AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsInformation ScienceHealth Care
Myocardial Reperfusion InjuryReperfusion InjuryMyocardial IschemiaMyocardial ReperfusionIschemic PostconditioningMyocardiumMyocardial InfarctionIschemiaCardiotonic AgentsIschemic Preconditioning, MyocardialReperfusionMyocytes, CardiacCreatine KinaseRats, Sprague-DawleyDisease Models, AnimalPeroxidaseHeartBrain IschemiaRats, WistarCoronary CirculationHemodynamicsVentricular Function, LeftIschemic PreconditioningMyocardial ContractionTime FactorsMitochondria, HeartApoptosisL-Lactate DehydrogenaseCardioplegic SolutionsMice, Inbred C57BLReceptor, Adenosine A3Heart Function TestsMice, KnockoutOxidative StressDogsRandom AllocationWarm IschemiaNeutrophilsP-SelectinPerfusionNitric OxideElectrocardiographySignal TransductionProtective AgentsWounds and InjuriesNecrosisCoronary VesselsCold IschemiaProto-Oncogene Proteins c-aktNitric Oxide Synthase Type IIMalondialdehydeNitric Oxide Synthase Type IIIRabbitsHeart Arrest, InducedArrhythmias, CardiacReactive Oxygen SpeciesKidneyAntioxidantsNeutrophil InfiltrationCytoprotectionAcute Kidney InjuryNeuroprotective AgentsSwineLiverCoronary DiseaseIschemic Attack, TransientInfarction, Middle Cerebral ArteryConstrictionCaspase 3Heart VentriclesPeroxynitrous AcidBrain InjuriesCells, CulturedSuperoxide DismutaseMicrocirculationOrgan PreservationCoronary AngiographySpinal Cord IschemiaModels, AnimalIn Situ Nick-End LabelingEnzyme InhibitorsAspartate AminotransferasesBlotting, WesternOrgan Preservation SolutionsTroponin IAlanine TransaminaseKATP ChannelsHeart RateMyocardial StunningBlood PressureTumor Necrosis Factor-alphaMitochondrial Membrane Transport ProteinsAngioplasty, Balloon, CoronaryThrombectomyTioproninEndothelium, VascularHeme Oxygenase-1Treatment OutcomeCyclic S-OxidesFree Radical Scavengers
InfarctionAcuteApoptosisSubjected to ischemia followed by reperfusionMyocytesMyocardiumVivoNecrosisAttenuate Renal IschemiaReducing the infarct sizeCardioprotectiveRatsStrategies for inducing mRole in myocardialMitochondriaMitochondrialInfarct size comparedEndogenousTissueOxidative stressHypertrophyHypoxiaInducePerfusionEndothelialTherapeuticApoptoticInflammationPathwayCoronary arteryNitric OxideInflammatory responseExperimentalHypercholesterolemiaCardiovascularDamageResulting in impaired cardiacPathophysiologicalRenalAbstractMortalityMechanismsSignificantlyHeartBiomarkersAdultIncreasesMediatorsPerioperativeProteinModelSympathetic
Infarction32
Acute7
  • Contrast-Induced Acute Kidney Injury and Cardiovascular Imaging: Danger or Distraction? (amedeo.com)
  • Renal ischemia-reperfusion injury (IRI) is considered as a major cause of acute kidney injury. (frontiersin.org)
  • Reactive oxygen species damage drives cardiac and mitochondrial dysfunction following acute nano-titanium dioxide inhalation exposure. (wvu.edu)
  • 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)
  • Takotsubo cardiomyopathy (TCM) is a transient cardiac syndrome that involves left ventricular apical akinesis and mimics acute coronary syndrome. (medscape.com)
  • [ 6 ] These include multivessel coronary artery spasm, impaired cardiac microvascular function, impaired myocardial fatty acid metabolism, acute coronary syndrome with reperfusion injury, and endogenous catecholamine-induced myocardial stunning and microinfarction. (medscape.com)
  • Some authors have proposed a unifying hypothesis stating that in susceptible individuals, notably women, neurohormonal stimulation results in acute myocardial dysfunction, as reflected by the characteristic left ventricular wall-motion abnormality of TCM. (medscape.com)
Apoptosis17
  • The pathophysiological nature of MIRI is the short-term disturbance of myocardial energy and metabolism caused by reflow after ischemia and hypoxia in the coronary artery and the dynamic changes in apoptosis and the prosurvival signaling pathways in response to related injury factors. (hindawi.com)
  • HPC protected neonatal rat cardiomyocytes against H/R injury by increasing cell viability, while reducing LDH release and cell apoptosis. (spandidos-publications.com)
  • However, the knockdown of miR‑133b‑5p in the cardiomyocytes blocked HPC‑mediated cardioprotection as reflected by the aggravation of cell injury and apoptosis. (spandidos-publications.com)
  • In conclusion, the present study demonstrated that SA inhibits the apoptosis of H9c2 cardiomyocytes following H/R injury via reduced activation of the p38MAPK and JNK signaling pathways. (spandidos-publications.com)
  • The underlying mechanisms behind myocardial I/R injury are associated with a number of factors, including substantial free radical production, intracellular calcium overload, increased inflammation, myocardial necrosis and apoptosis ( 6 ). (spandidos-publications.com)
  • Thus, inhibition of oxidative stress and myocardial apoptosis is beneficial in the treatment of myocardial I/R injury. (spandidos-publications.com)
  • The results demonstrated that SA inhibited apoptosis signaling in H9c2 cardiomyocytes via downregulation of p38 mitogen-activated protein kinase (p38MAPK) and c-Jun N-terminal kinase (JNK) signaling pathways following hypoxia/reoxygenation (H/R) injury. (spandidos-publications.com)
  • 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)
  • The effect of turmeric on myocardial apoptosis and cardiac function was examined in an ischemia and reperfusion model of myocardial injury. (sydneyaviationtheory.com.au)
  • Here we investigated roles for miR-126 in stress kinase activation, induction of inflammatory cytokines and apoptosis caused by exposure of cultured cardiac myocytes to hypoxia/acidosis or acidosis alone. (biomedres.us)
  • Cardiac myocyte cell death by apoptosis accompanies heart disease of both ischemic and nonischemic origin [1-3]. (biomedres.us)
  • In animal models, increased apoptosis accompanies both phases of ischemia and reperfusion [8]. (biomedres.us)
  • Our group reported that severe chronic hypoxia alone does not cause apoptosis of cardiac myocytes in culture. (biomedres.us)
  • Inhibition of Na+/H+ exchange is protective against ischemic injury, while inhibition of the vacuolar ATPase promotes apoptosis, in part by shifting the proton load toward the Na+/H+ transporter and thus increasing Ca2+ uptake, and in part by reducing the myocyte capacity to control [pH]i. (biomedres.us)
  • 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)
  • 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)
Subjected to ischemia followed by reperfusion1
  • 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)
Myocytes13
  • Cardiac myocytes isolated from neonatal or adult rat hearts were cultured in control or in three different hypercholesterolemic media with increasing cholesterol content (hiChol) or hiChol + hyperglycemic medium, respectively. (nih.gov)
  • Cholesterol uptake was tested by Filipin staining in neonatal cardiac myocytes. (nih.gov)
  • Neonatal cardiac myocytes took up cholesterol from the different hiChol media at a concentration-dependent manner. (nih.gov)
  • In normoxia, viability of hiChol neonatal cardiac myocytes was not significantly changed, however, superoxide levels were increased as compared to vehicle. (nih.gov)
  • After SI/R, the viability of hiChol neonatal cardiac myocytes was decreased and total ROS level was increased as compared to vehicle. (nih.gov)
  • Viability of hiChol adult cardiac myocytes was significantly decreased and superoxide level was increased in normoxia and these changes were further aggravated by SI/R. HiChol combined with hyperglycemia further aggravated cell death, however level of oxidative stress increased only in normoxic condition. (nih.gov)
  • HiChol rat cardiac myocytes showed reduction of cell viability and increased oxidative stress, which were further aggravated by SI/R and with additional hyperglycemia. (nih.gov)
  • This is the first demonstration that the combination of the current hypercholesterolemic medium and SI/R in cardiac myocytes mimics the cardiac pathology of the comorbid heart with I/R and hypercholesterolemia. (nih.gov)
  • hERG is the pore-forming subunit of potassium channels that create delayed rectifier potassium ion currents in many cells, including cardiac myocytes. (wikipedia.org)
  • The delayed rectifier potassium ion current is largely responsible for the repolarization of ventricular cardiac myocytes by permitting potassium efflux. (wikipedia.org)
  • Hypoxic cardiac myocytes generate excess H+ through increased anaerobic glycolysis, net hydrolysis of ATP, and CO2 retention. (biomedres.us)
  • 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)
  • 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)
Myocardium11
  • The most effective early treatment for reducing AMI injury and limiting the infarcted myocardium is timely coronary revascularization using thrombolytic therapy or primary percutaneous coronary intervention (PPCI) [ 2 - 4 ]. (hindawi.com)
  • This coupled comorbidity of pathological ischemia and therapeutic reinjury of infarcted myocardium, namely, myocardial ischemia-reperfusion injury (MIRI), is particularly refractory to treatment [ 4 , 5 ]. (hindawi.com)
  • During injury stimulation, the major effects on the cardiac function may be those involving mitochondria-dominated events along with potential nucleus-governed genetic/epigenetic alternations within the cardiomyocytes as well as the macrophage-led inflammation and T-cell-led immune responses underlying the myocardium-vessel interactive cascade. (hindawi.com)
  • Adult rats were subjected to myocardial ischemia/reperfusion (I/R) injury with or without ischemic preconditioning (IPC), and the level of miR‑133b‑5p in myocardium was measured. (spandidos-publications.com)
  • Following myocardial I/R injury, the expression of miR‑133b‑5p was decreased in myocardium, while this decrease was restored by IPC. (spandidos-publications.com)
  • Restoration of blood supply, termed reperfusion, has been used to treat ischemic myocardium and prevent further tissue damage. (spandidos-publications.com)
  • Reperfusion has the potential to salvage ischemic myocardium but paradoxically can cause injury, a phenomenon called as 'reperfusion injury' (IR). (aku.edu)
  • One of the most promising injectable hydrogels in cardiac regeneration is a cardiac extracellular matrix hydrogel that is derived from decellularized porcine myocardium. (bvsalud.org)
  • These pleiotropic effects thus have a major role in protecting the myocardium against ischemic injury. (ac.ir)
  • 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)
  • Last year, Dharmakumar and Kumar observed that damage to the heart from MI was not only a result of ischemia caused by a blocked artery, but also a result of bleeding in the myocardium after the artery had been opened. (medscape.com)
Vivo5
  • Hypoxia/reoxygenation (H/R) as well as hypoxic preconditioning (HPC) is widely used for simulating in vivo myocardial I/R and ischemic preconditioning (IPC) in a cell culture model. (spandidos-publications.com)
  • The obtained information from this study is very critical toward the future in vivo evaluation of fibrin-enriched cardiac extracellular matrix hydrogels in promoting myocardial angiogenesis. (bvsalud.org)
  • METHODS:A literature-based meta-analysis was performed to evaluate the clinical efficacy of SXSM on bradycardia, which was confirmed by a rat ex vivo cardiac model. (pubmed.pro)
  • Transcription factor GATA4-targeted compounds that have previously shown in vivo efficacy in cardiac injury models were tested for stage-specific activation of atrial and ventricular reporter genes in differentiating pluripotent stem cells using a dual reporter assay. (biomedcentral.com)
  • When cardiac MRI came around, around the year 2000, suddenly there was a noninvasive imaging method where we could investigate patients in vivo," said Kumar. (medscape.com)
Necrosis3
Attenuate Renal Ischemia1
Reducing the infarct size1
  • Although intralipid inhibits the opening of the mitochondrial permeability transition pore as efficiently as cyclosporine-A, intralipid is more effective in reducing the infarct size and improving the cardiac functional recovery. (silverchair.com)
Cardioprotective4
Rats2
  • 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)
  • 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)
Strategies for inducing m1
  • Several different strategies for inducing myocardial angiogenesis have been explored, including exogenous delivery of angiogenic genes, proteins, microRNAs, cells, and extracellular vesicles. (bvsalud.org)
Role in myocardial1
  • 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)
Mitochondria7
  • The mitochondria has been known to protect the heart from ischemic-reperfusion injury through the opening of the ATP-sensitive K+ channel. (wikipedia.org)
  • Given the central role that mitochondria play during hypoxia, we hypothesized that Txnip deletion would enhance ischemia-reperfusion damage. (jci.org)
  • Thus, although Txnip deletion suppresses mitochondrial function, protection from myocardial ischemia is enhanced as a result of a coordinated shift to enhanced anaerobic metabolism, which provides an energy source outside of mitochondria. (jci.org)
  • Intralipid was as efficient as cyclosporine-A in inhibiting the mitochondrial permeability transition pore opening (calcium retention capacity = 280 ± 8.2 vs. 260.3 ± 2.9 nmol/mg mitochondria protein in cyclosporine-A, P = 0.454, n = 6) and in reducing cardiac mitochondrial superoxide production. (silverchair.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)
  • In this application, we present the first evidence that HNE upregulation following cardiac I/R injury activates the translocation of AIFm2 from the mitochondria to the nucleus. (lsuhs.edu)
  • 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)
Mitochondrial2
  • 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)
  • Whereas mitochondrial ATP synthesis was minimally decreased by Txnip deletion, cellular ATP content and lactate formation were higher in Txnip-KO hearts after ischemia-reperfusion injury. (jci.org)
Infarct size compared1
  • Anastrozole blocked DES induced preconditioning and increased infarct size compared to DES alone (37.94615.5% vs. 17.163.62%) without affecting area at risk and systemic hemodynamic parameters following ischemia/reperfusion. (uni-wuerzburg.de)
Endogenous1
  • Chemical compounds that modulate atrial and ventricular cell fate could be used to improve subtype-specific differentiation of endogenous or exogenously delivered progenitor cells in order to promote cardiac regeneration. (biomedcentral.com)
Tissue4
  • Various types of injectable hydrogels have been investigated for cardiac tissue repair. (bvsalud.org)
  • We here investigated macrophage lineages and ablated tissue macrophages in homeostasis and after I/R injury in a CSF1R-dependent manner. (elifesciences.org)
  • 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)
  • 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)
Oxidative stress1
  • Post-ischemic stroke-induced myocardial dysfunction is associated with nitro-oxidative stress and sympathetic overactivity. (escardio.org)
Hypertrophy2
  • Long noncoding-RNAs (lncRNAs) are critical regulators of cardiac development as well as pathological hypertrophy and heart failure (HF). (researchgate.net)
  • Background: Physiological cardiac hypertrophy occurs commonly in response to exercise and can protect against pathological stress. (researchgate.net)
Hypoxia1
  • Neonatal rat cardiomyocytes were isolated and subjected to hypoxia/reoxygenation (H/R) injury, with or without HPC. (spandidos-publications.com)
Induce1
  • Our in vitro results demonstrate that fibrin-enriched cardiac extracellular matrix hydrogels can induce robust endothelial cell tube formation from human umbilical vein endothelial cells and promote the sprouting of human mesenchymal stem cell spheroids. (bvsalud.org)
Perfusion2
  • this may be an important mechanism of decreased coronary perfusion and subsequent myocardial injury during reflow. (elsevierpure.com)
  • Patients with TCM are found to shift toward the glucose pathway despite relatively normal myocardial perfusion and lack of ischemia in left ventricular segments. (medscape.com)
Endothelial2
  • Hypercholesterolemia causes endothelial and myocardial dysfunction, as well as aggravates ischemia/reperfusion (I/R)-induced myocardial injury. (nih.gov)
  • Our investigation indicates that most of these studies examined endothelial progenitor cells, hematopoietic stem cells, mesenchymal stem cells, adipose-derived stem cells, and a few others were about less-discussed types of stem cells such as cardiac stem cells, myeloblasts, and induced pluripotent stem cells. (magiran.com)
Therapeutic4
  • Importance Mortality is high among patients heart failure (HF) who are receiving treatment, and therefore identifying new pathways rooted in preclinical cardiac remodeling phenotypes may afford novel biomarkers and therapeutic avenues. (researchgate.net)
  • The main mechanisms underlying the therapeutic benefits of cardiac extracellular matrix hydrogels have been elucidated and involved in the modulation of the immune response, downregulation of pathways related to heart failure progression and fibrosis, upregulation of genes important for cardiac muscle contraction, and enhancing cardiomyocyte differentiation and maturation from stem cells. (bvsalud.org)
  • As the prevalence of the metabolic syndrome is increasing, better understanding of cardiac metabolism is needed to identify potential new targets for therapeutic intervention. (jci.org)
  • Collectively, these results indicate the potential for therapeutic alteration of cell fate decisions and pathological gene regulatory networks by GATA4-targeted compounds modulating chamber-specific transcriptional programs in multipotent cardiac progenitor cells and cardiomyocytes. (biomedcentral.com)
Apoptotic3
  • Cellular injury was evaluated by detecting cell viability, lactate dehydrogenase (LDH) activity and apoptotic rate. (spandidos-publications.com)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
  • It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
Inflammation1
  • Extracellular small non-coding RNAs (exRNAs) have been associated with cardiac inflammation and fibrosis and we hypothesized that they are associated with post-MI LVRm phenotypes. (researchgate.net)
Pathway2
  • Sef preconditioning ameliorated myocardial I/R injury by modulating MAPKs pathway activity via upregulating TIMP3. (perfusion.com)
  • During ischemia, this pathway is suppressed and instead glucose is largely utilized, resulting in impaired cardiac function. (medscape.com)
Coronary artery1
  • Reperfusion after cardiac ischemia increases cell death and infarct size (IS), called myocardial ischemia/reperfusion (I/R) injury, which is the main cause of myocardial injury during the cardiac surgery particularly in coronary artery bypass graft surgery ( 1 , 2 ). (spandidos-publications.com)
Nitric Oxide2
  • 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)
  • The goal of this project is to study the role of neurogranin in regulating peripheral nitric oxide and cardiac function. (lsuhs.edu)
Inflammatory response1
  • Reperfusion triggers an inflammatory response and often results in oxidative damage. (wikipedia.org)
Experimental3
  • 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)
  • The volatile anesthetic desflurane (DES) effectively reduces cardiac infarct size following experimental ischemia/reperfusion injury in the mouse heart. (uni-wuerzburg.de)
  • Aromatase metabolizes testosterone to 17b- estradiol (E2) and thereby significantly contributes The volatile anesthetic desflurane (DES) effectively reduces cardiac infarct size following experimental ischemia/reperfusion injury in the mouse heart. (uni-wuerzburg.de)
Hypercholesterolemia1
  • Therefore, our aim was to develop a medium throughput comorbidity cell-based test system of myocardial I/R injury, hypercholesterolemia and hyperglycemia that mimics comorbidity conditions. (nih.gov)
Cardiovascular2
  • The anesthesiology module now included in the Adult Cardiac Surgery Database (ACSD) component of the STS database, created through a partnership with the Society of Cardiovascular Anesthesiologists (SCA), will only further enhance perioperative care. (medscape.com)
  • See also the American Heart Association [AHA] 2020 guidelines for CPR and emergency cardiovascular care and 2022 AHA Interim Guidance to Health Care Providers for Basic and Advanced Cardiac Life Support in Adults, Children, and Neonates With Suspected or Confirmed COVID-19. (msdmanuals.com)
Damage1
Resulting in impaired cardiac1
  • Specific absence of homeostatic, monocyte-independent macrophages altered the immune cell crosstalk in response to injury and induced proinflammatory neutrophil polarization, resulting in impaired cardiac remodelling without influencing infarct size. (elifesciences.org)
Pathophysiological2
  • 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)
  • Renal ischemia-reperfusion injury (IRI) is a common pathophysiological phenomenon in clinical settings. (frontiersin.org)
Renal1
Abstract2
  • 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)
  • The exclusion criteria were studies published as an abstract only, crossover studies, and studies with a lack of data on the cardiac index. (pubmed.pro)
Mortality2
  • Cardiopulmonary Resuscitation (CPR) in Infants and Children Despite the use of cardiopulmonary resuscitation (CPR), mortality rates for out-of-hospital cardiac arrest are about 90% for infants and children. (msdmanuals.com)
  • Mortality rates for in-hospital cardiac arrest. (msdmanuals.com)
Mechanisms3
  • 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)
  • Conceptual diagram of the development and unknown mechanisms of myocardial ischemia-reperfusion injury. (hindawi.com)
  • However, the molecular mechanisms involved in AIFm2 translocation that mediates cardiac injury remain unknown. (lsuhs.edu)
Significantly3
  • 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)
  • 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)
Heart6
  • Reperfusion injury is a significant threat to myocardial function that arises with the reintroduction of blood flow to the heart following an ischemic episode. (wikipedia.org)
  • Moreover, it was observed that, PGRN protects the heart against ischemia-reperfusion injury. (biomedcentral.com)
  • We have recently shown that postischemic administration of intralipid protects the heart against ischemia-reperfusion injury. (silverchair.com)
  • In addition, it has been shown that atorvastatin can protect the isolated mouse heart against reperfusion-induced injury [ 6 ]. (ac.ir)
  • Preliminary data from our lab show that 'binge and crash' infusion of methamphetamine in mice causes both electrical and structural remodeling of the heart and contribute to the increase in cardiac arrhythmias. (lsuhs.edu)
  • We reported that there is infarct expansion after reperfusion, so once you open up the vessel, the heart attack actually gets larger. (medscape.com)
Biomarkers2
  • Guha D, Mukerji SS, Chettimada S, Misra V, Lorenz DR, Morgello S, Gabuzda D. Cerebrospinal fluid extracellular vesicles and neurofilament light protein as biomarkers of central nervous system injury in HIV-infected patients on antiretroviral therapy. (biovendor.com)
  • Machine-learning to stratify diabetic patients using novel cardiac biomarkers and integrative genomics. (wvu.edu)
Adult2
  • Enhanced antioxidant capacity prevents epitranscriptomic and cardiac alterations in adult offspring gestationally-exposed to ENM. (wvu.edu)
  • In summary, available evidence from the present meta-analysis suggests that perioperative administration of dexmedetomidine in adult cardiac surgery might reduce the incidence of AKI. (medscape.com)
Increases1
  • Our lab has shown that infusion of methamphetamine in mice increases the incidence of inducible atrial fibrillation and ventricular tachycardia, suggesting that methamphetamine acutely impacts cardiac electrophysiology. (lsuhs.edu)
Mediators1
Perioperative2
  • The more than 6.5 million surgical records in this database have helped create surgical risk calculators and have led to improvements in perioperative care for cardiac surgery patients. (medscape.com)
  • Our specialists have selected 3 seminal papers that have been recently published in each speciality (perioperative medicine, cardiac imaging, cardiology, cardiothoracic surgery). (shda.org.au)
Protein1
  • Specific Aim # 2: Determine the cytosolic transport protein involved in the translocation of the HNE-adducted AIFm2 complex from the cytosol to the nucleus following cardiac injury. (lsuhs.edu)
Model1
  • Using a novel rodent model, this project is uniquely positioned to make a significant contribution to the understanding of methamphetamine-associated cardiomyopathy and cardiac arrhythmias. (lsuhs.edu)
Sympathetic2
  • Clinical trials in the area of advanced imaging include radiotracer imaging of cardiac sympathetic innervation, Single photon emission computed tomography (SPECT) imaging of fatty acid tracers and validation of coronary CT angiography. (uc.edu)
  • Other evidence for this theory has been demonstrated through myocardial imaging studies using catecholamine analogues, that evaluated cardiac sympathetic activity. (medscape.com)