• The most effective early treatment for reducing AMI injury and limiting the infarcted myocardium is timely coronary revascularization using thrombolytic therapy or primary percutaneous coronary intervention (PPCI) [ 2 - 4 ]. (hindawi.com)
  • This coupled comorbidity of pathological ischemia and therapeutic reinjury of infarcted myocardium, namely, myocardial ischemia-reperfusion injury (MIRI), is particularly refractory to treatment [ 4 , 5 ]. (hindawi.com)
  • During injury stimulation, the major effects on the cardiac function may be those involving mitochondria-dominated events along with potential nucleus-governed genetic/epigenetic alternations within the cardiomyocytes as well as the macrophage-led inflammation and T-cell-led immune responses underlying the myocardium-vessel interactive cascade. (hindawi.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)
  • Following myocardial I/R injury, the expression of miR‑133b‑5p was decreased in myocardium, while this decrease was restored by IPC. (spandidos-publications.com)
  • Both ischemic and reperfused rat myocardium can undergo apoptotic cell death, however the myocardium, which is subjected to ischemia followed by reperfusion, undergoes accelerated apoptosis [ 3 ]. (ac.ir)
  • These pleiotropic effects thus have a major role in protecting the myocardium against ischemic injury. (ac.ir)
  • Restoration of blood supply, termed reperfusion, has been used to treat ischemic myocardium and prevent further tissue damage. (spandidos-publications.com)
  • REPERFUSION of the myocardium after sustained ischemia induces myocardial cell necrosis and apoptosis, resulting in increased infarct size despite the restoration of coronary blood flow. (silverchair.com)
  • 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)
  • Ischemic injury, however, may be located in the mid myocardium or even the subepicardium if the level of the coronary occlusion is distal within the myocardium. (medscape.com)
  • BACKGROUND: Coagulation disorders and reperfusion of ischemic myocardium are major causes of morbidity and mortality. (regionh.dk)
  • 2002 - defended ahead of time his PhD thesis in Pathologic Physiology entitled «Comparative evaluation of the cardioprotective efficacy of local and distant ischemic adaptation of the myocardium» dedicated to myocardial protection against ischemia injury in the experiment. (almazovcentre.ru)
  • Both sildenafil and vardenafil protect the ischemic myocardium against reperfusion injury through a mechanism dependent on mitochondrial K(ATP) channel opening. (nih.gov)
  • 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)
  • HPC protected neonatal rat cardiomyocytes against H/R injury by increasing cell viability, while reducing LDH release and cell apoptosis. (spandidos-publications.com)
  • However, the knockdown of miR‑133b‑5p in the cardiomyocytes blocked HPC‑mediated cardioprotection as reflected by the aggravation of cell injury and apoptosis. (spandidos-publications.com)
  • 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)
  • Also, curcumin reduces cell apoptosis induced by myocardial IRI, curcumin reduces cell apoptosis induced by myocardial IRI and activates the Nrf-2/HO-1 signaling pathway during myocardial. (edu.iq)
  • In conclusion, the present study demonstrated that SA inhibits the apoptosis of H9c2 cardiomyocytes following H/R injury via reduced activation of the p38MAPK and JNK signaling pathways. (spandidos-publications.com)
  • The underlying mechanisms behind myocardial I/R injury are associated with a number of factors, including substantial free radical production, intracellular calcium overload, increased inflammation, myocardial necrosis and apoptosis ( 6 ). (spandidos-publications.com)
  • Thus, inhibition of oxidative stress and myocardial apoptosis is beneficial in the treatment of myocardial I/R injury. (spandidos-publications.com)
  • The results demonstrated that SA inhibited apoptosis signaling in H9c2 cardiomyocytes via downregulation of p38 mitogen-activated protein kinase (p38MAPK) and c-Jun N-terminal kinase (JNK) signaling pathways following hypoxia/reoxygenation (H/R) injury. (spandidos-publications.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)
  • End of the experiments we collected blood samples for the measurement of endothelial dysfunction parameter asymmetric dimethylarginine (ADMA), apoptosis parameters M30 and M65, cardiac risk factors homocysteine and serum lipid profile.CDP-choline treatment significantly attenuated the size of infarct area induced by long term ischemia-reperfusion versus saline group. (uludag.edu.tr)
  • 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)
  • 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)
  • In vivo, treatment of mice with rAAV9-BAG3 prior to I/R significantly decreased infarct size and improved left ventricular function when compared with mice receiving rAAV9-GFP and improved markers of autophagy and apoptosis. (uthscsa.edu)
  • Wild‐type C57BL/6J mice (male, 8-10 weeks old) were used and murine myocardial ischemia and reperfusion injury (IRI) model was conducted, cardiac function was evaluated by echocardiography. (edu.iq)
  • This augmented adverse remodelling after I/R and led to an increased infarct size and deterioration of cardiac function. (elifesciences.org)
  • Surprisingly, Txnip-KO hearts had greater recovery of cardiac function after an ischemia-reperfusion insult. (jci.org)
  • Consistently, knockdown of CLU4A reduced the myocardial infarct size and improved cardiac function in vivo . (engreen.com.cn)
  • 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)
  • Atorvastatin has been shown to be cardioprotective in ischemia-reperfusion (I/R) injury. (ac.ir)
  • The present study aimed to clarify the cardioprotective effect of SA in myocardial I/R injury in vitro and explore the potential molecular mechanisms. (spandidos-publications.com)
  • In rodents, Bbeta(15-42) inhibits proinflammatory cytokine release and is cardioprotective during ischemia-reperfusion injury. (bris.ac.uk)
  • However, clinical and preclinical results using various cardioprotective strategies to attenuate reperfusion injury have generally not been applicable for every day clinical practice. (eurekaselect.com)
  • Although, CDP-choline treatment did not significantly alter the blood levels of any parameter (ADMA, M30, M65, homocysteine, serum lipid profile).Results of this study show that CDP-choline exerts cardioprotective effects in long term myocardial ischemia-reperfusion injury. (uludag.edu.tr)
  • Phosphodiesterase-5 (PDE-5) inhibitors including sildenafil and vardenafil induce powerful preconditioning-like cardioprotective effect against ischemia/reperfusion injury through opening of mitochondrial K(ATP) channels in the heart. (nih.gov)
  • 5-HD blocked the cardioprotective effects of sildenafil and vardenafil as shown by an increase in infarct size (34.0+/-1.1% and 28.3+/-1.9%, respectively). (nih.gov)
  • Oral dosing of rats with SCN-, before acute ischemia-reperfusion injury (30 min occlusion, 24 h or 4 week recovery), significantly reduced the infarct size as a percentage of the total reperfused area (54% versus 74%), and increased the salvageable area (46% versus 26%) as determined by MRI imaging. (ku.dk)
  • These data indicate that elevated levels of the MPO substrate SCN-, which can be readily modulated by dietary means, can protect against acute ischemia-reperfusion injury. (ku.dk)
  • 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)
  • In this study, we investigated that if CDP-choline has protective effects against long-term myocardial ischemia-reperfursion injury in rats.Long term ischemia-reperfusion was produced in anaesthetized rats by ligature of the left main coronary artery for 30 minutes followed by reperfusion period for the next 180 minutes. (uludag.edu.tr)
  • 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)
  • 4. Ren C, Gao X, Niu G, Yan Z, Chen X, Zhao H. Delayed postconditioning protects against focal ischemic brain injury in rats. (ac.ir)
  • Interrupting reperfusion as a stroke therapy: ischemic postconditioning reduces infarct size after focal ischemia in rats. (ac.ir)
  • Ischemic postconditioning may not influence early brain injury induced by focal cerebral ischemia/reperfusion 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)
  • Effects of three types of bariatric interventions on myocardial infarct size and vascular function in rats with type 2 diabetes mellitus. (almazovcentre.ru)
  • Hypoxia/reoxygenation (H/R) as well as hypoxic preconditioning (HPC) is widely used for simulating in vivo myocardial I/R and ischemic preconditioning (IPC) in a cell culture model. (spandidos-publications.com)
  • An intravital model for imaging the adult and aged IR-injured beating heart in real time in vivo was used to demonstrate heightened basal and injury-induced neutrophil recruitment, and poorer blood flow, in the aged coronary microcirculation when compared with adult hearts. (jci.org)
  • 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)
  • 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)
  • 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)
  • corresponding, respectively, to 189 control- and 170 NA-1-treated animals) showed a significant 42.8% reduction in infarct size in the NA-1-treated group. (pdesignaling.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)
  • Left main coronary artery occlusion generally results in a large anterolateral infarct, whereas occlusion of the left anterior descending coronary artery causes necrosis limited to the anterior wall. (medscape.com)
  • In hearts with a right coronary dominance (with the right artery supplying the posterior descending branch), a right coronary artery occlusion causes a posterior (inferior) infarct. (medscape.com)
  • Five dogs were fed with α-tocopherol (1000 IU/kg, bw) for ten days prior to 90 min of left anterior descending coronary artery occlusion followed by 4 hours of reperfusion. (manipal.edu)
  • Adult male New Zealand white rabbits were anesthetized and subjected to ischemia by 30 min of coronary artery occlusion followed by 3 h of reperfusion. (nih.gov)
  • All animals were subjected to 45 minutes ischemia following 180 minutes reperfusion. (uni-wuerzburg.de)
  • Tripathi, Y & Hegde, BM 1997, ' Effect of α-tocopherol pretreatment on infarct size following of 90 minutes ischemia and 4 hours of reperfusion in dogs ', Indian Journal of Physiology and Pharmacology , vol. 41, no. 3, pp. 241-247. (manipal.edu)
  • 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)
  • An IL-36R antagonist (IL-36Ra) decreased neutrophil recruitment, improved blood flow, and reduced infarct size in both adult and aged mice. (jci.org)
  • To test if ß1-containing integrins are required during repair following acute injury, we administered E. coli lipopolysaccharide (LPS) by intratracheal injection to mice with a postdevelopmental deletion of ß1 integrin in AT2 cells. (bvsalud.org)
  • While control mice recovered from LPS injury without structural abnormalities, ß1-deficient mice had more severe inflammation and developed emphysema. (bvsalud.org)
  • When subjected to myocardial ischemia-reperfusion injury, Caspase3 transgenic mice showed increased infarct size and a pronounced susceptibility to die. (uniroma5.it)
  • 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)
  • Neonatal rat cardiomyocytes were isolated and subjected to hypoxia/reoxygenation (H/R) injury, with or without HPC. (spandidos-publications.com)
  • Given the central role that mitochondria play during hypoxia, we hypothesized that Txnip deletion would enhance ischemia-reperfusion damage. (jci.org)
  • Gibson invented several of the measures of coronary blood flow that are widely used today (the TIMI frame count and the TIMI myocardial perfusion grade). (wikidoc.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)
  • 2007 - Head of Research Laboratory of Myocardial Metabolism, Almazov Federal Heart, Blood and Endocrinology Centre (Almazov National Medical Research Centre). (almazovcentre.ru)
  • Rotigaptide (ZP123) Prevents Spontaneous Ventricular Arrhythmias and Reduces Infarct Size During Myocardial Ischemia/Reperfusion Injury in Open-Chest Dogs. (wikipedia.org)
  • 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)
  • Infarct size measurement, cardiac troponin-I assays, oxidative stress analysis and histopathological analyzed. (edu.iq)
  • The resulted data showed that curcumin alleviates myocardial inflammatory responses and oxidative stress during myocardial IRI. (edu.iq)
  • 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)
  • Failure of normal alveolar repair mechanisms can lead to loss of alveolar structure (emphysema) or development of fibrosis, depending on the type and severity of injury. (bvsalud.org)
  • Intracellular mechanisms underlying this so-called reperfusion injury presumably include increased levels of reactive oxygen species, Ca 2+ overload, rapid restoration of physiologic pH, and inflammatory processes resulting in opening of the mitochondrial permeability transition pore (mPTP). (silverchair.com)
  • Focus areas: mechanisms of myocardial protection against ischemia-reperfusion injury, development of targeted drug delivery using nanocarriers. (almazovcentre.ru)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
  • Vascular endothelial cell (EC)-derived factors play an important role in endothelial-cardiomyocyte crosstalk and could save cardiomyocytes (CMs) from injury. (mdpi.com)
  • Large infarct size and coronary microvascular injury, as the consequence of ischaemia-reperfusion injury and distal embolization of atherothrombotic debris, account for suboptimal long-term prognosis of STEMI patients. (ox.ac.uk)
  • These device-based therapies can be categorized according to the pathophysiological pathways they target: (i) techniques to prevent distal atherothrombotic embolization, (ii) techniques to prevent or mitigate ischaemia/reperfusion injury, and (iii) techniques to enhance coronary microvascular function/integrity. (ox.ac.uk)
  • 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)
  • A wealth of studies now confirm that PQQ's cell-signaling activity translates into substantial protection against degenerative and age-related conditions, such as mitochondrial dysfunction, 1 heart degeneration, 18-20 brain injury, and cognitive decline. (lifeextension.com)
  • While altered BAG3 expression has been associated with cardiac dysfunction, its role in ischemia/reperfusion (I/R) is unknown. (uthscsa.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)
  • Acute kidney injury (AKI) can result from a variety of etiologies (e.g., ischemia, toxicity, and sepsis) and is characterized by high rates of morbidity and mortality. (biolifesas.org)
  • However, beta-adrenergic signaling displays a differential role in cardioprotection during reperfusion. (silverchair.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)
  • abstract = "Many compounds have been shown to prevent reperfusion injury in various animal models, although to date, translation into clinic has revealed several obstacles. (bris.ac.uk)
  • abstract = "The present study was designed to evaluate the effects of pretreatment with antioxidants on free radical mediated reprefusion injury. (manipal.edu)
  • Renal ischemia-reperfusion injury (IRI) is a common pathophysiological phenomenon in clinical settings. (frontiersin.org)
  • We also implicate Caspase3 in determining myocardial infarct size after ischemia-reperfusion injury, because its cardiomyocyte-specific overexpression increases infarct size. (uniroma5.it)
  • Similarly, cardiomyocyte-specific Txnip deletion reduced infarct size after reversible coronary ligation. (jci.org)
  • 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)
  • Ischemia decreases intracellular pH and increases intracellular Na and intracellular Ca in all age groups. (asahq.org)
  • It receives blood from a vein in the nasal cavity, runs backwards, and gradually increases in size as blood drains from veins of the brain and the DURA MATER. (bvsalud.org)
  • Interleukin-36 (IL-36), a newly discovered proinflammatory member of the IL-1 superfamily, may mediate this injury, but its role in the injured heart is currently not known. (jci.org)
  • The aim of the study is to investigate the effects of curcumin in attenuates myocardial ischemia and reperfusion-induced proinflammatory response through activation of the Nrf-2/HO-1 signaling pathway. (edu.iq)
  • Inconclusion, this study demonstrates that curcumin attenuates myocardial IRI by inhibiting proinflammatory cytokines through a mechanism that may be related to activation of the Nrf-2/HO-1 signaling pathway. (edu.iq)
  • 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)
  • Cellular injury was evaluated by detecting cell viability, lactate dehydrogenase (LDH) activity and apoptotic rate. (spandidos-publications.com)
  • It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
  • Acute myocardial infarctions (MIs) are common. (medscape.com)
  • 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)
  • Esmolol given during the initial 30 min of reperfusion had no effect on infarct size (54 +/- 4%) but blocked desflurane-induced postconditioning (58 +/- 5%), whereas esmolol administered throughout reperfusion reduced infarct size in the absence or presence of desflurane to 42 +/- 6% and 41 +/- 7%, respectively. (silverchair.com)
  • ICI 118,551 and KN-93 did not affect infarct size (62 +/- 4% and 62 +/- 6%, respectively) but abolished desflurane-induced postconditioning (57 +/- 5% and 64 +/- 3%, respectively). (silverchair.com)
  • H-89 decreased infarct size in the absence (36 +/- 5%) or presence (33 +/- 5%) of desflurane. (silverchair.com)
  • We here investigated macrophage lineages and ablated tissue macrophages in homeostasis and after I/R injury in a CSF1R-dependent manner. (elifesciences.org)
  • Infarct size, as percentage of myocardial tissue at risk in α-tocopherol pretreated animals was 5.86 ± 0.83 and was 39.35 ± 7.58 in the untreated animals. (manipal.edu)
  • Following reprefusion in untreated group, the values of serum and myocardial tissue lipid peroxidation were significantly higher than observed values in α-tocopherol treated animals. (manipal.edu)
  • 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)
  • Myocardial infarct size was assessed by triphenyltetrazolium staining. (silverchair.com)
  • The goal of these studies was to demonstrate the protective effect of sildenafil and vardenafil on reperfusion injury and to compare it with the antianginal vasodilator nitroglycerin (NTG). (nih.gov)
  • In summary, resident macrophages orchestrate inflammatory responses improving cardiac remodelling, while recruited macrophages determine infarct size after I/R injury. (elifesciences.org)
  • Supplementation also decreased antibody recognition of HOCl-damaged myocardial proteins. (ku.dk)
  • For example, research with animals found that supplementation with PQQ decreased the size of the area of the heart injured by acute coronary artery blockage . (lifeextension.com)
  • In addition, it has been shown that atorvastatin can protect the isolated mouse heart against reperfusion-induced injury [ 6 ]. (ac.ir)
  • 20. Zhao H. The protective effect of ischemic postconditioning against ischemic injury: from the heart to the brain. (ac.ir)
  • Cytidine diphosphocholine (CDP-choline) is in use for treatments of stroke and head trauma in Japan and several European countries for many years because of its protective effect against cerebral injury. (uludag.edu.tr)
  • APC decreased intracellular Na and intracellular Ca accumulation during ischemia in young adult and middle-aged hearts. (asahq.org)
  • Fas expression was significantly higher in the ischemia-reperfusion group as compared to sham-operated group, but was decreased significantly in atorvastatin treated group as compared with I/R group. (ac.ir)
  • Delayed postconditionig initiates additive mechanism necessary for survival of selectively vulnerable neurons after transient ischemia in rat brain. (ac.ir)
  • Despite extensive research, our understanding of the precise role of different subsets of macrophages in ischemia/reperfusion injury remains incomplete. (elifesciences.org)