• The main reason for the acute phase of ischemia-reperfusion injury is oxygen deprivation and, therefore, arrest of generation of ATP (cellular energy currency) by mitochondria oxidative phosphorylation. (wikipedia.org)
  • 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)
  • Using a mouse model, we investigated cardiac remodeling under the influence of acute cigarette smoke (CS) exposure following ischemic injury in both sexes. (biomedcentral.com)
  • Xenon may prevent or ameliorate acute neuronal injury, but it also may aggravate injury during cardiac surgery by increasing bubble embolism. (asahq.org)
  • 1 The pathogenic mechanisms involved in the development of PONCD may be similar to those involved in the propagation of acute neuronal injury from other causes. (asahq.org)
  • For the end point infarct size, estimated by biomarkers of myocardial necrosis, an overall pooled effect was SMD =−0.58, 95% CI: −0.96 to −0.19. (dovepress.com)
  • 2 Paradoxically, reperfusion itself can enlarge the infarct size, by complex mechanisms collectively termed ischemia/reperfusion injury. (dovepress.com)
  • 3 In 2003, Zhao and et all published experimental data demonstrating a considerable reduction of infarct size by a reperfusion procedure termed ischemic postconditioning (IPost), consisting of brief, repetitive cycles of reperfusion and reocclusion, followed by sustained reperfusion. (dovepress.com)
  • The accumulation of cardiac lactate was attenuated by PLCA during myocardial I/R, and infarct size was smaller in rats treated with PLCA (1 mg/kg) than in those treated with caffeic acid (1 mg/kg). (biomedcentral.com)
  • Facilitation of glucose utilization contributes to the protective effect of AKT signaling to reduce infarct size and improve myocardial function in a heart subjected to I/R [ 15 ]. (biomedcentral.com)
  • MG53 KO mice lack IPC-mediated cardioprotection as evidenced by a failure of IPC to reduce IR-induced myocardial infarct size. (biomedcentral.com)
  • 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)
  • Our previous studies have reported that EA could relieve neurological disorders, reduce infarct volumes after focal cerebral ischemia (Wang et al. (biomedcentral.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)
  • 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)
  • 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)
  • and is an intrinsic process through which repeated short episodes of ischemia are instituted to protect the myocardium against subsequent ischemic insults [ 7 ]. (biomedcentral.com)
  • 9. Sasayama S, Nonogi H , Fujita M, Sakurai T, Wakabayashi A, Kawai C, Eiho S, Kuwahara M: Changes in diastolic properties of the regional myocardium during pacing-induced ischemia in human subjects. (fiercecert.com)
  • Its applications include assessment of myocardial ischemia and viability, cardiomyopathies, myocarditis , iron overload , vascular diseases and congenital heart disease . (alchetron.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)
  • Reperfusion injury, sometimes called ischemia-reperfusion injury (IRI) or reoxygenation injury, is the tissue damage caused when blood supply returns to tissue (re- + perfusion) after a period of ischemia or lack of oxygen (anoxia or hypoxia). (wikipedia.org)
  • We aimed to investigate the effect of PLCA on hypoxia/reoxygenation (H/R) in neonatal rat ventricular myocytes (NRVM) and on myocardial I/R in rats. (biomedcentral.com)
  • Cardiomyocytes were isolated and subjected to 6 h hypoxia followed by 18 h reperfusion. (biomedcentral.com)
  • Ischemia/reperfusion (I/R) in mouse hearts and hypoxia/oxidative stress in neonatal rat cardiomyocytes have been associated with a downregulation of MG53. (biomedcentral.com)
  • The fate of the brain tissue after focal cerebral ischemia is determined by the degree and duration of ischemia, and even without preconditioning, resident brain cells naturally respond to brain ischemia by mobilizing a host of defences and counter responses to mitigate cell injury and death [ 5 ]. (biomedcentral.com)
  • For example brain ischemia/reperfusion injury is mediated via complex I redox-dependent inactivation. (wikipedia.org)
  • Ischemic injury due to coronary artery disease is the most common pathological cause of cardiac remodeling [ 6 ]. (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)
  • In adult male Sprague-Dawley rats, the focal cerebral ischemic injury was induced by middle cerebral artery occlusion (MCAO) models for 1.5 h. (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)
  • In the scenario of IT, PC stimulus primes the brain for subsequent injurious ischemic injury. (biomedcentral.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)
  • Since cardiomyocytes are terminally differentiated cells with limited self-renewal capacity, and membrane rupture is a major cause of cardiomyocyte cell death following injury, membrane repair is a necessary process for preserving cardiomyocyte viability [ 6 ]. (biomedcentral.com)
  • The uncoupling of glycolysis and glucose oxidation induces lactate accumulation during myocardial ischemia/reperfusion (I/R) injury. (biomedcentral.com)
  • Reperfusion injury is distinct from cerebral hyperperfusion syndrome (sometimes called "Reperfusion syndrome"), a state of abnormal cerebral vasodilation. (wikipedia.org)
  • 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)
  • 2012 ). Our team has proposed a new approach of electroacupuncture (EA) neuroprotection for the prevention of cerebral ischemia injury. (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)
  • CONCLUSIONS: Together, our findings demonstrated that CTRP5 overexpression could protect the heart from oxidative stress and inflammatory injury induced by DOX through inhibiting TLR4/NLRP3 signaling, suggesting that CTRP5 might be a potential therapeutic target in the prevention of DOX-induced cardiotoxicity. (bvsalud.org)
  • 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)
  • A therapeutic drug that targets ischemia reperfusion (I/R) injury is needed and has yet to be developed. (biomedcentral.com)
  • The blood is a forward Early salvage into an oxidation file and is concentrations to regulate its digoxin through the polypeptides. (augenta.net)
  • Subsequently, cardiac staining and molecular biological analysis were performed to analyze the morphological and biochemical effects of CTRP5 on the cardiac injury. (bvsalud.org)
  • CTRP5 overexpression significantly attenuated DOX-induced cardiac injury, cardiac dysfunction, inhibited oxidative stress and inflammatory response. (bvsalud.org)
  • BACKGROUND: Remote ischaemic preconditioning attenuates cardiac injury at elective surgery and angioplasty. (ox.ac.uk)
  • Treatment with (30 or 50 mg/kg, IP) phycocyanin significantly attenuated inflammatory nociception and the induction of iNOS and COX-2 and was accompanied by an inhibition of the formation of TNF-alpha, prostaglandin E2, nitrate and myeloperoxidase activity. (algaesciences.com)
  • The mechanism of action of Spirulina may be directly linked to the antioxidant activity of its chromophore, phycocyanobilin that is closely related to bilirubin and biliverdin intermediates of the human heme biosynthetic and salvage pathways (Manirafasha 2016). (algaesciences.com)
  • Ischemic tolerance defines transient resistance to lethal ischemia gained by a prior sublethal noxious stimulus (i.e., preconditioning). (biomedcentral.com)
  • [ 3 , 4 ] Further refinements in CPB hardware and techniques, perfusion methods, myocardial and brain protection over the past seven decades contributed to improved outcomes of surgical treatment of CHD. (medscape.com)
  • 6. Sasayama S, Nonogi H , Fujita M, Sakurai T, Wakabayashi A, Kawai C, Eiho S, Kuwahara M: Three-dimensional analysis of regional myocardial function in response to nitroglycerin in patients with coronary artery disease. (fiercecert.com)
  • 11. Sasayama S, Asanoi H, Kameyama T, Nonogi H , Kawai C: The mechanism of improvement of pacing-induced ischemia by nifedipine in patients with coronary artery disease. (fiercecert.com)
  • Tissue damage due to the general energy deficit during ischemia is followed by reperfusion (increase of oxygen level) when the injury is enhanced. (wikipedia.org)
  • Mitochondrial complex I is thought to be the most vulnerable enzyme to tissue ischemia/reperfusion but the mechanism of damage is different in different tissues. (wikipedia.org)
  • However, accumulating evidence suggests that MG53 has a potentially protective role in heart tissue, including in ischemia/reperfusion injury of the heart, cardiomyocyte membrane injury repair, and atrial fibrosis. (biomedcentral.com)
  • The expression of NLRP3 inflammasome in the penumbral tissue following reperfusion was assessed by western blotting and immunoflourescent staining. (biomedcentral.com)
  • One such area of interest is the ability to modulate myocardial glucose uptake and its impact on cardioprotection. (biomedcentral.com)
  • The possible underlying mechanism of the cardioprotective effect of T. terrestris could be due to restoration of endogenous myocardial antioxidant status or free radical scavenging activity along with correction of the altered hemodynamic parameters and preservation of histoarchitectural and ultrastructural alterations. (scialert.net)
  • 1999) demonstrated that phycocyanin inhibited inflammatory cell infiltration and reduced cell injury in acetic acid induced colitis in rats. (algaesciences.com)
  • More importantly, this study revealed that pharmacological PDE1 inhibition attenuated the progression of pre-established AAA. (rochester.edu)
  • 3 In a previous study, different pharmacological principles that aimed to reduce ischemia/reperfusion injury failed to show effect. (dovepress.com)
  • Cardiac ischemia is modelled in vitro through the application of hypoxic and oxidative stress. (biomedcentral.com)
  • 2 Glutamate may act as an excitotoxin, and antagonists of the N -methyl-d-aspartate (NMDA) subtype of the glutamate receptor have been protective in in vitro models of neuronal injury. (asahq.org)
  • Burn wounds can be classified into 6 separate groups based on the mechanism of injury: scalds, contact burns, fire, chemical, electrical, and radiation. (medscape.com)
  • The mechanism of burn injury can be used as a predictor of outcome. (medscape.com)
  • The mechanism of minor burn injury varies considerably with the age of the victim. (medscape.com)
  • Prevention of nervous system injury by xenon should be tested in a large placebo-controlled, randomized clinical trial. (asahq.org)
  • In this review, we focus on the role of cardiomyocyte-derived and cardiac fibroblast-derived microRNAs that are involved in the regulation of genes associated with cardiomyocyte and fibroblast function and in atherosclerosis-related cardiac ischemia. (archivesofmedicalscience.com)
  • Given these advantages, ADSCs may be better candidates for myocardial regeneration than bone marrow-derived stem cells. (biomedcentral.com)
  • Continuous pressure limits blood supply and causes ischemia, and the inflammation occurs during reperfusion. (wikipedia.org)
  • The highest incidence of serious burn injury occurs in young adults (20-29 y) followed by children younger than 9 years. (medscape.com)
  • Delayed phase of IT occurs in days, when the latent cerebroprotective phenotype is complete, the brain is again ischemia-tolerant. (biomedcentral.com)
  • We have recently shown that postischemic administration of intralipid protects the heart against ischemia-reperfusion injury. (silverchair.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)
  • In vivo rat hearts or isolated Langendorff-perfused mouse hearts were subjected to ischemia followed by reperfusion with intralipid (0.5%, 1% and 2% ex-vivo, and 20% in vivo), cyclosporine-A (0.2 μM, 0.8 μM, and 1.5 μM ex- vivo and 10 mg/kg in vivo), or vehicle. (silverchair.com)
  • The cAMP analogue 8-Br-cAMP-AM (8-Br) confers marked protection against global ischaemia/reperfusion of isolated perfused heart. (mdpi.com)
  • Clinically, beneficial effects of GLP-1 have also been demonstrated in patients with myocardial ischemia and heart failure. (biomedcentral.com)
  • While the heart is capable of utilizing a variety of available substrates to generate adenosine triphosphate, this metabolic flexibility is compromised under circumstances in which the heart is stressed, particularly by myocardial ischemia. (biomedcentral.com)
  • In addition, a significant decrease in the activities of myocardial injury markers i.e., creatine phosphokinase-MB (CK-MB isoenzyme) and lactate dehydrogenase (LDH) was also observed in the heart of ISP control group as compared to sham control. (scialert.net)
  • Coronary heart disease is a leading cause of death in the world and therapy to reduce injury is still needed. (biomedcentral.com)
  • With ischemia in coronary heart disease, impairment of the oxygen supply and metabolic disorder both occur [ 2 ]. (biomedcentral.com)
  • if MCAO is applied during this phase, mainly cortical areas are spared (early ischemia-tolerant phenotype). (biomedcentral.com)
  • Reperfusion of ischemic tissues is often associated with microvascular injury, particularly due to increased permeability of capillaries and arterioles that lead to an increase of diffusion and fluid filtration across the tissues. (wikipedia.org)
  • FINDINGS: 82 patients were excluded on arrival at hospital because they did not meet inclusion criteria, 32 were lost to follow-up, and 77 did not complete the follow-up with data for salvage index. (ox.ac.uk)
  • For example, patients with flame burns and electrical burn injuries often require hospitalization. (medscape.com)
  • In addition to its function in skeletal muscle, MG53 has been shown to have protective effects on various forms of cardiac muscle injury. (biomedcentral.com)
  • 10. Sasayama S, Nonogi H , Asanoi H, Yamanishi K, Kawai C: Effects of nifedipine on pacing-induced ischemia:modification of regional myocardial function and coronary hemodynamics. (fiercecert.com)
  • Some theorize that this delayed reaction derives from the various inflammatory immune responses that occur during reperfusion. (wikipedia.org)
  • These inflammatory responses cause intracranial pressure, pressure which leads to cell injury and in some situations cell death. (wikipedia.org)
  • Hypothermia has been shown to help moderate intracranial pressure and therefore to minimize the harmful effect of a patient's inflammatory immune responses during reperfusion. (wikipedia.org)
  • When the lethal ischemic insult is applied onto this latent protective phenotype, a separate set of responses are triggered that constitute ischemia-tolerant phenotype, which strikingly differs from the unprimed or unpreconditioned brain's phenotype (Figure 1 ). (biomedcentral.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)
  • 15. Nakamura Y, Sasayama S, Nonogi H , Miyazaki S, Fujita M, Kihara Y, Konishi T, Kawai C: Effects of pacing-induced ischemia on early left ventricular filling and regional myocardial dynamics and their modification by nifedipine. (fiercecert.com)
  • AMPK and AKT are synergistically activated by PLCA, which lead facilities glucose utilization, thereby attenuating lactate accumulation and cell death. (biomedcentral.com)
  • Another school of thought focuses on hypothermia's ability to prevent the injuries that occur after circulation returns to the brain, or what is termed reperfusion injuries. (wikipedia.org)