• 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)
  • However, whether GRh2 has a protective effect on ischaemia/reperfusion (I/R) in the myocardium has yet to be elucidated. (spandidos-publications.com)
  • Restoration of blood supply, termed reperfusion, has been used to treat ischemic myocardium and prevent further tissue damage. (spandidos-publications.com)
  • Although the mechanisms of ischemic preconditioning and APC are thought to be similar, it is not known whether the beneficial effects of APC are also reduced in the aged myocardium. (asahq.org)
  • Immature calcium handling in immature myocardium raises intracellular calcium concentrations after ischemia and reperfusion. (medscape.com)
  • Because of the increased ability of the immature myocardium to rely on anaerobic glycolysis, it can withstand ischemic injury better than adult myocardium can. (medscape.com)
  • In the ischemic myocardium, an increase in glucose uptake and subsequent ATP generated through glycolysis helps to sustain myocardial electric and mechanical performance, maintains cellular ultrastructure, promotes myocardial recovery. (biomedcentral.com)
  • The injured myocardium develops an evolving dependence on glucose as its preferred metabolic substrate while development of myocardial insulin resistance is associated with the progression of heart failure and increased incidence as well as severity of the damaged hearts. (biomedcentral.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)
  • These studies will not only extend our understanding of the fundamental mechanism by which these protein adducts are regulated in the myocardium but will also provide a solid rationale towards the specific putative binding sites available on AIFm2 in regulating NADH oxidoreductase activity during I/R injury-induced mitochondrial oxidative stress. (lsuhs.edu)
  • Before ischemia, acute troglitazone treatment had no effect on LV function, electrocardiogram, or substrate utilization. (diabetesjournals.org)
  • Acute treatment with troglitazone increases susceptibility to ventricular fibrillation during myocardial ischemia and reperfusion. (diabetesjournals.org)
  • Renal ischemia-reperfusion injury (IRI) is considered as a major cause of acute kidney injury. (frontiersin.org)
  • Protection of the heart against injury from acute ischemia remains challenging for emergency physicians and cardiologists because there are no therapies proven to directly protect the heart against the deleterious effects of ischemia in humans. (mcw.edu)
  • Acute kidney injury (AKI) is a common clinical syndrome characterized by rapid deterioration of renal function. (biomedcentral.com)
  • Insulin, glucose and potassium (GIK) are touted as useful metabolic adjuvant, associated with improvement of cardiac function in acute myocardial function, but the general acceptance of this therapeutic approach is limited by requirements for concomitant infusion of glucose and concerns regarding hypoglycemia. (biomedcentral.com)
  • Therefore, we studied whether an acute bout of endurance or interval exercise is able to protect against endothelial I/R injury. (artinis.com)
  • Current treatments for acute ischemic stroke include IV thrombolytic therapy with tissue-type plasminogen activator ( t-PA ) and endovascular therapies using stent retriever devices. (medscape.com)
  • [ 5 ] . A 2015 update of the American Heart Association/American Stroke Association guidelines for the early management of patients with acute ischemic stroke recommends that patients eligible for intravenous t-PA should receive intravenous t-PA even if endovascular treatments are being considered and that patients should receive endovascular therapy with a stent retriever if they meet criteria. (medscape.com)
  • Reperfusion triggers an inflammatory response and often results in oxidative damage. (wikipedia.org)
  • H2S decreases injury through many different effects such a decrease in oxidative stress, maintenance of mitochondrial function, and increased eNOS (endothelial nitric oxide synthase) activation. (wikipedia.org)
  • In conclusion, the present study confirmed that GRh2 could reduce oxidative stress and inflammation in cardiomyocytes after reperfusion, and its mechanism of action may be related to its regulation of the Nrf2/HO‑1/NLRP3 signalling pathway. (spandidos-publications.com)
  • Meng X, Zhang L, Han B and Zhang Z: PHLDA3 inhibition protects against myocardial ischemia/reperfusion injury by alleviating oxidative stress and inflammatory response via the Akt/Nrf2 axis. (spandidos-publications.com)
  • The authors carried out tests on an animal model to investigate the individual and combined effects of melatonin and NMN on myocardial function, mitochondrial activity, and oxidative stress status following ischemia/reperfusion injury in aged rat hearts. (prohealth.com)
  • Thus, inhibition of oxidative stress and myocardial apoptosis is beneficial in the treatment of myocardial I/R injury. (spandidos-publications.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)
  • Post-ischemic stroke-induced myocardial dysfunction is associated with nitro-oxidative stress and sympathetic overactivity. (escardio.org)
  • Accumulated evidence indicates that oxidative stress in mitochondria plays a vital role in cardiac injury, but how mitochondrial redox mechanisms are involved in cardiac dysfunction remains unclear. (lsuhs.edu)
  • The ischemic injury underlying these illnesses is complex, involving intricate interplays among many biological functions including energy metabolism, vascular regulation, hemodynamics, oxidative stress, inflammation, platelet activation, and tissue repair that take place in a context- and time-dependent manner. (cdc.gov)
  • Ischemic preconditioning and anesthetic preconditioning (APC) are reported to decrease myocardial infarct size during ischemia-reperfusion injury. (asahq.org)
  • Interrupting reperfusion as a stroke therapy: ischemic postconditioning reduces infarct size after focal ischemia in rats. (ac.ir)
  • 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 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)
  • 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)
  • 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)
  • Observe and count:â' The Amount of Apoptosis Positive Cell Nucleus, Total Cell Nucleus, and rate of myocardial cell apoptosis. (dpi-journals.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)
  • 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)
  • HNE mediates necrosis, apoptosis, and autophagy within the area rendered ischemic over the first 6 to 24 hours. (lsuhs.edu)
  • Ischemic postconditioning may not influence early brain injury induced by focal cerebral ischemia/reperfusion in rats. (ac.ir)
  • MB research in ischemic heart stroke While low-dose MB has been shown to lessen neurobehavioral impairment in neurodegenerative illnesses (Parkinson's disease [23 29 Alzheimer disease [30-32]) the neuroprotective ramifications of MB on cerebral ischemia in vivo had been only. (immune-source.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)
  • Ischemic heart disease is the leading cause of mortality worldwide, therefore, identification of novel drug targets for cardioprotection is of great importance. (nih.gov)
  • Ischemia reperfusion injury and cardioprotection by conditioning have been shown to affect global myocardial gene expression profile at the transcript level. (nih.gov)
  • Heusch G: Myocardial ischaemia-reperfusion injury and cardioprotection in perspective. (spandidos-publications.com)
  • Heusch G: Molecular basis of cardioprotection: Signal transduction in ischemic pre-, post-, and remote conditioning. (spandidos-publications.com)
  • One such area of interest is the ability to modulate myocardial glucose uptake and its impact on cardioprotection. (biomedcentral.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)
  • This study aimed to evaluate the effects of TQ on spatial memory and hippocampal long-term potentiation (LTP) in rats with thioacetamide (TAA)-induced liver injury and hepatic encephalopathy. (magiran.com)
  • This study aims to explore the protective effects of sufentanil-postconditioning on myocardial cells in rats. (dpi-journals.com)
  • Methods: Choosing 80 healthy rats, all was established in Myocardial Ischemia-reperfusion Model. (dpi-journals.com)
  • Conclusion: Post-treatment with sufentanil alleviates myocardial ischemia-reperfusion injury in rats. (dpi-journals.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)
  • 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)
  • 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)
  • 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)
  • SA also attenuated renal I/R injury ( 11 ). (spandidos-publications.com)
  • The objective of present study was to assess the effects of MK-886 and DITPA on renal I/R injury. (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)
  • Cardiac cells that survive this first wave of injuries will often have their mitochondrial functions compromised, and this can lead to further dysfunction and even cellular death. (prohealth.com)
  • These factors affect the way in which the immature heart handles calcium, which, in turn, contributes to the myocardial dysfunction observed after CPB. (medscape.com)
  • Ischemic preconditioning, postconditioning, and remote conditioning trigger endogenous cardioprotective mechanisms that render the heart more resistant to lethal ischemic-reperfusion injury. (nih.gov)
  • However, major cardiovascular co-morbidities such as hyperlipidemia, diabetes, and their co-medications interfere with these cardioprotective mechanisms thereby limiting the efficacy of cardioprotective ischemic conditioning maneuvers. (nih.gov)
  • Cardioprotective effects of acidified sodium nitrite in myocardial ischemia with reperfusion. (aspetjournals.org)
  • Thus, acidified NaNO2 exerts a significant protective action during ischemia and reperfusion injury, which suggests that endothelium-derived relaxing factor has a cardioprotective effect in MI. (aspetjournals.org)
  • Research done in animals shows that treatment with NAD+ precursors like NMN have cardioprotective effects against ischemia/reperfusion injury (4). (prohealth.com)
  • 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)
  • Our current projects are focused on: 1) Rescue and Role of Complex I in Myocardial Ischemic Injury 2) Subcellular Regulation of Autophagy 3) Mitochondria and Stem Cells in Anthracycline-Induced Heart Failure 4) Development of Small-Molecular Cardioprotective Agents for Treatment of Reperfusion Injury and 5) Microbial Basis of Cardiovascular Disease. (pewtrusts.org)
  • 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)
  • Here we aimed to identify differentially methylated genes that play a functional role in ischemic stroke in a Chinese population. (biomedcentral.com)
  • Altered DNA methylation of the TRIM6 , TLN2, and FLRT2 genes may play a functional role in ischemic stroke in Chinese populations. (biomedcentral.com)
  • Nitric oxide generation during reperfusion and ischemia plays a substantial role in ischemic and reperfusion injury [56]. (immune-source.com)
  • A rat model of myocardial I/R injury was constructed by ligating the left anterior descending coronary artery, which was subsequently treated with GRh2. (spandidos-publications.com)
  • The effects of acidified sodium nitrite (NaNO2) which releases nitric oxide, a substance which is thought to be indistinguishable from endothelium-derived relaxing factor, were investigated in a 6-h model of myocardial ischemia (MI) with reperfusion in open-chest, anesthetized cats. (aspetjournals.org)
  • Cysteine hydropersulfide reduces lipid peroxidation and protects against myocardial ischaemia-reperfusion injury - Are endogenous persulfides mediators of ischaemic preconditioning? (southampton.ac.uk)
  • However, the beneficial effects of ischemic preconditioning have been shown to decrease with advancing age. (asahq.org)
  • 1 demonstrated the phenomenon in dogs, ischemic preconditioning (IPC) has been shown to occur in every mammalian species in which it has been investigated. (asahq.org)
  • Preconditioning, i.e., repeated exposure to short periods of ischemia, effectively reduces endothelial I/R injury. (artinis.com)
  • In the present study, we examined the hypothesis that exercise has preconditioning effects on endothelial I/R injury. (artinis.com)
  • Acidified NaNO2 (12.5-50 mmol/kg/hr) was infused i.v., starting 30 min postocclusion followed by reperfusion 1 hr later, in cats subjected to MI by occlusion of the left anterior descending coronary artery. (aspetjournals.org)
  • Coronary artery smooth muscle function was comparable in hearts before and after ischemia. (elsevierpure.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)
  • 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)
  • Endothelial ischemia-reperfusion (I/R) injury importantly contributes to the poor prognosis during ischemic (myocardial) events. (artinis.com)
  • In conclusion, a single bout of lower limb interval exercise, but not moderate-intensity endurance exercise, effectively prevents brachial artery endothelial I/R injury. (artinis.com)
  • Reperfusion injury increases the damage done after events such as heart attacks. (prohealth.com)
  • In experimental groups A (n = 10) and B (n = 10), metabolic control of autoregulation was assessed by plots of myocardial oxygen consumption versus coronary flow generated by incremental increases in heart rate. (elsevierpure.com)
  • Ischemia decreases intracellular pH and increases intracellular Na and intracellular Ca in all age groups. (asahq.org)
  • 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)
  • 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)
  • During myocardial ischemia (lack of blood flow to the muscle tissue of the heart, commonly referred to as a "heart attack"), blood flow is interrupted because of damage to one or more of the coronary blood vessels that irrigate the heart. (prohealth.com)
  • In many cases, damage to heart tissue by reperfusion injury is greater than the damage done by the interruption of blood flow. (prohealth.com)
  • For the study, the researchers performed tests to measure the condition of cardiac tissue before and after an ischemic event and after perfusion was re-established. (prohealth.com)
  • but reperfusion may introduce additional harm to the tissue through a process known as ischemia/reperfusion injury. (cdc.gov)
  • Excessive glutamate release resulting in excessive Ca +2 entry into cells is the excitotoxicity which initiates the brain ischemic damage seen in stroke and cardiac arrest. (benbest.com)
  • 18. Wang CX, Yang T, Shuaib A. An improved version of embolic model of brain ischemic injury in the rat. (ac.ir)
  • Sun W, Wang Z, Sun M, Huang W and Wang Y and Wang Y: Aloin antagonizes stimulated ischemia/reperfusion-induced damage and inflammatory response in cardiomyocytes by activating the Nrf2/HO-1 defense pathway. (spandidos-publications.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)
  • This paper provides a review on the current evidence supporting the use of GLP-1 in experimental animal models and human trials with the ischemic and non-ischemic heart and discusses their molecular mechanisms and potential as a new therapeutic approach. (biomedcentral.com)
  • However, the molecular mechanisms involved in AIFm2 translocation that mediates cardiac injury remain unknown. (lsuhs.edu)
  • Ischemia and reperfusion can cause serious brain damage in stroke or cardiac arrest. (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)
  • DNA methylation has previously been associated with ischemic stroke, but the specific genes and their functional roles in ischemic stroke remain to be determined. (biomedcentral.com)
  • Genome-wide DNA methylation assessed with the Illumina Methylation EPIC Array in a discovery sample including 80 Chinese adults (40 cases vs . 40 controls) found that patients with ischemic stroke were characterized by increased DNA methylation at six CpG loci (individually located at TRIM6 , FLRT2 , SOX1 , SOX17 , AGBL4, and FAM84A , respectively) and decreased DNA methylation at one additional locus (located at TLN2 ). (biomedcentral.com)
  • Stroke is one of the leading causes of mortality and morbidity worldwide, second only to ischemic heart disease (IHD) [ 1 ]. (biomedcentral.com)
  • Methylene blue provides been shown to boost blood circulation pressure and myocardial function by inhibiting nitric oxide activities in individual septic surprise disease [41 47 50 52 These research Zotarolimus showed that methylene blue provides vascular results and causes vasoconstriction transiently thus improving blood circulation pressure that could help to reduce the chances of hypoperfusion during heart stroke. (immune-source.com)
  • Not only can both produce symptoms that mimic ischemic stroke, but they can also aggravate ongoing neuronal ischemia. (medscape.com)
  • In patients with transient ischemic attacks (TIAs), failure to recognize the potential for near- term stroke, failure to perform a timely assessment for stroke risk factors, and failure to initiate primary and secondary stroke prevention exposes the patient to undue risk of stroke and exposes clinicians to potential litigation. (medscape.com)
  • Therapeutic hypothermia (TH) aims to ameliorate further injury in infants with moderate and severe hypoxic ischemic encephalopathy (HIE). (nature.com)
  • However, mitigation strategies to preserve cardiac function after an ischemic event have often only focused on individual therapeutic agents, and the results have not been ideal. (prohealth.com)
  • Accordingly, mechanism of enhancing myocardial energetic efficiency by stimulating glucose availability and utilization has led to the vigorous pursuit of therapeutic approaches designed to augment glucose uptake and oxidation. (biomedcentral.com)
  • Here we review the current literature on scutellarin to provide a comprehensive understanding of the pharmacological activity, mechanism of action, toxicity, and therapeutic potential of scutellarin for the treatment of ischemia, diabetic complications, and other chronic diseases. (cdc.gov)
  • abstract = "To determine the mechanism(s) responsible for decreased coronary flow after global cardiac ischemia and reperfusion, we studied 40 isolated rabbit hearts before and after 30 minutes of normothermic ischemic arrest and reperfusion. (elsevierpure.com)
  • There is proof that MB lowers or inhibits nitric oxide era might have the aftereffect of neuroprotection in ischemia/reperfusion damage. (immune-source.com)
  • We previously demonstrated that chronic pretreatment with a thiazolidinedione peroxisome proliferator-activated receptor (PPAR)-γ activator, troglitazone, improves recovery of left ventricular (LV) function and substrate metabolism after ischemia and reperfusion, without causing arrhythmias. (diabetesjournals.org)
  • Ischemia is the condition suffered by tissues & organs when deprived of blood flow -- mostly the effects of inadequate nutrient & oxygen. (benbest.com)
  • Hypoxic ischemic encephalopathy (HIE) occurs in 1-6 per 1,000 live full-term births and is caused by the interruption of blood and/or oxygen supply to the brain in the perinatal period ( 1 , 2 ). (nature.com)
  • As such, new drugs that would complement reperfusion by providing neural and cardiovascular protection and by targeting multiple abnormalities in ischemia are receiving increased attention. (cdc.gov)
  • Therefore, we hypothesize that HNE adduction to AIFm2 mediates mitochondrial stress signaling through translocation of AIFm2 from mitochondria to the nucleus and contributes to the pathogenesis of heart failure following I/R injury. (lsuhs.edu)
  • Neonatal rat cardiomyocytes were also used to evaluate the protective effect of GRh2 on hypoxia/reoxygenation (H/R)‑induced myocardial injury in vitro. (spandidos-publications.com)
  • It is being developed as a treatment for diabetic retinopathy, pressure ulcers, wound healing, and Myocardial ischemia/Reperfusion Injury. (tradekorea.com)
  • this may be an important mechanism of decreased coronary perfusion and subsequent myocardial injury during reflow. (elsevierpure.com)
  • When blood flow is re-established (reperfusion), a series of inflammatory responses take place because of the damage sustained by the tissues affected by the previous lack of blood. (prohealth.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)
  • Delayed postconditionig initiates additive mechanism necessary for survival of selectively vulnerable neurons after transient ischemia in rat brain. (ac.ir)
  • Sham group (n = 6), mice underwent same anesthetic and surgical procedures except for ischemia induction. (biomedcentral.com)
  • For a more quantitative approach less concerned with molecular biology, see Quantifying Ischemic Damage for Cryonics Rescue . (benbest.com)
  • APC decreased intracellular Na and intracellular Ca accumulation during ischemia in young adult and middle-aged hearts. (asahq.org)
  • 3, 5-diiodothyropropionic acid (DITPA) have evidences of improving effects on I/R in heart through modulation of cellular signaling in response to ischemic stress. (biomedcentral.com)
  • its ability to attenuate glutamate toxicity, its ability to protect against cellular damage, its ability to protect brains from ischemic damage, its anxiolytic effect, and its superior antioxidant activity which can be used in the prophylaxis and treatment of oxidation associated diseases. (drphilipblair.com)