recorder. After the ischemia-reperfusion process the infarcted areas were assessed. The levels of lactate dehydrogenase (LDH), creatinephosphokinase (CK), malondialdehyde (MDA), super-oxide dismutase (SOD) and C-reactive protein (CRP) in serum were determined. Cardiomyocytic apoptosis was measured by terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) staining. Pre-treatment with MA (50, 10 mg/kg) attenuated myocardial damage characteristic of decreasing infarct size, decreasing LDH and CK release. Activities of ...

Author Summary Myocardial ischemia, commonly observed when arteries supplying the heart become occluded, results when cardiac tissue receives inadequate blood perfusion. In order to minimize the amount of cardiac damage, ischemic tissue must be reperfused. However, reperfusion can result in deleterious effects that leave the heart muscle sicker than if the ischemia had been allowed to continue. Examples of these reperfusion injuries include lethal arrhythmias and an increased region of cell death. Some of the early events that result in reperfusion injury include changes in pH and an overload of sodium inside the cell. During reperfusion, the sodium-proton exchanger (NHE) removes protons from the cell in an effort to restore normal pH, in turn importing sodium ions. Many strategies have been attempted to prevent reperfusion injury, including inhibition of the NHE, with little clinical effect. Using a mathematical model that we developed to study ischemia and reperfusion in cardiac cells, we found that

We analyzed the effects of acute ischemia-reperfusion (KIR) injury on the status of kidney function and architecture in dipeptidyl peptidase4-difficient (DPP4(D)) rats and the effect of remote small bowel ischemia-reperfusion (BIR) preconditioning. DPP4-deficient (DPP4(D)) and normal Fischer344 (F344) rats were divided into 6 groups: (1) sham-F344, (2) sham-DPP4(D), (3) KIR-F344 (4) KIR-DPP4(D), (5) DPP4(D)-KIR-extendin-9-39 and (6) BIR-KIR-F344. Blood creatinine and urea nitrogen levels and the urinary protein-to-creatinine ratio was higher in KIR-F344 rats than BIR-KIR-F344 or KIR-DPP4(D) rats 72 h after acute KIR. Conversely, the circulating glucagon-like peptide 1 (GLP-1) levels were higher in BIR-KIR-F344 and KIR-DPP4(D) than KIR-F344 rats after acute KIR. KIR-F344 rats showed greater inflammation, oxidative stress, apoptosis, DNA damage and kidney injury than other rat groups. Damage to the kidney architecture in KIR-F344 rats was greater than in BIR-KIR-F344 or KIR-DPP4(D) rats. ...

The effect of hyaluronidase on myocardial ischemic injury was examined in 13 patients with acute myocardial infarction, and the results were compared with 11 patients who did not receive hyaluronidase. A 35-electrode precordial mapping method was used to assess the rate of resolution of ST segment elevations. In the 11 control patients, the sum of ST segment elevations (ΣST) fell after 2 hours to an average of 93.5% ± 17.3% (SEM) and after 24 hours to 89.6% ± 7.6% of the initial values, while the number of electrodes exhibiting ST segment elevations exceeding 0.1 mV (NST) fell to 98.0% ± 12.3% and 94.3% ± 10.4% of the initial values respectively. In the hyaluronidase-treated group, at the same time ΣST fell significantly more (P , 0.05), to 54.1% ± 5.0% and 51.3% ± 11.8% and NST was also more markedly reduced (P , 0.05) to 50.7% ± 7.8% and 50.1% ± 12.4%, thus indicating that hyaluronidase can accelerate the reduction of myocardial ischemic injury in patients with acute myocardial ...

Heme Oxygenase-1 Induction Improves Cardiac Function following Myocardial Ischemia by Reducing Oxidative Stress. . Biblioteca virtual para leer y descargar libros, documentos, trabajos y tesis universitarias en PDF. Material universiario, documentación y tareas realizadas por universitarios en nuestra biblioteca. Para descargar gratis y para leer online.

Discussion. In this study, we used the ischemia/reperfusion model developed for kidney function and injury studies at the Department of Anesthesiology, Botucatu Medical School. This model consists of right nephrectomy in all animals, followed by randomization of the animals into four groups of 10 animals per group: Ischemia, Ischemia + drug, Non-ischemia, and Non-ischemia + drug. Thus, parecoxib was tested in two groups, in the presence and absence of I/R (IP and NIP groups), and NGAL levels were measured in all groups at four times to evaluate renal function.. Nephrectomy followed by ischemia/reperfusion may trigger mechanisms of renal preconditioning, reducing histological lesions and preserving or facilitating recovery of renal function in the ischemic kidney. For instance, animals that had not been nephrectomized prior to ischemia/reperfusion had oliguric renal failure, whereas animals that had been nephrectomized prior to I/R developed polyuric renal failure with better prognosis and ...

TY - JOUR. T1 - Enhanced cardioprotection against ischemia-reperfusion injury with combining sildenafil with low-dose atorvastatin. AU - Rosanio, Salvatore. AU - Ye, Yumei. AU - Atar, Shaul. AU - Rahman, Atiar M.. AU - Freeberg, Sheldon Y.. AU - Huang, Ming He. AU - Uretsky, Barry F.. AU - Birnbaum, Yochai. PY - 2006/2. Y1 - 2006/2. N2 - Purpose: Both ATV and SL reduce myocardial infarct size (IS) by enhancing expression and activity of NOS isoforms. We investigated whether atorvastatin (ATV) and sildenafil (SL) have synergistic effects on myocardial infarct size (IS) reduction and enhancing nitric oxide synthase (NOS) expression. Method: Rats were randomized to nine groups: ATV-1 (1 mg/kg/d); ATV-10 (10 mg/kg/d); SL-0.7 (0.7 mg/kg); SL-1 (1 mg/kg); ATV-1 + SL-0.7; water alone (controls); 1400W (iNOS inhibitor; 1 mg/kg); ATV-10 + 1400W; and ATV-1 + SL-0.7 + 1400W. ATV was administered orally for 3 days. SL was administered intraperitoneally 18 h before surgery and 1400W intravenously 15 min ...

Ischemia/reperfusion (I/R) injury remains a major complication of liver resection, transplantation, and hemorrhagic shock. Although the mechanisms that contribute to hepatic I/R are complex and diverse involving the interaction of cell injury in hepatocytes, immune cells, and endothelium, mitochondrial dysfunction is a cardinal event culminating in hepatic reperfusion injury. Mitochondrial autophagy, so-called mitophagy, is a key cellular process that regulates mitochondrial homeostasis and eliminates damaged mitochondria in a timely manner. Growing evidence accumulates that I/R injury is attributed to defective mitophagy. This review aims to summarize the current understanding of autophagy and its role in hepatic I/R injury and highlight the various therapeutic approaches that have been studied to ameliorate injury.

Reperfusion injury or reperfusion insult, sometimes called ischemia-reperfusion injury (IRI) or reoxygenation injury, is the tissue damage caused when blood supply returns to tissue (re- + perfusion) after a period of ischemia or lack of oxygen (anoxia or hypoxia). The absence of oxygen and nutrients from blood during the ischemic period creates a condition in which the restoration of circulation results in inflammation and oxidative damage through the induction of oxidative stress rather than (or along with) restoration of normal function. Reperfusion of ischemic tissues is often associated with microvascular injury, particularly due to increased permeability of capillaries and arterioles that lead to an increase of diffusion and fluid filtration across the tissues. Activated endothelial cells produce more reactive oxygen species but less nitric oxide following reperfusion, and the imbalance results in a subsequent inflammatory response. The inflammatory response is partially responsible for ...

Many pharmacological agents were investigated for the prevention of renal ischemic reperfusion (IR) injury as well as the phosphodiesterase (PDE) inhibitors. The aim of the study was to examine the possible renoprotective effect of enoximone as a member of this family on IR injury. Thirty-six Wistar-Albino rats were allocated to six groups. Sham (S) and control groups (E1, E2) only received 0.09% NaCl, 5 mg/kg and 10 mg/kg enoximone via caudal caval vein, respectively. In ischemia (I) and treatment groups (IE1, IE2), the rats were subjected to bilateral renal artery occlusion and were given 0.09% NaCl, 5 mg/kg and 10 mg/kg enoximone in the same route, respectively. Bilateral kidneys were removed at the sixth hour of laparotomy for histopathological and biochemical analysis, such as superoxide dismutase, myeloperoxidase, malonyldialdehyde, and nitric oxide end products. Blood samples were taken in order to evaluate renal function tests. The data were analyzed by using one-way analysis of ...

TY - JOUR. T1 - Cardiac vagal afferent stimulation by free radicals during ischaemia and reperfusion. AU - Schultz, Harold D.. AU - Ustinova, Elena E.. PY - 1996/1/1. Y1 - 1996/1/1. N2 - 1. Myocardial ischaemia and reperfusion can evoke excitation of cardiac vagal afferent nerve endings and activation of a cardiogenic depressor reflex (Bezold-Jarisch effect). We postulate that oxygen free radicals, which are well known to be produced during ischaemia and reperfusion, contribute to this excitation. 2. Activity from vagal afferent fibres in rats, whose endings were located in the walls of all four chambers of the heart, was recorded in response to topical application of pro-oxidant chemicals to the surface of the heart. Activity was also recorded from vagal afferent fibres, whose endings were located in the left ventricle, in response to occlusion of the left anterior coronary artery (LAC) for 30 min and subsequent reperfusion. A majority of the recorded fibres were classified as chemosensitive ...

TY - JOUR. T1 - Gender affects reperfusion injury in rat liver. AU - Gasbarrini, Antonio. AU - Addolorato, Giovanni. AU - Gasbarrini, Giovanni Battista. AU - Di Campli, Cristiana. AU - Castagneto, Marco. AU - Padalino, Cristiano. AU - Pola, Paolo. PY - 2001. Y1 - 2001. KW - rat liver. KW - reperfusion injury. KW - rat liver. KW - reperfusion injury. UR - http://hdl.handle.net/10807/20509. M3 - Article. SP - 1305. EP - 1312. JO - American Journal of Digestive Diseases. JF - American Journal of Digestive Diseases. SN - 0002-9211. ER - ...

Context: Traditionally, Clematis tangutica Korsh. (Ranunculaceae) is used as a Tibetan herb for treating indigestion and blood stasis in China. Recently, a flavonoid glycoside, apigenin-7-O-ß-d-(6â ³-p-coumaroyl)-glucopyranoside (APG), was isolated from the whole plant of C. tangutica.Objective: To investigate the cardioprotective effects of APG against myocardial ischaemia/reperfusion injury (MI/RI) and the possible mechanism.Materials and methods: Animals were subjected to 30 min/3 h MI/RI model. At the end of reperfusion, infarct size (IS), histopathology, serum levels CK-MB, LDH, TNF-α, IL-6 and MPO activities were detected. Phospho-IκB-α, ICAM-1 and NF-κB were assessed in vivo. Neonatal rat cardiomyocytes were pre-treated with or without APG, followed by stimulation with 8 h/2 h oxygen and glucose deprived/reoxygenation (OGD/R) model. Cell viability, LDH and cardiomyocyte apoptosis were assessed. The expression levels of phospho-IκB-α and NF-κB were measured in vitro.Results: ...

OBJECTIVES: Complement activation is considered an important mediator of myocardial ischaemia/reperfusion (I/R) injury. Although complement inhibitors are highly effective in animals, clinical trials fail to show a substantial benefit in humans. This raises questions on the role of complement activation in human myocardial I/R injury. METHODS: Soluble C5b-9, i.e. terminal complement complex, and C5a were assessed in patients with non-ischaemic (n = 10) and ischaemic heart failure (n = 10), and p... Abstract ...

TY - JOUR. T1 - Hyperoxic ventilation exacerbates lung reperfusion injury. AU - Ellman, Peter I.. AU - Alvis, Jeffrey S.. AU - Tache-Leon, Carlos. AU - Singh, Ramesh. AU - Reece, T. Brett. AU - Kern, John A.. AU - Tribble, Curtis G.. AU - Kron, Irving L.. N1 - Funding Information: Supported by the National Institutes of Health under RO1 grant HL506093-03. PY - 2005/11. Y1 - 2005/11. N2 - Objective: It is well known that hyperoxia can be potentially harmful to the ventilated patient, although little is known about the potential effects in the setting of lung reperfusion. We hypothesized that hyperoxic ventilation at the time of reperfusion could worsen the effects of lung reperfusion injury. Methods: Using an ex vivo, blood perfused, isolated rabbit lung system, we evaluated the effects of hyperoxic (fraction of inspired oxygen = 100%, n = 10) versus normoxic (room air, n = 10) ventilation after 18 hours of cold ischemia. Lungs were ventilated and perfused for 2 hours. A control group was ...

TY - JOUR. T1 - The effect of hyperbaric oxygenation on ischemia-reperfusion injury of the small intestine. AU - Yamada, T.. AU - Taguchi, T.. AU - Hirata, Y.. AU - Toyohara, T.. AU - Hirose, R.. AU - Suita, S.. AU - Yagi, H.. PY - 1994/1/1. Y1 - 1994/1/1. UR - http://www.scopus.com/inward/record.url?scp=0028359583&partnerID=8YFLogxK. UR - http://www.scopus.com/inward/citedby.url?scp=0028359583&partnerID=8YFLogxK. M3 - Article. C2 - 8030012. AN - SCOPUS:0028359583. VL - 26. SP - 1506. EP - 1507. JO - Transplantation Proceedings. JF - Transplantation Proceedings. SN - 0041-1345. IS - 3. ER - ...

The Food and Drug Administration (FDA) is announcing a public workshop to discuss the effects of ischemia/reperfusion injury (IRI) on outcomes in kidney transplantation. This public workshop is intended to obtain information from health care providers, academic, and industry on various aspects of the pathophysiology, clinical management, and outcomes following IRI. The meeting will include a discussion of animal models, devices, and clinical trial design. The input from this public workshop will help in developing topics for further discussion and may serve to inform recommendations on clinical trial design for products for the mitigation of IRI and/or for the prophylaxis and/or treatment of delayed graft function (DGF) and related conditions in kidney transplant recipients.. Registration is free for the public workshop. Interested parties are encouraged to register early because space is limited. Seating will be available on a first-come-first-served basis. To register electronically, email ...

TY - CONF. T1 - Influence of estrogen on the early recovery of hepatobiliary secretory function after ischemia/reperfusion injury in rats [abstract[. AU - de Vries, A.H. AU - Ponds, F.A.M. AU - Padbury, Robert. AU - Porte, Robert. AU - Nieuwenhuijs, Vincent. AU - Barritt, Gregory. PY - 2009. Y1 - 2009. M3 - Paper. T2 - 44th Annual Meeting of the European Association for the study of the liver (EASL). Y2 - 22 April 2009 through 26 April 2009. ER - ...

TY - GEN. T1 - Glutaminase in ischaemia reperfusion injury. AU - Heel, Kathy. AU - Blennerhasett, L.. AU - Kong, S-E.. AU - Mccauley, Rosalie. AU - Hall, John. PY - 1998. Y1 - 1998. M3 - Conference paper. VL - 68. SP - 522. BT - Not available. A2 - Faris, I.. A2 - Fletcher, J.. A2 - Ludbrook, J.. PB - Blackwell. CY - Carlton, Victoria, Australia. ER - ...

Ischemia reperfusion injury is a complex process consisting of a seemingly chaotic but actually organized and compartmentalized shutdown of cell function, of which oxidative stress is a key component. Studying oxidative stress, which results in an imbalance between reactive oxygen species (ROS) production and antioxidant defense activity, is a multi-faceted issue, particularly considering the double function of ROS, assuming roles as physiological intracellular signals and as mediators of cellular component damage. Herein, we propose a comprehensive overview of the tools available to explore oxidative stress, particularly in the study of ischemia reperfusion. Applying chemistry as well as biology, we present the different models currently developed to study oxidative stress, spanning the vitro and the silico, discussing the advantages and the drawbacks of each set-up, including the issues relating to the use of in vitro hypoxia as a surrogate for ischemia. Having identified the limitations of historical

TY - JOUR. T1 - Regulation of Inositol 1,4,5-triphosphate receptor, type 1 (IP3R1) in hypoxic/reperfusion injury of white matter. AU - Kesherwani, Varun. AU - Agrawal, Sandeep K.. PY - 2012/6/1. Y1 - 2012/6/1. N2 - Objective: Calcium overloading is responsible for initiating the cell death in neuronal tissue after hypoxic injury. Inositol 1,4,5-triphosphate receptors (IP3Rs) is an important calcium channel which regulates cellular calcium homeostasis. IP3R1 is widely expressed in brain and spinal tissue. In the present study, we have studied the regulation of IP3R1 in hypoxic/reperfusion injury of spinal cord dorsal column in vitro. Methods: Dorsal columns were isolated from the spinal cord of adult rats and injury was induced by exposing to hypoxic condition for 1 hour. After injury, reperfusion was carried out for 0, 2, 4, and 8 hours. Tissues were collected and processed for western blotting, immunohistochemistry and real-time PCR. Results: In the present study, we have found increased ...

This study was undertaken to evaluate whether peroxisome proliferator-activated-receptor-gamma (PPAR-gamma) agonist-rosiglitazone (ROSI) induces postischemic functional recovery in Langendorf heart model. Hearts isolated from normal rats were subjected to 20 min of normoxia or 25 min zero-flow ischemia followed by 50 min reperfusion. In this acute protocol, ROSI (20 microgram/ml) administered 10 min before ischemia had no effect on hemodynamic cardiac function, but had protective effect on lipid peroxidation in in vitro experiments. In chronic protocol in which ROSI was given by daily gavage (4 mg/kg) for three consecutive days, ROSI could not prevent the hemodynamic alteration on cardiac performance, but has protective effect on the activity of superoxide dismutase (SOD). There was no significant difference in the contents of reduced glutathione (GSH) and catalase activity between ischemia-reperfusion (IR) and ROSI treated IR hearts. Although ROSI had no effect on hemodynamic factor, it had ...

NKT cells play a protective role in ischemia reperfusion (IR) injury, of which the trafficking in the body and recruitment in injured organs can be influenced by immunosuppressive therapy. Therefore, we investigated the effects of rapamycin on kidneys exposed to IR injury in early stage and on trafficking of NKT cells in a murine model. Balb/c mice were subjected to kidney 30 min ischemia followed by 24 h reperfusion. Rapamycin (2.5 ml/kg) was administered by gavage daily, starting 1 day before the operation. Renal function and histological changes were assessed. The proportion of NKT cells in peripheral blood, spleen and kidney was detected by flow cytometry. The chemokines and corresponding receptor involved in NKT cell trafficking were determined by RT-PCR and flow cytometry respectively. Rapamycin significantly improved renal function and ameliorated histological injury. In rapamycin-treated group, the proportion of NKT cells in spleen was significantly decreased but increased in peripheral blood

Rationale: Nitric oxide (NO) bioavailability is reduced in the setting of heart failure. Nitrite (NO2) is a critically important NO intermediate that is metabolized to NO during pathological states. We have previously demonstrated that sodium nitrite ameliorates acute myocardial ischemia/reperfusion injury. Objective: No evidence exists as to whether increasing NO bioavailability via nitrite therapy attenuates heart failure severity after pressure-overload-induced hypertrophy. Methods and results: Serum from patients with heart failure exhibited significantly decreased nitrosothiol and cGMP levels. Transverse aortic constriction was performed in mice at 10 to 12 weeks. Sodium nitrite (50 mg/L) or saline vehicle was administered daily in the drinking water postoperative from day 1 for 9 weeks. Echocardiography was performed at baseline and at 1, 3, 6, and 9 weeks after transverse aortic constriction to assess left ventricular dimensions and ejection fraction. We observed increased cardiac ...