AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsInformation ScienceHealth Care
Myocardial Reperfusion InjuryReperfusion InjuryMyocardial IschemiaMyocardial ReperfusionIschemic PostconditioningMyocardiumMyocardial InfarctionCardiotonic AgentsIschemic Preconditioning, MyocardialIschemiaReperfusionCreatine KinaseRats, Sprague-DawleyMyocytes, CardiacPeroxidaseDisease Models, AnimalHeartRats, WistarCoronary CirculationHemodynamicsBrain IschemiaIschemic PreconditioningVentricular Function, LeftCardioplegic SolutionsL-Lactate DehydrogenaseApoptosisMyocardial ContractionMice, Inbred C57BLTime FactorsMitochondria, HeartReceptor, Adenosine A3Heart Function TestsMice, KnockoutOxidative StressDogsRandom AllocationNeutrophilsP-SelectinWarm IschemiaNitric OxideWounds and InjuriesSignal TransductionProtective AgentsNecrosisProto-Oncogene Proteins c-aktNitric Oxide Synthase Type IIMalondialdehydePerfusionNitric Oxide Synthase Type IIICold IschemiaCoronary VesselsElectrocardiographyRabbitsKidneyNeutrophil InfiltrationAntioxidantsReactive Oxygen SpeciesAcute Kidney InjuryCytoprotectionLiverHeart Arrest, InducedSwineBrain InjuriesCaspase 3Peroxynitrous AcidNeuroprotective AgentsSuperoxide DismutaseConstrictionOrgan PreservationInfarction, Middle Cerebral ArteryMicrocirculationAspartate AminotransferasesIn Situ Nick-End LabelingOrgan Preservation SolutionsAlanine TransaminaseModels, AnimalEnzyme InhibitorsBlotting, WesternKATP ChannelsIschemic Attack, TransientMitochondrial Membrane Transport ProteinsTumor Necrosis Factor-alphaSpinal Cord IschemiaThrombectomyMyocardial StunningTroponin ITioproninCyclic S-OxidesAngioplasty, Balloon, CoronaryHeme Oxygenase-1Coronary DiseaseEndothelium, VascularCells, CulturedFree Radical ScavengersRats, Inbred LewCoronary AngiographyBlood PressureHydroxy AcidsArrhythmias, CardiacDecanoic Acids
InfarctionMyocardiumInfarct sizeAcuteRatsPostconditioningCardioprotectionInhibitionOxidativeRole in ischemicModel of myocardialPreconditioningTissue reperfusionKnown as reperfusion injuryApoptosisCardiac functionPercutaneous coronary intCardioprotective effectsCerebral ischemiaPost ischemicEndogenousSusceptibilityEndothelialHypoxiaTherapeuticRenalTransientBrain ischemicDiabetesDysfunctionProtective effectNitric oxideMechanismsHeartIntracellularGlucose oxidationDiabeticCardiovascularPerfusionMitochondrialInsultStrokeOxidationInflammationLeft ventricularClinicalInflammatory responseNormothermicNrf2PharmacologicalTissuesOxygenInduces
Infarction20
Myocardium10
  • 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)
  • 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)
  • 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)
Infarct size8
  • 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 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)
  • 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)
Acute11
  • 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)
  • Renal ischemia-reperfusion injury (IRI) is considered as a major cause of acute kidney injury. (frontiersin.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)
  • Therefore, we studied whether an acute bout of endurance or interval exercise is able to protect against endothelial I/R injury. (artinis.com)
  • 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)
  • Plasma protein acute-phase response in unstable angina is not induced by ischemic injury. (ox.ac.uk)
  • To determine whether ischemia-reperfusion injury causes this acute-phase response, we studied the temporal relation between plasma levels of CRP and ischemic episodes in 48 patients with unstable angina and 20 control patients with active variant angina, in which severe myocardial ischemia is caused by occlusive coronary artery spasm. (ox.ac.uk)
  • 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)
  • 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)
Rats10
  • 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)
  • Ischemic postconditioning may not influence early brain injury induced by focal cerebral ischemia/reperfusion 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)
  • 16. Wang Q, Zhang X, Ding Q, Hu B, Xie Y, Li X, Yang Q, Xiong L. Limb Remote Postconditioning Alleviates Cerebral Reperfusion Injury Through Reactive Oxygen Species-Mediated Inhibition of Delta Protein Kinase C in Rats. (ac.ir)
  • 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)
Postconditioning9
  • Ischemic preconditioning, postconditioning, and remote conditioning trigger endogenous cardioprotective mechanisms that render the heart more resistant to lethal ischemic-reperfusion injury. (nih.gov)
  • Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. (ac.ir)
  • 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)
  • Postconditioning in reperfusion injury: a status report. (ac.ir)
  • 20. Zhao H. The protective effect of ischemic postconditioning against ischemic injury: from the heart to the brain. (ac.ir)
  • 21. Zhao H. Ischemic postconditioning as a novel avenue to protect against brain injury after stroke. (ac.ir)
  • Another endogenous form of cardioprotection, similar to PC but applicable at the time of reperfusion, termed postconditioning (PostC), has been recently described. (eurekaselect.com)
  • Ischaemic postconditioning with a comparable sequence of brief periods of local ischaemia, when applied immediately after the ischaemic insult, confers benefits similar to preconditioning. (uea.ac.uk)
Cardioprotection6
  • 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)
Inhibition2
  • 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)
  • discovered that constant infusion of MB counteracts early myocardial dysfunction and derangement of hemodynamics and gas exchange by inhibition of nitric oxide pathway within an ovine endotoxemia model [48]. (immune-source.com)
Oxidative4
  • 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)
  • The absence of oxygen and nutrients from blood during the ischemic period creates a condition in which the restoration of circulation results in inflammation and oxidative damage through the induction of oxidative stress rather than (or along with) restoration of normal function. (wikipedia.org)
  • 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)
  • 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)
Role in ischemic3
  • 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)
Model of myocardial2
  • 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)
Preconditioning6
  • 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)
  • Ischaemic preconditioning results in a reduction in ischaemic-reperfusion injury to the heart. (uea.ac.uk)
Tissue reperfusion1
  • 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)
Known as reperfusion injury2
Apoptosis2
  • 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)
Cardiac function1
  • 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)
Percutaneous coronary int1
Cardioprotective effects3
  • Research done in animals shows that treatment with NAD+ precursors like NMN have cardioprotective effects against ischemia/reperfusion injury (4). (prohealth.com)
  • Cardioprotective effects of acidified sodium nitrite in myocardial ischemia with reperfusion. (aspetjournals.org)
  • The cardioprotective effects of DOEO were examined by histopathological observation, myocardial enzyme detection, peroxidation, anti-oxidant level detection, and related protein expression. (wjtcm.net)
Cerebral ischemia1
  • 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)
Post ischemic2
  • 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)
Endogenous1
  • 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)
Susceptibility1
Endothelial3
  • Activated endothelial cells produce more reactive oxygen species but less nitric oxide following reperfusion, and the imbalance results in a subsequent inflammatory response. (wikipedia.org)
  • 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)
Hypoxia4
  • 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)
  • 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)
  • Cardiomyocytes were isolated and subjected to 6 h hypoxia followed by 18 h reperfusion. (biomedcentral.com)
  • The degree of CNS injury depends on the severity and duration of hypoxia. (medscape.com)
Therapeutic5
  • 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)
  • 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)
  • Mitochondrial ROS production is implicated as one of the major contributors to cell death in the reperfused heart and the importance of mitophagic processes (mitochondrial housekeeping) could be a potential therapeutic target to prevent ischemia/reperfusion injury (I/R-I). Aspalathus linearis (commonly known as rooibos) is an indigenous South African plant grown exclusively in the Western Cape fynbos region. (sun.ac.za)
  • A therapeutic drug that targets ischemia reperfusion (I/R) injury is needed and has yet to be developed. (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)
Renal1
  • Renal ischemia-reperfusion injury (IRI) is a common pathophysiological phenomenon in clinical settings. (frontiersin.org)
Transient2
  • Delayed postconditionig initiates additive mechanism necessary for survival of selectively vulnerable neurons after transient ischemia in rat brain. (ac.ir)
  • 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)
Brain ischemic2
  • 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)
Diabetes1
  • 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)
Dysfunction2
  • 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)
  • All of 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)
Protective effect1
  • This study aimed to determine the potential myocardial protective effect and possible mechanism of action of D. odorifera essential oil (DOEO). (wjtcm.net)
Nitric oxide3
  • 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)
  • There is proof that MB lowers or inhibits nitric oxide era might have the aftereffect of neuroprotection in ischemia/reperfusion damage. (immune-source.com)
  • Compared to the myocardial ischemia group, the DOEO pretreatment groups had lower levels of myocardial injury, creatinine kinase, lactate dehydrogenase, alanine transaminase, aspartate transaminase, hydrogen peroxide, and nitric oxide, and higher levels of glutathione and superoxide dismutase. (wjtcm.net)
Mechanisms2
  • 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)
Heart17
  • Cryonics patients frequently experience ischemic & reperfusion injury between the time when the heart stops and cryostorage begins. (benbest.com)
  • Most myocardial infarctions, commonly known as heart attacks, happen in people once they get older, and aging makes it more difficult to recover from this type of injury. (prohealth.com)
  • What Happens During a Heart Attack and Reperfusion Injury? (prohealth.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)
  • Reperfusion injury increases the damage done after events such as heart attacks. (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)
  • 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)
  • Stroke is one of the leading causes of mortality and morbidity worldwide, second only to ischemic heart disease (IHD) [ 1 ]. (biomedcentral.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)
  • The plant Tribulus terrestris Linn, a deciduous tree of the Zygophyllaceae family, is an important herb from Indian and Chinese traditional medicine literature for the treatment of various diseases especially ischemic heart diseases (Warrier, 1994). (scialert.net)
  • Furthermore, diabetic patients are particularly at risk for developing ischemic heart disease and strokes. (sun.ac.za)
  • Regarding cardiac and mitochondrial signaling, prior to ischemia HCD heart had a decreased dependence on insulin-dependent AMPK and increased inflammation via upregulated p38, whereas GRT treatment presented with decreased insulindependent PKB and AS160 signaling (together with increased FA OxPhos compared to carbohydrates, however showed more mitochondrial uncoupling, decreasing basal metabolic rate and thereby potentially less ROS production), inhibited GSK3β and conferred an anti-inflammatory effect by significantly reducing p38 activation. (sun.ac.za)
  • 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)
  • Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)
Intracellular2
  • Ischemia decreases intracellular pH and increases intracellular Na and intracellular Ca in all age groups. (asahq.org)
  • APC decreased intracellular Na and intracellular Ca accumulation during ischemia in young adult and middle-aged hearts. (asahq.org)
Glucose oxidation1
  • The uncoupling of glycolysis and glucose oxidation induces lactate accumulation during myocardial ischemia/reperfusion (I/R) injury. (biomedcentral.com)
Diabetic2
  • Repeated bouts of ischemia and reperfusion injury also are thought to be a factor leading to the formation and failure to heal of chronic wounds such as pressure sores and diabetic foot ulcer. (wikipedia.org)
  • It is being developed as a treatment for diabetic retinopathy, pressure ulcers, wound healing, and Myocardial ischemia/Reperfusion Injury. (tradekorea.com)
Cardiovascular1
  • 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)
Perfusion3
  • 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)
  • this may be an important mechanism of decreased coronary perfusion and subsequent myocardial injury during reflow. (elsevierpure.com)
  • [ 3 , 4 ] Further refinements in CPB hardware and techniques, perfusion methods, myocardial and brain protection over the past 2 decades contributed to improved outcomes of surgical treatment of CHD. (medscape.com)
Mitochondrial1
  • 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)
Insult1
  • In fact an individual suffering from an ischemic insult continues suffering injuries well after circulation is restored. (wikipedia.org)
Stroke6
  • Reperfusion injury plays a major part in the biochemistry of hypoxic brain injury in stroke. (wikipedia.org)
  • 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)
  • Not only can both produce symptoms that mimic ischemic stroke, but they can also aggravate ongoing neuronal ischemia. (medscape.com)
Oxidation1
  • 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)
Inflammation1
Left ventricular1
  • 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)
Clinical1
  • 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)
Inflammatory response2
  • 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)
  • The inflammatory response is partially responsible for the damage of reperfusion injury. (wikipedia.org)
Normothermic1
  • 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)
Nrf21
  • 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)
Pharmacological3
  • At present, pharmacological PC and PostC are possible alternative methods that may substitute pharmaceutical treatments the short ischemic insults. (eurekaselect.com)
  • Adenosine, nicorandil and other agents have been already used as pharmacological mimetics of ischemic PC in multicenter trials. (eurekaselect.com)
  • 3 In a previous study, different pharmacological principles that aimed to reduce ischemia/reperfusion injury failed to show effect. (dovepress.com)
Tissues3
  • 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)
  • Ischemia is the condition suffered by tissues & organs when deprived of blood flow -- mostly the effects of inadequate nutrient & oxygen. (benbest.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)
Oxygen1
Induces1
  • Surgical ACL reconstruction performed with a tourniquet induces compression and ischemic stress of the quadriceps femoris (QF) muscle which can accelerate postoperative weakness. (artinis.com)