• The present study aimed to investigate the effects of changes in heat shock protein (HSP)90β expression and verify whether HSP90β regulates EAAT2 expression in a cerebral ischemia‑reperfusion injury model. (spandidos-publications.com)
  • A model of cerebral ischemia‑reperfusion was established using the MCAO method. (spandidos-publications.com)
  • These results suggested that HSP90β is involved in the process of cerebral ischemia‑reperfusion injury in rats and that inhibition of HSP90β expression increases EAAT2 levels, conferring a neuroprotective effect in MCAO model rats. (spandidos-publications.com)
  • When ischemic stroke occurs, cerebral ischemia and hypoxia cause the release of excessive excitatory amino acids, mainly glutamic acid and aspartic acid, which exert excitotoxic effects on the central nervous system. (spandidos-publications.com)
  • These excitotoxic effects play important roles in neuronal and blood-brain barrier damage after cerebral ischemia ( 5 , 6 ). (spandidos-publications.com)
  • When cerebral ischemia-reperfusion injury happened in patients, multiple pathological processes occur, such as leukocyte infiltration, platelet, and complement activation, which would result in cognitive dysfunction and inflammation. (hindawi.com)
  • The original phenolic hydroxyl in the puerarin molecules was substituted in order to change the blood-brain barrier permeability and thus enhance the efficacy for preventing cerebral ischemia/reperfusion injury. (hindawi.com)
  • The mouse model of cerebral artery ischemia/reperfusion injury was established to test the anticerebral ischemia-reperfusion injury activity of the puerarin derivatives. (hindawi.com)
  • The results showed that puerarin derivative P1-EA and P2-EA were resulting in an increased lipophilicity that enabled the derivatives to pass more efficiently through the blood-brain barrier, thus, improving the protective effects against cerebral ischemia/reperfusion injury. (hindawi.com)
  • Studies have shown that puerarin reduced cerebral edema in rats with cerebral ischemia-reperfusion injury, removed lipid peroxidation products, enhanced antioxidant capacity, improved antioxidant activity of the brain tissue, and reduced the degree of focal cerebral ischemic injury [ 2 - 4 ]. (hindawi.com)
  • Ischemia-reperfusion injured rat model was induced by middle cerebral artery occlusion and reperfusion (MCAO/R). EA treatment at the DU 20 and DU 24 acupoints treatment were conducted to rats from the 12 h after MCAO/R injury for consecutive 7 days. (biomedcentral.com)
  • It is well-documented that extracellular ATP triggers surrounding glial purinergic receptors signaling pathway and pro-inflammatory cytokines release to aggravate neural injury in cerebral ischemia [ 8 , 9 ]. (biomedcentral.com)
  • Our previous studies have demonstrated that EA protects cerebral neural cells against inflammatory injury after cerebral ischemia, which appears at 24 h to 14 days after treatment. (biomedcentral.com)
  • OBJECTIVES: FTO is known to be involved in cerebral ischemia/reperfusion (I/R) injury. (bvsalud.org)
  • Mechanical thrombectomy (MT) has become an effective re-airway method for cerebral ischemia-reperfusion injury (CI/RI). (bvsalud.org)
  • Neuroinflammation is acknowledged as a pivotal pathological event after cerebral ischemia. (bvsalud.org)
  • In former studies the expression of two different two-pore domain potassium \((K_{2P})\) channels (TASK1, TREK1) were shown to ameliorate neuronal damage due to cerebral ischemia. (uni-wuerzburg.de)
  • Methods In C57Bl/6 (wildtype, WT), \(hcn2^{+/+}\) and \(hcn2^{-/-}\) mice we used an in vivo model of cerebral ischemia (transient middle cerebral artery occlusion (tMCAO)) to depict a functional impact of HCN2 in stroke formation. (uni-wuerzburg.de)
  • Infarct volume, hemorrhagic transformation, and mortality were determined at 24 hours after cerebral ischemia. (bmj.com)
  • I/R injury was induced by blocking the right middle cerebral artery for 2 hours with reperfusion for 2 hours and 22 hours, respectively using the intraluminal method. (hku.hk)
  • Cerebral ischemia-reperfusion injury (CIRI) refers to the phenomenon that the ischemic injury of brain leads to the injury of brain cells, and ischemic injury is further aggravated after the recovery of blood reperfusion. (sciencegate.app)
  • Cerebral ischemia-reperfusion injury (CIRI) caused by ischemic stroke seriously affects the prognosis of stroke patients. (sciencegate.app)
  • Cerebral ischemia/reperfusion (I/R) injury is closely related to dysfunctional glucose metabolism. (sciencegate.app)
  • Celastrol is a bioactive compound that has been found to exhibit neuroprotective effects in cerebral ischemia, while whether it can protect against cerebral I/R injury by regulating glycolysis remains unclear. (sciencegate.app)
  • Transient focal cerebral ischemia (90 min) was induced by occlusion of the left middle cerebral artery that followed by 24 h reperfusion periods. (ac.ir)
  • Induction of cerebral ischemia in the control group produced severe neurological sensorimotor deficits in conjunction with considerable cerebral infarctions. (ac.ir)
  • Abstract BACKGROUND: Several β-adrenergic receptor (βAR) antagonists have been shown to have neuroprotective effects against cerebral ischemia. (starrlifesciences.com)
  • We used β2AR knockout mice and a β2selective antagonist to test the effect of loss of β2ARs on outcome from transient focal cerebral ischemia. (starrlifesciences.com)
  • METHODS: Ischemia was induced by the intraluminal suture method, for 60 min of middle cerebral artery occlusion (MCAO) followed by 24 h reperfusion. (starrlifesciences.com)
  • After cerebral ischemia, total levels of Hsp72 and the number of Hsp72 immunopositive cells were greater in mice lacking β2 AR. (starrlifesciences.com)
  • This is consistent with a shift away from prosurvival signaling to prodeath signaling in the presence of β2AR activation in cerebral ischemia. (starrlifesciences.com)
  • The effect of β2AR signaling in the setting of cerebral ischemia is complex and warrants further study. (starrlifesciences.com)
  • This article describes the pathophysiology of, and treatment strategy for, cerebral ischemia. (nih.gov)
  • Reperfusion plays an important role in the pathophysiology of cerebral ischemia. (nih.gov)
  • Magnetic resonance imaging (MRI) and histological studies in rat focal ischemia models using transient middle cerebral artery (MCA) occlusion indicate that reperfusion after an ischemic episode of 2- to 3-hour duration does not result in reduction of the size of the infarct. (nih.gov)
  • Cerebral hyperexcitability in migraine experiencers might sensitize brain tissue to ischemia. (medscape.com)
  • [ 1 ] A recent hypothesis to explain the migraine-stroke association, based on experimental data obtained in mice expressing familial hemiplegic migraine type 1 mutations, is that the cerebral hyperexcitability phenotype associated with migraine might sensitize brain tissue to ischemia. (medscape.com)
  • Along with the observation that migraine mutants had an elevated minimum cerebral blood flow threshold required for tissue survival and developed larger infarcts, these findings directly support the hypothesis that brain tissue in migraineurs is more susceptible to ischemic injury. (medscape.com)
  • Based on these premises, taking advantage of the reliability of computed tomography perfusion (CTP) imaging in the estimation of cerebral tissue viability in both clinical and research settings, [ 4 ] we conducted a case-control study comparing CTP maps of migraineurs and nonmigraineurs patients with acute ischemic stroke aimed at investigating whether a personal history of migraine is associated with vulnerability to brain ischemia. (medscape.com)
  • METHODS: Vehicle (dimethyl sulfoxide), a GPER agonist (G-1, 30 mug/kg), or a GPER antagonist (G-15, 300 mug/kg) were administered alone or in combination to young or aged male mice, or young intact or ovariectomized female mice, 1 hour before or 3 hours after cerebral ischemia-reperfusion. (monash.edu)
  • The Sprague-Dawley (SD) rats that underwent right-sided middle cerebral artery occlusion (MCAO) were used for assessment of NKCC1, TNF-α and IL-1β expression using Western blotting, double immunofluorescence and real time RT-PCR, and the model also was used for evaluation of brain water content (BWC) and infarct size. (biomedcentral.com)
  • In conclusion CVR-L-Arg is a promising noninvasive research method that could provide means for evaluation of cerebral endothelial function in physiological and pathological conditions. (hindawi.com)
  • In the past few decades the immense development of neuroradiological methods enabled better imaging of cerebral blood vessels. (hindawi.com)
  • Ultrasound remains the ultimate method for real time functional cerebral blood flow imaging. (hindawi.com)
  • 6. Xing B, Chen H, Zhang M, Zhao D, Jiang R, Liu X, Zhang S. Ischemic postconditioning inhibits apoptosis after focal cerebral ischemia/reperfusion injury in the rat. (ac.ir)
  • Ischemic postconditioning may not influence early brain injury induced by focal cerebral ischemia/reperfusion in rats. (ac.ir)
  • 16. Wang Q, Zhang X, Ding Q, Hu B, Xie Y, Li X, Yang Q, Xiong L. Limb Remote Postconditioning Alleviates Cerebral Reperfusion Injury Through Reactive Oxygen Species-Mediated Inhibition of Delta Protein Kinase C in Rats. (ac.ir)
  • This study attempted to determine whether neutrophil sequestration in reperfused myocardium can be inhibited and infarct size reduced by treatment with a chimeric, monoclonal IgG4 antibody (CLB54) directed against CD18 in a primate model of acute myocardial ischemia and reperfusion. (johnshopkins.edu)
  • In the heart, IPC is an intrinsic process whereby repeated short episodes of ischaemia protect the myocardium against a subsequent ischaemic insult. (wikipedia.org)
  • This study explores if long-term feeding of an obesogenic high fat diet renders the myocardium less susceptible to ischemic-reperfusion induced injury via Epac-dependent signaling. (uib.no)
  • Ischemia-reperfusion injury (IRI) is a syndrome affecting the myocardium upon blood flow restoration following a sufficiently long interruption, such as encountered in a coronary thrombosis or heart surgery [1,2]. (justia.com)
  • Adult rats were subjected to myocardial ischemia/reperfusion (I/R) injury with or without ischemic preconditioning (IPC), and the level of miR‑133b‑5p in myocardium was measured. (spandidos-publications.com)
  • In the situation of acute coronary occlusion, the myocardium supplied by the occluded vessel is subject to ischemia and is referred to as the myocardium at risk (MaR). Single photon emission computed tomography has previously been used for quantitative assessment of the MaR. It is, however, associated with considerable logistic challenges for employment in clinical routine. (biomedcentral.com)
  • Paradoxically, reperfusion of the ischemic myocardium, as achieved with early percutaneous intervention, results in substantial damage to the heart (ischemia/reperfusion injury) caused by cell death due to aggravated inflammatory and oxidative stress responses. (tocotrienolresearch.org)
  • Protection of the ischemic myocardium is known to occur as a result of ischemic preconditioning (PC), in which repetitive brief periods of ischemia protect the heart from a subsequent prolong ischemic insult. (eurekaselect.com)
  • Last year, Dharmakumar and Kumar observed that damage to the heart from MI was not only a result of ischemia caused by a blocked artery, but also a result of bleeding in the myocardium after the artery had been opened. (medscape.com)
  • BACKGROUND: Coagulation disorders and reperfusion of ischemic myocardium are major causes of morbidity and mortality. (regionh.dk)
  • Methods The intraluminal filament tMCAO model was established in hyperglycemic rats (n=106) with 5 hours ischemia followed by 19 hours reperfusion. (bmj.com)
  • Various concentrations of SUF, especially 5, 10 and 25 μg/kg of SUF, all alleviated the infarct size, neurological function and brain edema of MCAO rats. (sciencegate.app)
  • Methods A total of 67 male Wistar rats were divided into a non-PTP control group, 24 or 72 hours after a single cycle or 3 consecutive cycles of PTP in a 42°C water bath (1-24, 1-72, 3-24, and 3-72 groups). (ntnu.edu.tw)
  • Results Coronary arterial ischemia/reperfusion depressed cardiac microcirculation, induced ST-segment elevation and increased infarct size in non-PTP and PTP rats. (ntnu.edu.tw)
  • Compared to I/R injury groups, H 2 S pretreatment had reduced spinal cord infarct zone, improved hind motor function in rats. (biomedcentral.com)
  • The accumulation of cardiac lactate was attenuated by PLCA during myocardial I/R, and infarct size was smaller in rats treated with PLCA (1 mg/kg) than in those treated with caffeic acid (1 mg/kg). (biomedcentral.com)
  • 2. Ren C, Yan Z, Wei D, Gao X, Chen X, Zhao H. Limb remote ischemic postconditioning protects against focal ischemia in rats. (ac.ir)
  • Interrupting reperfusion as a stroke therapy: ischemic postconditioning reduces infarct size after focal ischemia in rats. (ac.ir)
  • 10. Allahtavakoli M, Jarrott B. Sigma-1 receptor ligand PRE-084 reduced infarct volume, neurological deficits, pro-inflammatory cytokines and enhanced anti-inflammatory cytokines after embolic stroke in rats. (ac.ir)
  • 13. Zhang W, Miao Y, Zhou S, Jiang J, Luo Q, Qiu Y. Neuroprotective effects of ischemic postconditioning on global brain ischemia in rats through upregulation of hippocampal glutamine synthetase. (ac.ir)
  • Interestingly, however, the HFD did not reduce infarct size in Epac1−/− deficient mice hearts (Epac1−/− HFD 65.1 ± 5.1% vs. Epac1−/− ND 56.1 ± 3.5%, ns. (uib.no)
  • However the 3-AR agonist BRL37344 could not reduce infarct size. (sun.ac.za)
  • Post-conditioning, or relief of myocardial ischemia in a stuttered manner, has been shown to reduce infarct size, in part because of up-regulation of survival kinases (extracellular-signal regulated kinase [ERK] 1/2 or PI3-kinase/Akt) during the early min of reperfusion. (nih.gov)
  • Facilitation of glucose utilization contributes to the protective effect of AKT signaling to reduce infarct size and improve myocardial function in a heart subjected to I/R [ 15 ]. (biomedcentral.com)
  • Such injury would occur when a patient has an acute myocardial infarct followed by reperfusion by either percutaneous coronary intervention or thrombolysis. (wikipedia.org)
  • Primary percutaneous coronary intervention (PCI) is the preferred method of reperfusion if this can be performed within recommended time frames. (dovepress.com)
  • The advent of coronary care units and early reperfusion therapy (lytic or percutaneous coronary intervention) has substantially decreased in-hospital mortality rates and has improved the outcome in survivors of the acute phase of MI. (medscape.com)
  • This group exposed anesthetised open-chest dogs to four periods of 5 minute coronary artery occlusions followed by a 5-minute period of reperfusion before the onset of a 40-minute sustained occlusion of the coronary artery. (wikipedia.org)
  • Mechanisms of ischemia resulting from internal carotid artery occlusion are, most commonly, artery-to-artery embolism or propagating thrombus and perfusion failure from distal insufficiency. (medscape.com)
  • Occlusion of the M1 segment of the MCA prior to the origin of the lenticulostriate arteries in the presence of a good collateral circulation can give rise to the large striatocapsular infarct. (medscape.com)
  • Occlusion of the MCA or its branches is the most common type of anterior circulation infarct, accounting for approximately 90% of infarcts and two thirds of all first strokes. (medscape.com)
  • Often, ischemia in the distribution of the ophthalmic artery is transient in the setting of symptomatic internal carotid artery occlusion (ie, transient monocular blindness, occurring in approximately 25% of patients), but central retinal artery ischemia is relatively uncommon, presumably because of the efficient collateral supply. (medscape.com)
  • Short series of repetitive cycles of brief reperfusion and re-occlusion of the coronary artery applied at the onset of reperfusion, reduce the infarct size and coronary artery endothelial dysfunction. (eurekaselect.com)
  • The present invention is based on the surprising finding that the peptides of the invention have protective cardiovascular effects without simultaneous administration of other compounds, specifically they have protective effects on the heart against ischemia-reperfusion injury. (justia.com)
  • We have recently shown that postischemic administration of intralipid protects the heart against ischemia-reperfusion injury. (silverchair.com)
  • During ischemic stroke (IS), adenosine 5′-triphosphate (ATP) is released from damaged nerve cells of the infract core region to the extracellular space, invoking peri-infarct glial cellular P2 purinoceptors singling, and causing pro-inflammatory cytokine secretion, which is likely to initiate or aggravate motor and cognitive impairment. (biomedcentral.com)
  • The neurological outcomes, infarction volumes and the level of astroglial and microglial/macrophage hyperplasia, inflammatory cytokine and P2X7R and P2Y1R expression in the peri-infarct hippocampal CA1and sensorimotor cortex were investigated after IS to evaluate the MCAO/R model and therapeutic mechanism of EA treatment. (biomedcentral.com)
  • Astroglial and microglial/macrophage P2 purinoceptors-mediated neuroinflammation and hyperplasia in peri-infarct hippocampal CA1 and sensorimotor cortex were attenuated by EA treatment after ischemic stroke accompanied by the improved motor and memory behavior performance. (biomedcentral.com)
  • RESULTS: Surprisingly, G-1 worsened functional outcomes and increased infarct volume in males poststroke, in association with an increased expression of cleaved caspase-3 in peri-infarct neurons. (monash.edu)
  • Most peri-infarct arrhythmias are benign and self-limited. (medscape.com)
  • Cerebrovascular diseases (CVDs) have become a global public health problem and ischemia‑reperfusion injury, the major cause of neurological impairment exacerbation, is closely related to excitotoxicity. (spandidos-publications.com)
  • Background Brain ischemia is known to include neuronal cell death and persisting neurological deficits. (uni-wuerzburg.de)
  • In neurons, TASK channels carrying hyperpolarizing \(K^+\) leak currents, and the pacemaker channel HCN2, carrying depolarizing Background Brain ischemia is known to include neuronal cell death and persisting neurological deficits. (uni-wuerzburg.de)
  • Compared with the enalapril or alpha tocopherol groups, the combined treatment significantly improved neurological motor and sensory functions ( p =0.038 and p =0.034, respectively) and also reduced the infarct volume ( p =0.032). (ac.ir)
  • Neurological score was determined at 24 h reperfusion and infarct size was determined by cresyl violet or 2,3,5-triphenyltetrazolium chloride staining. (starrlifesciences.com)
  • In contrast to findings in males, G-1 reduced neurological deficit, apoptosis, and infarct volume in ovariectomized females, but had no significant effect in intact females. (monash.edu)
  • 9. Allahtavakoli M, Moloudi R, Arababadi MK, Shamsizadeh A, Javanmardi K. Delayed post ischemic treatment with Rosiglitazone attenuates infarct volume, neurological deficits and neutrophilia after embolic stroke in rat. (ac.ir)
  • Inhibition of neutrophil sequestration with CLB54 administered before reperfusion reduces infarct size, preserves ischemic zone microvascular perfusion and minimizes the decline of regional wall motion. (johnshopkins.edu)
  • In adult mouse hearts, post-conditioning significantly reduced infarct size via up-regulation of ERK (but not Akt) signaling. (nih.gov)
  • Creatine kinase and infarct sizes were significantly reduced and left ventricular developed pressure was improved with APC in the young adult and middle-aged groups but not the aged group. (asahq.org)
  • Conclusions PTP significantly reduced cardiac ischemia/reperfusion injury by upregulating antioxidant, antiapoptotic, and antiautophagic mechanisms. (ntnu.edu.tw)
  • α-TOH significantly reduced infarct size, restored cardiac function as measured by ejection fraction, fractional shortening, cardiac output, and stroke volume, and prevented pathological changes as assessed by state-of-the-art strain and strain-rate analysis. (tocotrienolresearch.org)
  • We suggest PTP might efficiently diminish cardiac ischemia/reperfusion-induced apoptosis and autophagy injury. (ntnu.edu.tw)
  • 7. Yuan Y, Guo Q, Ye Z, Pingping X, Wang N, Song Z. Ischemic postconditioning protects brain from ischemia/reperfusion injury by attenuating endoplasmic reticulum stress-induced apoptosis through PI3K-Akt pathway. (ac.ir)
  • Although steady-state conditions revealed no increase in primitive cell proliferation in p21-null mice, a significantly larger fraction of quiescent neural precursors was activated in the hippocampus and subventricular zone after brain ischemia. (rupress.org)
  • We investigated whether a personal history of migraine is associated with vulnerability to brain ischemia in humans. (medscape.com)
  • Migraine is likely to increase individual vulnerability to ischemic stroke during the process of acute brain ischemia and might represent, therefore, a potential new therapeutic target against occurrence and progression of the ischemic damage. (medscape.com)
  • Similarly, cardiomyocyte-specific Txnip deletion reduced infarct size after reversible coronary ligation. (jci.org)
  • Coronary flow was determined using radiolabeled microspheres, infarct size by triphenyltetrazolium chloride staining, global and regional ventricular function by contrast ventriculography and neutrophil accumulation by a myeloperoxidase assay. (johnshopkins.edu)
  • The random effects model pooled estimate for the outcome infarct size assessed by cardiac magnetic resonance was estimated by the standardized mean difference (SMD) =−0.06, 95% confidence interval (CI): −0.34 to 0.21, ie, no effect of IPost. (dovepress.com)
  • For the end point infarct size, estimated by biomarkers of myocardial necrosis, an overall pooled effect was SMD =−0.58, 95% CI: −0.96 to −0.19. (dovepress.com)
  • 2 Paradoxically, reperfusion itself can enlarge the infarct size, by complex mechanisms collectively termed ischemia/reperfusion injury. (dovepress.com)
  • 3 In 2003, Zhao and et all published experimental data demonstrating a considerable reduction of infarct size by a reperfusion procedure termed ischemic postconditioning (IPost), consisting of brief, repetitive cycles of reperfusion and reocclusion, followed by sustained reperfusion. (dovepress.com)
  • 4 An infarct-reducing effect of IPost was confirmed in several animal models, 3 and subsequently, in small-sized "proof of concept" clinical studies, reduction of infarct size by IPost was reported. (dovepress.com)
  • Endpoints were infarct size and functional recovery. (uib.no)
  • This beneficial effect of N-Ac-GLP-1(7-34)amide was manifested through a diminished diastolic hypercontracture and diminished infarct size. (justia.com)
  • Effect of N-Ac-GLP-1(7-34)amide on infarct size. (justia.com)
  • Columns represent mean infarct size (IS) (N=7-14) calculated as percentage of Area at Risk (AAR) (%IS/AAR), with bars indicating SEM. (justia.com)
  • Infarct size (IS) was determined using tetrazolium staining (TTC) and data were analyzed with ANOVA. (sun.ac.za)
  • The 1- and 2-AR blockers CGP-20712A and ICI-118551 completely abolished the isoproterenol-induced reduction in infarct size and improvement in mechanical recovery, while the 3-AR blocker was without effect. (sun.ac.za)
  • Both Rp-8-CPT-cAMPs and wortmannin significantly increased infarct size when administered before 1/ 2-AR preconditioning or at the onset of reperfusion while it reduced mechanical recovery during reperfusion. (sun.ac.za)
  • PTX pretreatment had no significant effect on the reduction in infarct size induced by 1/ 2-AR or 2-AR preconditioning, however it reduced mechanical recovery in the latter. (sun.ac.za)
  • The NOS inhibitors had no effect on the reduction in infarct size induced by 1/ 2-AR preconditioning, but depressed mechanical function during reperfusion. (sun.ac.za)
  • The significant reduction in infarct size by 1/ 2-PC, was associated with activation of ERKp44/p42 and PKB/Akt during the triggering phase, as well as during reperfusion. (sun.ac.za)
  • Primary end points were infarct size, cardiac expression of phospho-Akt, phospho-mitogen-activated protein kinase kinase 1/2 and phospho-ERK 1/2, and expression of mitogen-activated protein kinase-phosphatase-1 (MKP-1: phosphatase purported to play a primary role in ERK dephosphorylation). (nih.gov)
  • Old mouse hearts are refractory to infarct size reduction with post-conditioning, possibly because of an age-associated increase in MKP-1 and resultant deficit in ERK phosphorylation. (nih.gov)
  • Reperfusion after cardiac ischemia increases cell death and infarct size (IS), called myocardial ischemia/reperfusion (I/R) injury, which is the main cause of myocardial injury during the cardiac surgery particularly in coronary artery bypass graft surgery ( 1 , 2 ). (spandidos-publications.com)
  • The hemodynamic function, infarct size, calcium retention capacity, mitochondrial superoxide production, and phosphorylation levels of protein kinase B (Akt)/glycogen synthase kinase-3β (GSK-3β) were measured. (silverchair.com)
  • Although intralipid inhibits the opening of the mitochondrial permeability transition pore as efficiently as cyclosporine-A, intralipid is more effective in reducing the infarct size and improving the cardiac functional recovery. (silverchair.com)
  • Ischemic preconditioning and anesthetic preconditioning (APC) are reported to decrease myocardial infarct size during ischemia-reperfusion injury. (asahq.org)
  • Left ventricular developed pressure, creatine kinase, and infarct size were measured. (asahq.org)
  • Pretreatment with a β2AR selective antagonist, ICI 118,551, also decreased infarct size significantly, by 25.1%, compared with the saline control (32.8 ± 11.9 mm3vs 43.8 ± 10.3 mm3, n = 10/group, P = 0.041). (starrlifesciences.com)
  • Cardiac function and injury were determined by microcirculation, electrocardiography, and infarct size. (ntnu.edu.tw)
  • In a case-control design, we compared the proportion of subjects with no-mismatch, the volume of penumbra salvaged, as well as the final infarct size in a group of patients with migraine and a group of patients with no history of migraine. (medscape.com)
  • Conversely, there was no difference in final infarct size among the 3 migraine subgroups ( P =0.312). (medscape.com)
  • Methods and results: Hearts from PKN1 knockout (KO) or wild type (WT) littermate control mice were perfused in Langendorff mode and subjected to global ischaemia and reperfusion (I/R). Myocardial infarct size was doubled in PKN1 KO hearts compared to WT hearts. (figshare.com)
  • Conclusion: Loss of PKN1 in vivo significantly reduces endogenous cardioprotection and increases myocardial infarct size following I/R injury. (figshare.com)
  • In the last two decades, a remarkable scientific effort has focused on the limitation of infarct size. (eurekaselect.com)
  • BWC and infarct size decreased significantly after 10% HS treatment. (biomedcentral.com)
  • Short-term cardiac stress, induced by ischemia-reperfusion (I/R) injury resulted in impaired left ventricular (LV) recovery and increased infarct size in heterozygous Hmox1-deficient (Hmox1 +/− ) mice [ 55 ]. (springer.com)
  • METHODS AND RESULTS: In 2 mouse models, MAP-1 preserves cardiac function, decreases infarct size, decreases C3 deposition, inhibits MBL deposition, and prevents thrombogenesis. (regionh.dk)
  • Thus, we hypothesized that the endogenous mannose-binding lectin (MBL)/ficolin-associated protein-1 (MAP-1) that inhibits complement activation in vitro also could be an in vivo regulator by attenuating myocardial schema/reperfusion injury and thrombogenesis when used at pharmacological doses in wild-type mice.METHODS AND RESULTS: In 2 mouse models, MAP-1 preserves cardiac function, decreases infarct size, decreases C3 deposition, inhibits MBL deposition, and prevents thrombogenesis. (regionh.dk)
  • ENGLISH ABSTRACT: The Mechanism of -adrenergic preconditioning ( -PC) Ischaemic preconditioning (IPC), a potent endogenous protective intervention against myocardial ischaemia, is induced by exposure of the heart to repetitive short episodes of ischaemia and reperfusion. (sun.ac.za)
  • We have recently shown that the lectin pathway-specific carbohydrate recognition subcomponent mannose-binding lectin plays an essential role in the pathophysiology of thrombosis and ischemia/reperfusion injury. (regionh.dk)
  • Conversely, G-15 improved functional outcomes and reduced infarct volume after stroke in males, whether given before or after stroke. (monash.edu)
  • Targeting specific microRNAs may represent a novel intervention opportunity to improve outcome and reduce hemorrhagic transformation after mechanical reperfusion for acute ischemic stroke. (bmj.com)
  • Multicenter cohort study of patients with acute ischemic stroke who underwent a brain computed tomography perfusion and were scheduled to undergo reperfusion therapy. (medscape.com)
  • Therefore, we speculate that purinergic receptors might play dualistic roles in response to EA effects treating inflammatory injury induced by ischemia. (biomedcentral.com)
  • Current methods of cold static storage have reached their limits in storage time due to the extent of ischemia-reperfusion (I/R) injury induced during static cold storage. (gotomydoctor.com)
  • Overall, α-TOH inhibits ischemia/reperfusion injury-induced oxidative and inflammatory responses, and ultimately preserves cardiac function. (tocotrienolresearch.org)
  • Methods: Wild type (wt), Epac1 (Epac1−/− ) and Epac2 (Epac2−/− ) deficient mice were fed a high fat (HFD) or normal chow diet (ND) for 33 ± 1 weeks. (uib.no)
  • Isolated ex vivo mice hearts were perfused in a constant pressure Langendorff mode, and exposed to 30min of global ischemia (GI) and 60min of reperfusion. (uib.no)
  • A total of 24 Adult males of Swiss albino mice were randomized to four groups: I/R group (n = 6), mice underwent 30 minute bilateral renal ischemia and 48 hr reperfusion. (biomedcentral.com)
  • Sham group (n = 6), mice underwent same anesthetic and surgical procedures except for ischemia induction. (biomedcentral.com)
  • After the end of reperfusion phase mice were sacrificed, blood samples were collected directly from the heart for determination of serum TNF-a, IL-6, urea and Creatinine. (biomedcentral.com)
  • Isolated buffer-perfused hearts were obtained from 3- to 4-month-old (adult) and 20- to 24-month-old C57BL/6J mice and subjected to 30 min of ischemia. (nih.gov)
  • Ischemia-induced cell depolarization: does the hyperpolarization-activated cation channel HCN2 affect the outcome after stroke in mice? (uni-wuerzburg.de)
  • Results After 60 min of tMCAO induction in WT mice, we collected tissue samples at 6, 12, and 24 h after reperfusion. (uni-wuerzburg.de)
  • RESULTS: Compared with wild type littermates, infarct volume was decreased by 22.3% in β2AR knockout mice (39.7 ± 10.7 mm3 vs 51.0 ± 11.4 mm3, n = 10/group, P = 0.034) after 60 min of MCAO followed by 24 h reperfusion. (starrlifesciences.com)
  • Thus, we hypothesized that the endogenous mannose-binding lectin (MBL)/ficolin-associated protein-1 (MAP-1) that inhibits complement activation in vitro also could be an in vivo regulator by attenuating myocardial schema/reperfusion injury and thrombogenesis when used at pharmacological doses in wild-type mice. (regionh.dk)
  • One of the primary causes of ARF is ischemia/reperfusion (I/R). Inflammatory process and oxidative stress are thought to be the major mechanisms causing I/R. MK-886 is a potent inhibitor of leukotrienes biosynthesis which may have anti-inflammatory and antioxidant effects through inhibition of polymorphonuclear leukocytes (PMNs) infiltration into renal tissues. (biomedcentral.com)
  • Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. (ac.ir)
  • Several studies showed that α-MSH has protective effects against ischemia/reperfusion (I/R) induced organ damages. (hku.hk)
  • The goal of this proposal is to investigate a novel preservation method utilizing hydrogen sulfide (H2S) to induce a protective state of hibernation against I/R injury. (gotomydoctor.com)
  • In vivo rat hearts or isolated Langendorff-perfused mouse hearts were subjected to ischemia followed by reperfusion with intralipid (0.5%, 1% and 2% ex-vivo, and 20% in vivo), cyclosporine-A (0.2 μM, 0.8 μM, and 1.5 μM ex- vivo and 10 mg/kg in vivo), or vehicle. (silverchair.com)
  • When cardiac MRI came around, around the year 2000, suddenly there was a noninvasive imaging method where we could investigate patients in vivo," said Kumar. (medscape.com)
  • Given the central role that mitochondria play during hypoxia, we hypothesized that Txnip deletion would enhance ischemia-reperfusion damage. (jci.org)
  • Cardiomyocytes were isolated and subjected to 6 h hypoxia followed by 18 h reperfusion. (biomedcentral.com)
  • Surprisingly, Txnip-KO hearts had greater recovery of cardiac function after an ischemia-reperfusion insult. (jci.org)
  • Treatment strategies include adequate pain medication, diuresis to manage heart failure, oxygenation, volume repletion for hypovolemia, administration of anti-inflammatory agents to treat pericarditis, and use of beta-blockers and/or nitroglycerin to relieve ischemia. (medscape.com)
  • Another endogenous form of cardioprotection, similar to PC but applicable at the time of reperfusion, termed postconditioning (PostC), has been recently described. (eurekaselect.com)
  • The role of PKA and PI3-K/Akt was investigated by the administration of the blockers Rp-8-CPT-cAMPs (16 μM) and wortmannin (100 nM) respectively, prior to RI or at the onset of reperfusion. (sun.ac.za)
  • Chien, CY , Chien, CT & Wang, SS 2014, ' Progressive thermopreconditioning attenuates rat cardiac ischemia/reperfusion injury by mitochondria-mediated antioxidant and antiapoptotic mechanisms ', Journal of Thoracic and Cardiovascular Surgery , 卷 148, 編號 2, 頁 705-713. (ntnu.edu.tw)
  • The present study was undertaken to study the effects of exogenous H2S on ischemia/reperfusion (I/R) injury of spinal cord and the underlying mechanisms. (biomedcentral.com)
  • Methods: Isolated perfused rat hearts were subjected to 35 min regional ischaemia (RI) and reperfusion. (sun.ac.za)
  • Therapeutic hydrogen has been applied by different delivery methods including straightforward inhalation, drinking hydrogen dissolved in water and injection with hydrogen-saturated saline. (researchgate.net)
  • A therapeutic drug that targets ischemia reperfusion (I/R) injury is needed and has yet to be developed. (biomedcentral.com)
  • α-MSH significantly decreased relative infarct area, hemorrhage, glial cells activation as well as oxidative and nitrosative stress. (hku.hk)
  • Cardiomyocyte and microvascular necrosis leading to reperfusion hemorrhage. (medscape.com)
  • Ischemia decreases intracellular pH and increases intracellular Na and intracellular Ca in all age groups. (asahq.org)
  • Triphenyltetrazolium chloride staining was used to detect infarct areas. (spandidos-publications.com)
  • The effects of exogenous H2S on I/R injury were examined by using assessment of hind motor function, spinal cord infarct zone by Triphenyltetrazolium chloride (TTC) staining. (biomedcentral.com)
  • This is exacerbated by changes in the expression of membrane ion channels and under-expression and reorganization of gap junctions ( Luke and Saffitz, 1991 ) in the infarct border zone also slowing conduction ( Tse, 2016 ). (frontiersin.org)
  • Postconditioning using N-Ac-GLP-1(7-34)amide N-terminally blocked and C-terminally truncated results in a limitation of ischemia-reperfusion injury in an isolated rat heart. (justia.com)
  • Postconditioning in reperfusion injury: a status report. (ac.ir)
  • The study will reveal, in a pig model of ischaemia and reperfusion, whether this intervention can improve outcome after MI over and above that achieved using current standard clinical therapy. (ed.ac.uk)
  • The clinician must be aware of these arrhythmias, in addition to reperfusion strategies, and must treat those that require intervention to avoid exacerbation of ischemia and subsequent hemodynamic compromise. (medscape.com)