• 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)
  • 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)
  • 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)
  • 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)
  • Reperfusion has the potential to salvage ischemic myocardium but paradoxically can cause injury, a phenomenon called as 'reperfusion injury' (IR). (aku.edu)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • Post-ischemic stroke-induced myocardial dysfunction is associated with nitro-oxidative stress and sympathetic overactivity. (escardio.org)
  • 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)
  • 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)
  • Observe and count:â' The Amount of Apoptosis Positive Cell Nucleus, Total Cell Nucleus, and rate of myocardial cell apoptosis. (dpi-journals.com)
  • HNE mediates necrosis, apoptosis, and autophagy within the area rendered ischemic over the first 6 to 24 hours. (lsuhs.edu)
  • In conclusion, myocardial damage in MI is mainly due to ischemic necrosis and inflammatory mechanisms while apoptosis is the main mechanism of cell death in IR in addition to limited ischemic necrosis. (aku.edu)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • 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)
  • One such area of interest is the ability to modulate myocardial glucose uptake and its impact on cardioprotection. (biomedcentral.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)
  • Acute kidney injury (AKI) is a common clinical syndrome characterized by rapid deterioration of renal function. (biomedcentral.com)
  • 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)
  • 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)
  • Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)
  • While the bioactive glycerophospholipid lysophosphatidic acid (LPA) plays a well-known role in atherosclerotic disease, its role in myocardial function remains virtually unexplored. (lsuhs.edu)
  • 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)
  • 2. PI3K p85 and Bcl-2 are targets of miR-503, and the post-ischemic cardiac PI3K p85 protein level is decreased in vivo. (fullpicture.app)
  • 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)
  • 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)
  • 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)
  • This study aimed to determine the potential myocardial protective effect and possible mechanism of action of D. odorifera essential oil (DOEO). (wjtcm.net)
  • Ischemic preconditioning and anesthetic preconditioning (APC) are reported to decrease myocardial infarct size during ischemia-reperfusion injury. (asahq.org)
  • 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)
  • 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)
  • Ischemic cardiovascular and cerebrovascular diseases continue to represent the most common cause of death in modern society. (biomedcentral.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)
  • 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)
  • CONCLUSIONS: The normal levels of CRP in variant angina, despite a significantly larger number of ischemic episodes and greater total ischemic burden, and the failure of CRP values to increase in unstable angina indicate that transient myocardial ischemia, within the range of duration observed, does not itself stimulate an appreciable acute-phase response. (ox.ac.uk)
  • 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)
  • Cardioprotective effects of acidified sodium nitrite in myocardial ischemia with reperfusion. (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 cardioprotective effects of DOEO were examined by histopathological observation, myocardial enzyme detection, peroxidation, anti-oxidant level detection, and related protein expression. (wjtcm.net)
  • 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)
  • Here we aimed to identify differentially methylated genes that play a functional role in ischemic stroke in a Chinese population. (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)
  • Altered DNA methylation of the TRIM6 , TLN2, and FLRT2 genes may play a functional role in ischemic stroke in Chinese populations. (biomedcentral.com)
  • Stroke is one of the leading causes of mortality and morbidity worldwide, second only to ischemic heart disease (IHD) [ 1 ]. (biomedcentral.com)
  • 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)
  • 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)
  • Not only can both produce symptoms that mimic ischemic stroke, but they can also aggravate ongoing neuronal ischemia. (medscape.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)
  • 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 decreases intracellular pH and increases intracellular Na and intracellular Ca in all age groups. (asahq.org)
  • Reperfusion injury increases the damage done after events such as heart attacks. (prohealth.com)
  • 3. Agomir-503 treatment worsens hypoxia/reoxygenation-induced injuries, while antagomir-503 treatment attenuates them and increases phosphorylation of Stat3 (Y705) and Akt (T450). (fullpicture.app)
  • The degree of CNS injury depends on the severity and duration of hypoxia. (medscape.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)
  • 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)
  • Ischemia is the condition suffered by tissues & organs when deprived of blood flow -- mostly the effects of inadequate nutrient & oxygen. (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)
  • 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)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
  • Overall, the study showed that DOEO displayed myocardial protection by upregulating the NF-E2-related nuclear factor- antioxidant response element (Nrf2-ARE) and caspase pathways. (wjtcm.net)
  • 1. MicroRNA-503 (miR-503) exacerbates myocardial ischemia/reperfusion (I/R) injury by inhibiting prosurvival signaling pathways, including PI3K/Akt and STAT3. (fullpicture.app)
  • APC decreased intracellular Na and intracellular Ca accumulation during ischemia in young adult and middle-aged hearts. (asahq.org)
  • It is being developed as a treatment for diabetic retinopathy, pressure ulcers, wound healing, and Myocardial ischemia/Reperfusion Injury. (tradekorea.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)
  • 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)
  • 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)
  • 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)
  • but reperfusion may introduce additional harm to the tissue through a process known as ischemia/reperfusion injury. (cdc.gov)
  • EGT022 os a molecule for the treatment of ischemic diseases based on proteomic research. (tradekorea.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)
  • 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)
  • Relationships between structure and effects of ACE inhibitors: comparative effects in myocardial ischaemic/reperfusion injury. (cmich.edu)
  • Dive into the research topics of 'Relationships between structure and effects of ACE inhibitors: comparative effects in myocardial ischaemic/reperfusion injury. (cmich.edu)
  • Clinically, beneficial effects of GLP-1 have also been demonstrated in patients with myocardial ischemia and heart failure. (biomedcentral.com)
  • 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)
  • It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
  • These results showed that DOEO had significant myocardial cell protection, with IC 50 values ranging from 17.64 to 24.78 μg/mL in vitro . (wjtcm.net)
  • 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)
  • Before ischemia, acute troglitazone treatment had no effect on LV function, electrocardiogram, or substrate utilization. (diabetesjournals.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)
  • However, the necrotic area expressed as a percentage of the myocardial area at risk was significantly lower in the 25 and 50 mmol/kg/hr NaNO2-treated cats. (aspetjournals.org)
  • Cardiac myeloperoxidase activities indicated that significantly fewer neutrophils were attracted to the ischemic zone of the NaNO2-treated MI cats when compared to the vehicle-infused MI cats. (aspetjournals.org)