• Similarly, cardiomyocyte-specific Txnip deletion reduced infarct size after reversible coronary ligation. (jci.org)
  • For example inhibition of sEH reduced infarct size in a stroke model (Zhang et al. (mdm2-inhibitors.com)
  • In mice knock down or inhibition of specific platelets proteins like PAR-4, GPVI or P-selectin leads to reduced infarct size and reduced inflammation in the acute phase after I/R injury. (isth.org)
  • Thrombocytopenia in mice leads to reduced infarct size and an improved left ventricular function 24 hours and 21 days after myocardial infarction. (isth.org)
  • Whereas mitochondrial ATP synthesis was minimally decreased by Txnip deletion, cellular ATP content and lactate formation were higher in Txnip-KO hearts after ischemia-reperfusion injury. (jci.org)
  • however, whether inhibition of Rho-K would decrease infarct size in hearts after ischemia/reperfusion. (vcu.edu)
  • Reperfusion injury refers to the tissue damage inflicted when blood flow is restored after an ischemic period of more than about ten minutes. (benbest.com)
  • Cryonics patients frequently experience ischemic & reperfusion injury between the time when the heart stops and cryostorage begins. (benbest.com)
  • In this article I attempt to evaluate the nature & extent of ischemic & reperfusion injury -- primarily focused on the impact for cryonics (although certainly relevant to stroke and cardiac arrest). (benbest.com)
  • I focus my attention on ischemic/reperfusion injury to the brain. (benbest.com)
  • While effective early reperfusion of the criminal coronary artery after a confirmed AMI is the typical treatment at present, collateral myocardial ischemia-reperfusion injury (MIRI) and pertinent cardioprotection are still challenging to address and have inadequately understood mechanisms. (hindawi.com)
  • However, while myocardial reperfusion is well established, the process itself can trigger myocardial reperfusion injury by causing further cardiomyocyte death through multiple pathophysiological mechanisms [ 3 - 5 ]. (hindawi.com)
  • Conceptual diagram of the development and unknown mechanisms of myocardial ischemia-reperfusion injury. (hindawi.com)
  • The pathophysiological nature of MIRI is the short-term disturbance of myocardial energy and metabolism caused by reflow after ischemia and hypoxia in the coronary artery and the dynamic changes in apoptosis and the prosurvival signaling pathways in response to related injury factors. (hindawi.com)
  • The volatile anesthetic desflurane (DES) effectively reduces cardiac infarct size following experimental ischemia/reperfusion injury in the mouse heart. (uni-wuerzburg.de)
  • Aromatase metabolizes testosterone to 17b- estradiol (E2) and thereby significantly contributes The volatile anesthetic desflurane (DES) effectively reduces cardiac infarct size following experimental ischemia/reperfusion injury in the mouse heart. (uni-wuerzburg.de)
  • Renal ischemia-reperfusion injury (IRI) is considered as a major cause of acute kidney injury. (frontiersin.org)
  • Renal ischemia-reperfusion injury (IRI) is a common pathophysiological phenomenon in clinical settings. (frontiersin.org)
  • has been demonstrated to attenuate renal ischemia‑reperfusion (I/R) injury. (spandidos-publications.com)
  • However, reperfusion following a period of prolonged ischemia can often cause myocardial ischemia-reperfusion (I/R) injury, leading to damage of cardiac tissues ( 5 ). (spandidos-publications.com)
  • Thus, inhibition of oxidative stress and myocardial apoptosis is beneficial in the treatment of myocardial I/R injury. (spandidos-publications.com)
  • 2005 and was cardioprotective in a ischemia-reperfusion injury model (Motoki et al. (mdm2-inhibitors.com)
  • and the underlying mechanism of CLU4A in myocardial ischemia/reperfusion injury needs to be investigated. (engreen.com.cn)
  • myocardial ischemia/reperfusion injury. (engreen.com.cn)
  • Despite extensive research, our understanding of the precise role of different subsets of macrophages in ischemia/reperfusion injury remains incomplete. (elifesciences.org)
  • Specific absence of homeostatic, monocyte-independent macrophages altered the immune cell crosstalk in response to injury and induced proinflammatory neutrophil polarization, resulting in impaired cardiac remodelling without influencing infarct size. (elifesciences.org)
  • In summary, resident macrophages orchestrate inflammatory responses improving cardiac remodelling, while recruited macrophages determine infarct size after I/R injury. (elifesciences.org)
  • Using state-of-the-art fate-mapping models and genetic and pharmacological targeting approaches, the authors provide solid evidence that the absence of resident macrophages do not influence infarct size but instead alter the immune cell crosstalk in response to injury. (elifesciences.org)
  • Reperfusion injury, in part mediated by neutrophils, may limit the potential benefit of reestablishing infarctrelated artery patency in patients with acute myocardial infarction. (johnshopkins.edu)
  • 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)
  • Autophagy is a process that relies on lysosomal pathways for the degradation of cytoplasmic proteins and organelles and plays an important role in the pathology of brain injury such as hypoxia ischemia[ 3 ]. (ijpsonline.com)
  • Induction of NF-κB-dependent gene expression plays an important role in a number of biological processes including inflammation and ischemia-reperfusion injury. (umn.edu)
  • 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)
  • The present study was designed to investigate the expression changes of PPAR-alpha, -beta, -gamma and NF-kappa B in the hippocampus of rats with global cerebral ischemia/reperfusion injury (GCIRI) after treatment with agonists or antagonists of PPAR-gamma. (biomedcentral.com)
  • Global cerebral ischemia/reperfusion injury (GCIRI) occurs in patients who are successfully resuscitated from various clinical conditions such as cardiac arrest, asphyxia and shock, which are frequently accompanied by inflammation and can lead to serious neuronal injury, and further to neurodegeneration and learning and memory impairment [ 12 ]. (biomedcentral.com)
  • Proinflammatory cytokines, such as interleukin (IL)-1β, IL-6 and tissue necrosis factor (TNF)-α, have been implicated as important mediators of injury following cerebral ischemia [ 13 ] and contribute to pathogenesis, exacerbating brain tissue damage following ischemia/reperfusion (I/R) injury [ 14 ]. (biomedcentral.com)
  • 17β-Estradiol attenuates blood-brain barrier disruption induced by cerebral ischemia-reperfusion injury in female rats. (ac.ir)
  • Genistein exerts neuroprotective effect on focal cerebral ischemia injury in rats. (ac.ir)
  • Atorvastatin has been shown to be cardioprotective in ischemia-reperfusion (I/R) injury. (ac.ir)
  • In lpr mice, a naturally occurring mutant deficient in Fas, there is marked reduction in infarct size and abundance of apoptotic cardiac myocytes following ischemia and reperfusion that also signifies the importance of Fas pathway in ischemia-reperfusion injury [ 5 ]. (ac.ir)
  • In addition, it has been shown that atorvastatin can protect the isolated mouse heart against reperfusion-induced injury [ 6 ]. (ac.ir)
  • It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
  • Conclusions - Ticagrelor, but not clopidogrel, administered just before reperfusion protects against reperfusion injury. (utmb.edu)
  • Diabetes causes suppressed glucose oxidation leading to inefficient energy production, enhanced fatty acid metabolism, and increased susceptibility to myocardial ischemia and reperfusion injury. (biomedcentral.com)
  • The effect of reperfusion injury in vivo in similar vessels on the response to SIN-1 was also assessed. (eurekamag.com)
  • This inhibition is abolished following reperfusion injury or inhibition of NO synthesis. (eurekamag.com)
  • Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)
  • Above all, PGRN also provides protection in the initial phase following myocardial ischemia-reperfusion injury. (biomedcentral.com)
  • Our previous research confirmed that electroacupuncture (EA) stimulus elicits neuroprotective effects against cerebral ischemic injury through α7 nicotinic acetylcholine receptor (α7nAChR)-mediated inhibition of high-mobility group box 1 release mechanism. (biomedcentral.com)
  • 2012 ). Our team has proposed a new approach of electroacupuncture (EA) neuroprotection for the prevention of cerebral ischemia injury. (biomedcentral.com)
  • 2009 ) and regulate the Reperfusion Injury Salvage Kinase (RISK) signaling pathway (ERKε, PKC, GSK-3β, STAT3) via cannabinoid receptor 1 (CB1R)(Wang et al. (biomedcentral.com)
  • 2013 ). In addition, we demonstrated that EA could attenuate cerebral ischemic injury via regulation of α7nAChR-mediated inhibition of HMGB1 release in rats (Wang et al. (biomedcentral.com)
  • Recent studies have shown that ferroptosis is closely related to the pathophysiological processes of many diseases, such as tumors, nervous system diseases, ischemia-reperfusion injury, kidney injury, and blood diseases. (nature.com)
  • Ferroptosis plays an important regulatory role in the occurrence and development of many diseases, such as tumors, neurological diseases, acute kidney injury, ischemia/reperfusion, etc. (nature.com)
  • The cardioprotective effect of CLU4A inhibition was detected by monitoring the cell viability, cell apoptosis, and LDH activity in vitro and in vivo , and examining the infarct size and cardiac function in vivo . (engreen.com.cn)
  • Inhibition of CLU4A improved the cell viability, restrained the cell apoptosis, and suppressed LDH activity in vitro . (engreen.com.cn)
  • Inhibition of Fas expression prevents I/R induced apoptosis. (ac.ir)
  • Upregulation of Fas expression in myocardial ischemia-reperfusion can induce cardiomyocyte apoptosis, and atorvastatin can significantly inhibit cardiomyocyte apoptosis by inhibiting Fas expression. (ac.ir)
  • Apoptosis of the cardiomyocytes has been demonstrated in animal models with coronary artery occlusion [ 1 ], and experimental evidence suggests that myocardial cells are able to undergo apoptosis during ischemia followed by reperfusion [ 2 ]. (ac.ir)
  • Ticagrelor, but not clopidogrel, increased myocardial adenosine levels, increased phosphorylation of Akt, endothelial NO synthase, and extracellular-signal-regulated kinase 1/2 4 hours after reperfusion and decreased apoptosis. (utmb.edu)
  • Effects of (-)-epicatechin on myocardial infarct size and left ventricular remodeling after permanent coronary occlusion. (ucsd.edu)
  • There is a rupture track through the center of this posterior left ventricular transmural infarct. (medscape.com)
  • CLU4A expression was measured after myocardial ischemia/reperfusion in mice and in H9C2 cells with hypoxia/reoxygenation treatment by q-PCR and western blotting. (engreen.com.cn)
  • Rosuvastatin (80 mg) is shows to decrease infarct size and improve cardiac mechanical function after ischemia/reperfusion in animal model. (bioservuk.com)
  • Inhibition of CLU4A exhibited a cardioprotective role by an ERK-dependent pathway. (engreen.com.cn)
  • Dietary soy may not confound acute experimental stroke infarct volume outcomes in ovariectomized female rats. (ac.ir)
  • Thirty Wistar rats were selected and divided into three groups (n = 10): acute ischemia-reperfusion (I/R) group, acute ischemia-reperfusion and treated with atorvastatin group and sham-operated group. (ac.ir)
  • Pretreating the rats with simvastatin 18 hour prior to the induction of ischemiareperfusion has been shown to reduce cardiac dysfunction and improve coronary flow [ 7 ]. (ac.ir)
  • Approach and Results - Rats underwent 30-minute ischemia per 24-hour reperfusion. (utmb.edu)
  • Given the central role that mitochondria play during hypoxia, we hypothesized that Txnip deletion would enhance ischemia-reperfusion damage. (jci.org)
  • Hypoxia and ischemia of the brain are key pathophysiological mechanisms of ischemic stroke ( 5 , 6 ). (frontiersin.org)
  • In the early stage of ischemia and hypoxia, cells will increase the energy supply to the ischemic area, especially the functional area of the ischemic penumbra, by regulating glycolysis. (ijpsonline.com)
  • In the tracheobronchial (airway) vasculature, these include the inhibition of inflammatory hyperperfusion, microvascular hyperpermeability, mucosal oedema formation, and the formation of new blood vessels (angiogenesis). (ersjournals.com)
  • 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)
  • these socalled pleiotropic properties include anti-inflammatory effects, plaque stabilization, improved endothelial function and inhibition of vascular smooth muscle cell proliferation. (ac.ir)
  • The infarct size, neurological deficit score, TUNEL staining and the expression of proinflammatory factors or anti-inflammatory cytokines were evaluated at 72 h after reperfusion in the presence or absence of either α7nAChR antagonist (α-BGT) or agonist (PHA-543,613). (biomedcentral.com)
  • The contents of inflammasome proteins were gradually increased after cerebral ischemia/reperfusion (I/R). EA stimulus attenuated NLRP3 inflammasome mediated inflammatory reaction and regulated the balance between proinflammatory factors and anti-inflammatory cytokines. (biomedcentral.com)
  • 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)
  • Our previous studies have reported that EA could relieve neurological disorders, reduce infarct volumes after focal cerebral ischemia (Wang et al. (biomedcentral.com)
  • Anastrozole blocked DES induced preconditioning and increased infarct size compared to DES alone (37.94615.5% vs. 17.163.62%) without affecting area at risk and systemic hemodynamic parameters following ischemia/reperfusion. (uni-wuerzburg.de)
  • Hearts were stained and infarct size measured. (vcu.edu)
  • Consistently, knockdown of CLU4A reduced the myocardial infarct size and improved cardiac function in vivo . (engreen.com.cn)
  • This augmented adverse remodelling after I/R and led to an increased infarct size and deterioration of cardiac function. (elifesciences.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)
  • 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 the latter model, sustained infusion of PR39 peptide resulted in significant reduction of myocardial infarct size. (umn.edu)
  • Infarct size (IS) was determined using tetrazolium staining (TTC) and data were analyzed with ANOVA. (sun.ac.za)
  • However the 3-AR agonist BRL37344 could not reduce infarct size. (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)
  • One week after stroke, in both VAC and estrogen groups, the infarct size reduced in comparison with the control group. (ac.ir)
  • Prior data show that 7-day pretreatment with ticagrelor limits infarct size. (utmb.edu)
  • We explored the acute effects of ticagrelor and clopidogrel on infarct size and potential long-term effects on heart function. (utmb.edu)
  • Conclusions: Endothelium dependent vasodilatation is attenuated by ischaemia and reperfusion in both proximal and distal coronary arteries of the size studied. (eurekamag.com)
  • Hearts were put through 30 min global ischaemia and 2 h reperfusion as proven in = 16)= 15)= 12)Tukey check. (woofahs.com)
  • Control hearts had been perfused for 55 min ahead of 30 min global ischaemia and 2 h reperfusion (and Tukey check. (woofahs.com)
  • The cAMP analogue 8-Br-cAMP-AM (8-Br) confers marked protection against global ischaemia/reperfusion of isolated perfused heart. (mdpi.com)
  • We tested the hypothesis that 8-Br is also protective under clinically relevant conditions (regional ischaemia) when applied either before ischemia or at the beginning of reperfusion, and this effect is associated with the mitochondrial permeability transition pore (MPTP). (mdpi.com)
  • Methods: Isolated perfused rat hearts were subjected to 35 min regional ischaemia (RI) and reperfusion. (sun.ac.za)
  • Klier M, Ayhan A, Dannenberg L, Gorressen S, Polzin A, Elvers M. Role of Platelets in Processes of Myocardial Healing After Myocardial Ischemia and Reperfusion in Mice [abstract]. (isth.org)
  • 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)
  • Images were acquired starting at 2 or 24 hours after reperfusion over the ipsilateral and contralateral cortex before and for 3 hours after, MMPSense750 was injected. (biomedcentral.com)
  • As an integrated platform for triggering inflammation, inflammasome contributes to the pathogenesis of initiating innate immune response after cerebral ischemia/reperfusion (I/R)(Ismael et al. (biomedcentral.com)
  • Most peri-infarct arrhythmias are benign and self-limited. (medscape.com)
  • The microvascular and parenchymal organ damage induced upon ischemia tissue reperfusion is mainly attributed to the reactive oxygen-free radicals, and it has been demonstrated in many organs. (frontiersin.org)
  • Specifically, the gelatinases MMP-2 and MMP-9 have previously been considered to specifically injure the important components of the basal lamina around the cerebral blood vessels that precede microvascular damage in cerebral ischemia [ 1 ]. (biomedcentral.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)
  • Matrix-metalloproteinase upregulation in ischemia reperfusion can be imaged acutely in-vivo with NIRF using MMPSense750. (biomedcentral.com)
  • Assay of superoxide dismutase-mRNA by Northern blot analysis in in vivo rat heart subjected to 30 min ischaemia and 10 min reperfusion showed pretreatment with 10 -7 M trilinolein had a synergistic action with antioxidant systems preventing the rise in superoxide dismutase-mRNA. (tmu.edu.tw)
  • It has been shown that the Fas pathway is functional in cardiac myocytes and plays a critical role in myocardial death due to ischemia-reperfusion in vivo [ 4 ]. (ac.ir)
  • Methods: In vitro reactivity of preconstricted coronary arterial rings was studied in control dogs (group 1), and dogs in which the left circumflex coronary artery was subjected in vivo to four acute occlusions of 5 min duration, with three intervening reperfusion periods of 5 min and a final reperfusion period of 60 min (group 2). (eurekamag.com)
  • The production of antioxidant enzymes that scavenge free radicals in ischemic tissue is then impaired, thereby exacerbating the damage caused by these free radicals in the post ischemic reperfusion tissue. (frontiersin.org)
  • Venous thrombosis (sometimes called DVT, deep vein thrombosis) leads to a blood clot in the affected part of the body, while arterial thrombosis (and, rarely, severe venous thrombosis) affects the blood supply and leads to damage of the tissue supplied by that artery (ischemia and necrosis). (wikipedia.org)
  • Correia Miranda LE, Capellini VK, Reis GS, Celotto AC, Carlotti Jr CG, PRB: Effects of partial liver ischemia followed by global liver reperfusion on the remote tissue expression of nitric oxide synthase: lungs and kidneys evora. (edu.pl)
  • The expression of NLRP3 inflammasome in the penumbral tissue following reperfusion was assessed by western blotting and immunoflourescent staining. (biomedcentral.com)
  • Surprisingly, Txnip-KO hearts had greater recovery of cardiac function after an ischemia-reperfusion insult. (jci.org)
  • Thus, although Txnip deletion suppresses mitochondrial function, protection from myocardial ischemia is enhanced as a result of a coordinated shift to enhanced anaerobic metabolism, which provides an energy source outside of mitochondria. (jci.org)
  • Although the phenomenon of ischaemic preconditioning (IPC) is associated with the desired protective capacity, the necessity of its application before sustained ischaemia limits its clinical potential. (sun.ac.za)
  • 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)
  • Ischemia and reperfusion can cause serious brain damage in stroke or cardiac arrest. (benbest.com)
  • The objective of the present study was to determine whether an alternate MMP activatable probe with a shorter optical imaging time, MMPSense ™ 750 FAST (MMPSense750), could be used for visualization of MMP activity in the early stages of ischemia reperfusion in a mouse model of stroke. (biomedcentral.com)
  • The infarct volume, as well as serum levels of matrix metalloproteinase-9 (MMP-9) and interleukin-10 (IL-10), were measured one week after stroke. (ac.ir)
  • 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)
  • MiRNAs typically bind to the 3′ untranslated region (UTR) of their mRNA targets and downregulate gene expression via mRNA degradation or translational inhibition ( 8 - 10 ). (spandidos-publications.com)
  • Ticagrelor, but not clopidogrel, attenuated fibrosis and decreased collagen-III mRNA levels 4 weeks after ischemia/reperfusion. (utmb.edu)
  • Rosuvastatin inhibits the expressions of ICAM-1, MCP-1, IL-8, IL-6, and COX-2 mRNA and protein levels through inhibition of c-Jun N-terminal kinase and nuclear factor-kB in endothelial cells. (bioservuk.com)
  • Arginase inhibition by (-)-Epicatechin reverses endothelial cell aging. (ucsd.edu)
  • Rosuvastatin (1.25 mg/kg) significantly inhibits thrombin-induced transmigration of monocvtes across mesenteric venules via inhibition of the endothelial cell surface expression of P-selectin, and increases the basal rate of nitric oxide in aortic segments by 2-fold times. (bioservuk.com)
  • Upregulation of miR‑133b‑5p contributes to HPC‑mediated cardioprotection in cardiomyocytes, and the mechanism may be associated with inhibition of caspase‑8 and caspase‑3 apoptotic signaling. (spandidos-publications.com)
  • The inhibition of IκBα degradation abolishes induction ofNF-κB-dependent gene expression in cell culture and in mouse models of acute pancreatitis and myocardial infarction, including upregulation of endothelial adhesion proteins VCAM- 1 and ICAM-1. (umn.edu)
  • 1) Ticagrelor (10 or 30 mg/kg) or clopidogrel (12.5 mg/kg) was given via intraperitoneal injection 5 minutes before reperfusion. (utmb.edu)
  • The loss of cardioprotection after L-NAME administration indicates that cardioprotection by Rho-K inhibition is mediated through nitric oxide-dependent pathway. (vcu.edu)
  • Objective: The effect of the nitric oxide donor, SIN-1, in proximal and distal coronary arteries with normal endothelium was characterised before and after inhibition of NO synthesis with L-nitroarginine methyl ester (L-NAME). (eurekamag.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)
  • In group 2 the response to acetylcholine was significantly (p lt 0.05) attenuated in left circumflex coronary arteries exposed to ischaemia and reperfusion compared with left anterior descending control rings from the same heart. (eurekamag.com)
  • Furthermore, Fasudil administration at and throughout reperfusion showed similar cardioprotection. (vcu.edu)
  • Pharmacologic inhibition of glycolytic metabolism completely abolished the protection afforded the heart by Txnip deficiency under hypoxic conditions. (jci.org)
  • In this case, the infarct is diffusely hemorrhagic. (medscape.com)
  • This project investigates the potential for drugs that inhibit intracellular regeneration of glucocorticoid to modify repair after heart attack by preventing infarct expansion and reducing the stimulus for the subsequent maladaptive remodeling that leads to HF. (ed.ac.uk)
  • This acute treatment or chronic ticagrelor for 4 weeks or their combination improved heart function, whereas clopidogrel, despite achieving a similar degree of platelet inhibition, had no effect. (utmb.edu)
  • Clinically, beneficial effects of GLP-1 have also been demonstrated in patients with myocardial ischemia and heart failure. (biomedcentral.com)
  • Ischemia is the condition suffered by tissues & organs when deprived of blood flow -- mostly the effects of inadequate nutrient & oxygen. (benbest.com)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
  • Hearts were isolated, perfused in Langendorff mode and subjected to 30 min stabilization before 30 min ischemia and 60 min reperfusion. (vcu.edu)
  • This work investigated the mechanism of myocardial protection of trilinolein to determine if inhibition of calcium influx and alteration of activity of superoxide dismutase are involved. (tmu.edu.tw)
  • 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)