AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsHealth Care
Phosphodiesterase 5 InhibitorsCarbolinesReperfusion InjuryCyclic Nucleotide Phosphodiesterases, Type 5Muscular Dystrophy, AnimalMyocardial Reperfusion InjuryIschemiaReperfusionHeartMyocardial IschemiaMyocardial ReperfusionBrain IschemiaHeart RateMyocardiumIschemic PreconditioningIschemic Preconditioning, MyocardialRats, Sprague-DawleyRats, WistarDisease Models, AnimalMyocardial InfarctionCardiotonic AgentsTime FactorsIschemic PostconditioningWarm IschemiaMyocytes, CardiacPeroxidasePerfusionHeart FailureCold IschemiaMyocardial ContractionProtective AgentsMalondialdehydeIschemic Attack, TransientMice, Inbred C57BLHemodynamicsOxidative StressApoptosisInfarction, Middle Cerebral ArteryNeuroprotective AgentsNecrosisCreatine KinaseKidneyHeart DiseasesHeart TransplantationCoronary CirculationMitochondria, HeartL-Lactate DehydrogenaseHeart Arrest, InducedSpinal Cord IschemiaRandom AllocationDogsConstrictionVentricular Function, LeftHeart Function TestsCytoprotectionMice, KnockoutSuperoxide DismutaseLiverReactive Oxygen SpeciesAntioxidantsNitric OxideNeutrophil InfiltrationModels, AnimalHeart Defects, CongenitalOrgan PreservationRabbitsTioproninMyocardial StunningGerbillinaeAspartate AminotransferasesDecanoic AcidsHydroxy AcidsCoronary DiseaseAcute Kidney InjuryVentricular PressureMicrocirculationAlanine TransaminaseFree Radical ScavengersIn Situ Nick-End LabelingHindlimbBlotting, WesternSignal TransductionOrgan Preservation SolutionsCerebral InfarctionEnzyme InhibitorsCaspase 3IntestinesCardioplegic SolutionsImmunohistochemistryHeme Oxygenase-1Cerebrovascular CirculationAdenosineCell DeathMesenteric Artery, SuperiorRNA, MessengerNeutrophilsBrainFetal HeartOxygenRats, Inbred Lew
InjuryCardioprotectionEndogenousMyocardiumRegional ischaemiaHypoxiaOxidative stressMechanismsAcute myocardialInfarctApoptosisTransplantationCoronary heart dInhibitionApoptoticTherapyMetabolicIschemic zoneConverselyVascularHemodynamicNormoxicHypercholesterolemiaVivoPhenomenonIntracellularOxygenNeuronalVentricular tachycardiaTherapeuticArrhythmiasMyocardial infarctionInterventionsRoleRatsInfarctionCirculationSignificantly higherReceptorLeft ventricleCardiovascularIncreasesOrganEffectsReductionGlobalFunctionClinically
Injury56
  • The invention pertains to a polypeptide for the protection against heart ischemia-reperfusion injury. (justia.com)
  • This is called reperfusion injury. (justia.com)
  • Ischemia-reperfusion injury (IRI) is a syndrome affecting the myocardium upon blood flow restoration following a sufficiently long interruption, such as encountered in a coronary thrombosis or heart surgery [1,2]. (justia.com)
  • One object of the present invention is to provide a therapy of heart ischemia-reperfusion injury by applying GLP-1 analogues which can be administered as single component and avoiding administration of the drug with a second compound. (justia.com)
  • The present invention is based on the surprising finding that the peptides of the invention have protective cardiovascular effects without simultaneous administration of other compounds, specifically they have protective effects on the heart against ischemia-reperfusion injury. (justia.com)
  • Postconditioning using N-Ac-GLP-1(7-34)amide N-terminally blocked and C-terminally truncated results in a limitation of ischemia-reperfusion injury in an isolated rat heart. (justia.com)
  • Ischemic preconditioning, postconditioning, and remote conditioning trigger endogenous cardioprotective mechanisms that render the heart more resistant to lethal ischemic-reperfusion injury. (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)
  • This study explores if long-term feeding of an obesogenic high fat diet renders the myocardium less susceptible to ischemic-reperfusion induced injury via Epac-dependent signaling. (uib.no)
  • In pathological conditions, damaged cells transfer dysfunctional mitochondria toward recipient cells to ask for help and take up exogenous functional mitochondria to alleviate injury. (frontiersin.org)
  • In heart transplantation, donor hearts inevitably suffer from ischemia/reperfusion (I/R) injury, which leads to primary graft dysfunction and affects patients' survival rate. (researchsquare.com)
  • Previous studies have shown that ischemia/reperfusion (I/R) injury acts as a significant role in PGD(4), contributing to adverse short- and long-term clinical outcomes in the recipients. (researchsquare.com)
  • Therefore, attenuating myocardial I/R injury during the heart transplant procedure would have a favorable impact on improving short- and long-term graft function and recipient's survival(6). (researchsquare.com)
  • Protection of the heart against injury from acute ischemia remains challenging for emergency physicians and cardiologists because there are no therapies proven to directly protect the heart against the deleterious effects of ischemia in humans. (mcw.edu)
  • Conversely, Nrf1 overexpression protected the adult mouse heart from ischemia/reperfusion (I/ R ) injury. (nih.gov)
  • Ischaemia/reperfusion-induced organ injury in low dose streptozotocin diabetes. (nel.edu)
  • The influence of low dose streptozotocin diabetes on intestinal and vascular injury induced by mesenteric ischaemia/reperfusio. (nel.edu)
  • Effect of acetylcholine and ischaemia/reperfusion injury on the heart of rats with STZ-induced experimental diabetes. (nel.edu)
  • To investigate the effect of acetylcholine (ACh) and ischaemia/reperfusion injury on functional changes and dysrhythmias of th. (nel.edu)
  • Knezl V, Kysel'ová Z, Zúrová-Nedelcevová J, Navarová J, Tribulová N, Drímal J. Effect of acetylcholine and ischaemia/reperfusion injury on the heart of rats with STZ-induced experimental diabetes. (nel.edu)
  • Other compounds associated with MI are nitric oxide (NO) and its metabolites, which have been reported to protect the heart from ischemia/reperfusion (IR) injury and decrease MI in general [ 7 ]. (hindawi.com)
  • We hypothesized that overexpression of calpastatin, an endogenous calpain inhibitor, would attenuate the ischemia/reperfusion injury in the heart. (nii.ac.jp)
  • Adenovirus-mediated overexpression of calpastatin could be a novel biological storage to improve heart transplantation by minimizing ischemia/reperfusion injury. (nii.ac.jp)
  • dependent cytosolic cystein protease, is as an important key protease involved in the ischemic reperfusion injury such as cardiac stunning. (nii.ac.jp)
  • Endothelin-1 increases susceptibility of isolated rat hearts to ischemia/reperfusion injury by reducing coronary flow. (ox.ac.uk)
  • Endothelin-1 (ET-1) is the most potent vasoconstrictor known to date, and it was proposed that this peptide plays a major role in myocardial ischemia/reperfusion injury. (ox.ac.uk)
  • Under constant pressure perfusion, hearts were subjected to 15 min of control perfusion, 15 ("moderate injury") or 30 ("severe injury") min of global ischemia, followed by 30 min of reperfusion. (ox.ac.uk)
  • The authors conclude that ET-1 increases the susceptibility of isolated hearts to ischemia/reperfusion injury via reduction of coronary flow. (ox.ac.uk)
  • Despite the complexpathophysiology of ischemia, hypoxia alone is a sufficient stimulus to induce a variety of adaptive responsesthat protect against ischemia-reperfusion injury. (grantome.com)
  • Aim 1 will investigate the mechanisms by which EPO protects the heart from injury following ischemiaand reperfusion. (grantome.com)
  • Atorvastatin has been shown to be cardioprotective in ischemia-reperfusion (I/R) injury. (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)
  • In addition, it has been shown that atorvastatin can protect the isolated mouse heart against reperfusion-induced injury [ 6 ]. (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)
  • Although coronary reperfusion is the most straightforward treatment for limiting the MI size, it has nevertheless been shown to exacerbate ischemic myocardial injury. (bvsalud.org)
  • Exogenous administration of adenosine in the form of adenosine preconditioning may also protect heart from ischemia-reperfusion injury. (kyobobook.co.kr)
  • Endogenous release of adenosine during ischemic/remote preconditioning or exogenous adenosine during pharmacological preconditioning activates adenosine receptors to activate plethora of mechanisms, which either independently or in association with one another may confer cardioprotection during ischemia-reperfusion injury. (kyobobook.co.kr)
  • Coronary heart disease is a leading cause of death in the world and therapy to reduce injury is still needed. (biomedcentral.com)
  • The uncoupling of glycolysis and glucose oxidation induces lactate accumulation during myocardial ischemia/reperfusion (I/R) injury. (biomedcentral.com)
  • A therapeutic drug that targets ischemia reperfusion (I/R) injury is needed and has yet to be developed. (biomedcentral.com)
  • Preclinical studies have identified autophagy as a process that can be activated during vascular disorders, including ischemia - reperfusion injury of the heart and other organs, cardiomyopathy, myocardial injury, and atherosclerosis. (houstonmethodist.org)
  • Clinical evidence suggests that tissue injury in both acute kidney injury and heart failure has immune-mediated inflammatory consequences that can initiate remote organ dysfunction. (biomedcentral.com)
  • The lack of effective treatments to reduce the consequences of myocardial ischemia-reperfusion injury and the increased reliance on percutaneous and surgical treatments for coronary and valvular disease or end-stage heart failure make it critically important to identify new targets and strategies for cardioprotection. (duke.edu)
  • Our laboratory combines comparative biology approaches in multiple organisms with translational functional genomics to study the mechanisms underlying perioperative myocardial injury, with a particular emphasis on endogenous cardioprotective responses involving attenuation of nuclear factor-kappa B regulated inflammatory signaling and changes in myocardial fuel utilization. (duke.edu)
  • Hibernators such as arctic ground squirrels (AGS) depress their metabolic, heart, and respiratory rates as well as their core body temperature to enter a state called torpor during which they exhibit remarkable resistance to myocardial I/R injury and ventricular dysrhythmias normally associated with hypothermia. (duke.edu)
  • Despite extensive research, our understanding of the precise role of different subsets of macrophages in ischemia/reperfusion injury remains incomplete. (elifesciences.org)
  • Time to rethink comorbidities in the reperfusion-injury phenomenon? (escardio.org)
  • The Food and Drug Administration (FDA) is announcing a public workshop to discuss the effects of ischemia/ reperfusion injury ( IRI ) on outcomes in kidney transplantation. (myast.org)
  • Cold ischemia and subsequent reperfusion injury are non-immunologic cornerstones in the development of graft injury after heart transplantation. (frontierspartnerships.org)
  • The nitric oxide donor S-nitroso-human-serum-albumin (S-NO-HSA) is known to attenuate myocardial ischemia-reperfusion (I/R)-injury. (frontierspartnerships.org)
  • Chronic allograft injury (CAI), consisting of vasculopathy and interstitial fibrosis, affects approximately 50% of patients after 10 years and limits long-term survival following heart transplantation ( 1 ). (frontierspartnerships.org)
  • There is substantial evidence that endothelial injury during organ procurement and preservation, caused by ischemia and subsequent reperfusion, results in endothelial dysfunction. (frontierspartnerships.org)
  • he also performed research using an in vitro heart model to study ischemia-reperfusion induced myocardial injury and oxidative stress. (healthsnap.io)
  • Shown to improve metabolic function and reduce adipose tissue inflammation, sFRP‐5 also acts in a cardio‐protective manner after ischemia and reperfusion injury in the heart, suppressing the non‐canonical Wnt5a/JNK signaling pathway in macrophages and myocytes. (reliatech.de)
  • Previous studies of global brain hypoxia ischemia have primarily focused on injury to the cerebral cortex and to the hippocampus. (cdc.gov)
  • In contrast, functional consequences of injury to the thalamus are poorly understood but may be crucially important. (cdc.gov)
Cardioprotection2
  • Ischemic heart disease is the leading cause of mortality worldwide, therefore, identification of novel drug targets for cardioprotection is of great importance. (nih.gov)
  • Conclusion: Epac1-dependent signaling is involved in mediating the cardioprotection afforded by long-term feeding of an obesogenic high fat diet in mice hearts. (uib.no)
Endogenous2
  • ENGLISH ABSTRACT: The Mechanism of -adrenergic preconditioning ( -PC) Ischaemic preconditioning (IPC), a potent endogenous protective intervention against myocardial ischaemia, is induced by exposure of the heart to repetitive short episodes of ischaemia and reperfusion. (sun.ac.za)
  • There is currently tremendous interest inunderstanding the endogenous responses to ischemia and infarction. (grantome.com)
Myocardium4
  • These results suggest that protection of ischemic myocardium by diltiazem is mediated, at least in part, by preservation of vascular functional integrity. (utmb.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)
  • Ventricular fibrillation (VF) is a life-threatening cardiac arrhythmia in which the coordinated contraction of the ventricular myocardium is replaced by high-frequency, disorganized excitation, resulting in [the effective] failure of the heart to pump blood. (medscape.com)
  • CABG may be performed as an emergency procedure in the context of an ST-segment elevation MI (STEMI) in cases where it has not been possible to perform percutaneous coronary intervention (PCI) or where PCI has failed and there is persistent pain and ischemia threatening a significant area of myocardium despite medical therapy. (medscape.com)
Regional ischaemia2
  • 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)
  • Methods: Isolated perfused rat hearts were subjected to 35 min regional ischaemia (RI) and reperfusion. (sun.ac.za)
Hypoxia5
  • Ischemia is characterized by deprivation of oxygen (hypoxia), metabolicsubstrates, and cytokines/survival factors, as well as accumulation of toxic metabolites. (grantome.com)
  • Cardiomyocytes were isolated and subjected to 6 h hypoxia followed by 18 h reperfusion. (biomedcentral.com)
  • Global hypoxia-ischemia interrupts oxygen delivery and blood flow to the entire brain. (cdc.gov)
  • We therefore investigated the impact of global brain hypoxia-ischemia on the thalamic circuit function in the somatosensory system of young rats. (cdc.gov)
  • Global brain hypoxia-ischemia during cardiac arrest has a long-term impact on processing and transfer of sensory information by thalamic circuitry. (cdc.gov)
Oxidative stress2
  • However, harmful stimuli (such as ischemia-reperfusion, oxidative stress, and toxic chemicals) can change the direction and efficiency of intercellular mitochondrial transfer. (frontiersin.org)
  • Moreover, the ISO-induced myocardial changes were the result of an increase in oxidative stress through reductions of the components of the myocardial antioxidant system, including glutathione, glutathione reductase, glutathione-S-transferase, glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase, in rat hearts [ 3 , 5 ]. (hindawi.com)
Mechanisms4
  • The abnormal morphology and dysfunction of mitochondria have been proven as the principal mechanisms in the pathogenesis of cardiovascular diseases, such as heart failure, myocardial infarction, atherosclerosis, and hypertension ( 4 - 6 ). (frontiersin.org)
  • Although the mechanisms responsible for the occurrence of congestive heart failure after anti-cancer therapy are largely unkno. (nel.edu)
  • ET-1 could increase myocardial susceptibility to ischemia by two mechanisms: via coronary flow reduction and/or via direct, metabolic effects on the heart. (ox.ac.uk)
  • Despite recent findings regarding the functional implications of TRPM4 in cardiac diseases, the molecular and cellular mechanisms leading to altered conduction are poorly understood. (frontiersin.org)
Acute myocardial3
Infarct7
  • Endpoints were infarct size and functional recovery. (uib.no)
  • Interestingly, however, the HFD did not reduce infarct size in Epac1−/− deficient mice hearts (Epac1−/− HFD 65.1 ± 5.1% vs. Epac1−/− ND 56.1 ± 3.5%, ns. (uib.no)
  • Results: Infarct sizes of hearts preconditioned with isoproterenol of formoterol were significantly smaller compared to those of non-preconditioned hearts. (sun.ac.za)
  • Both Rp-8-CPT-cAMPs and wortmannin significantly increased infarct size when administered before 1/ 2-AR preconditioning or at the onset of reperfusion while it reduced mechanical recovery during reperfusion. (sun.ac.za)
  • The NOS inhibitors had no effect on the reduction in infarct size induced by 1/ 2-AR preconditioning, but depressed mechanical function during reperfusion. (sun.ac.za)
  • The significant reduction in infarct size by 1/ 2-PC, was associated with activation of ERKp44/p42 and PKB/Akt during the triggering phase, as well as during reperfusion. (sun.ac.za)
  • 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)
Apoptosis3
  • 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)
  • Ischaemia and reperfusion trigger cardiomyocyte death by necrosis and apoptosis. (mmu.ac.uk)
Transplantation5
Coronary heart d2
Inhibition1
  • Finally, addition of exogenous recombinant Wisp1 partially rescued myofibroblast-induced collagen gel contraction following HuR inhibition, demonstrating that HuR-dependent Wisp1 expression plays a functional role in HuR-dependent MF activity downstream of TGFβ. (harvard.edu)
Apoptotic2
  • HIF-1 target genes also encode survivalfactors, such as insulin-like growth factor 2 as well as EPO and VEGF, which can block apoptotic signalinginduced by ischemia. (grantome.com)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
Therapy5
  • The recent development of novel nanoparticle-based targeted cardiac therapy calls for novel simulation methods that can provide insights into the distribution patterns of therapeutic agents within the heart tissue. (cupidoproject.eu)
  • Delivery of therapy-loaded nanoparticles (NP) via inhalation is an innovative technology shown to successfully reduce heart failure in mice, improving the efficiency of drug delivery, and reducing adverse side effects. (cupidoproject.eu)
  • The advent of coronary care units and early reperfusion therapy (lytic or percutaneous coronary intervention) has substantially decreased in-hospital mortality rates and has improved the outcome in survivors of the acute phase of MI. (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)
  • Data from two pivotal trials suggest that a single infusion of the CRISPR-based gene therapy exagamglogene autotemcel (exa-cel) can provide a 'functional cure' for patients with transfusion-dependent beta-thalassemia or severe sickle cell disease. (cdc.gov)
Metabolic2
  • Intracellular calcium accumulation, the action of free radicals, metabolic alterations, and autonomic modulation are important influences on the development of VF during ischemia. (medscape.com)
  • Organ failure in the heart or kidney can initiate various complex metabolic, cell-mediated and humoral pathways affecting distant organs, contributing to the high therapeutic costs and significantly higher morbidity and mortality. (biomedcentral.com)
Ischemic zone3
  • The re-establishing of blood flow to an ischemic zone is called reperfusion [ 1 ]. (biomedcentral.com)
  • Eleven of these HuR-bound mRNAs also showed significant co-expression correlation with HuR, αSMA, and periostin in primary fibroblasts isolated from the ischemic-zone of infarcted mouse hearts. (harvard.edu)
  • Accordingly, we found Wisp1 expression to be increased in cardiac fibroblasts isolated from the ischemic-zone of mouse hearts following ischemia/reperfusion, and confirmed Wisp1 expression to be HuR-dependent in isolated fibroblasts. (harvard.edu)
Conversely1
  • conversely, presence of a thiazolidinedione moiety in the test compound experienced no independent effect on preload-adjusted external work during ischemia and reperfusion (= 0.85). (tam-receptor.com)
Vascular2
  • Effects of diltiazem on coronary vascular functional integrity were assessed in isolated rabbit hearts during reperfusion after 30 min of global, no-flow ischemia. (utmb.edu)
  • Diltiazem, 4 μM, blocked ischemia-reperfusion-induced increases in water content, extracellular space, vascular resistance, V 1 , and vascular permeability to [ 125 I]BSA, without reducing LV developed pressure or +dP/dt relative to nonischemic diltiazem controls. (utmb.edu)
Hemodynamic1
  • The clinician must be aware of these arrhythmias, in addition to reperfusion strategies, and must treat those that require intervention to avoid exacerbation of ischemia and subsequent hemodynamic compromise. (medscape.com)
Normoxic3
  • This figure outlines the time course for normoxic (A) and ischemia-reperfusion (B) experiments. (justia.com)
  • Donor hearts were explanted, stored in cardioplegic solution supplemented with either a medium (Vehicle), normoxic CM (N-CM), or hypoxic CM (H-CM), and then heterotopically transplanted. (researchsquare.com)
  • Antibody arrays revealed that nine proteins were significantly increased in hypoxic CM compared with normoxic CM. Furthermore, compared with vehicle and N-CM groups, the protein levels of PI3K and p‐Akt/Akt ratio in the transplanted hearts significantly increased in the H-CM group. (researchsquare.com)
Hypercholesterolemia1
  • Ischemic heart disease including myocardial infarction develops on the basis of several risk-factors and comorbidities such as obesity, diabetes, hypertension, and hypercholesterolemia. (nih.gov)
Vivo2
  • Isolated ex vivo mice hearts were perfused in a constant pressure Langendorff mode, and exposed to 30min of global ischemia (GI) and 60min of reperfusion. (uib.no)
  • 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)
Phenomenon2
  • The phenomenon may be modelled in an experimental setting, in this case on an isolated rat heart. (justia.com)
  • Although the phenomenon of ischaemic preconditioning (IPC) is associated with the desired protective capacity, the necessity of its application before sustained ischaemia limits its clinical potential. (sun.ac.za)
Intracellular2
  • In isolated, buffer-perfused rat hearts, function was measured with a left ventricular balloon, and energy metabolism (ATP, phosphocreatine, inorganic phosphate, intracellular pH) was estimated by 31NMR-spectroscopy. (ox.ac.uk)
  • In the control period, ET-1 reduced coronary flow, ventricular function, phosphocreatine and intracellular pH dose-dependently: during ischemia/reperfusion, coronary flow, functional recovery and high-energy phosphate metabolism were adversely affected by ET-1 in a dose-related manner. (ox.ac.uk)
Oxygen4
  • The elevated heart rate increases myocardial oxygen demand, and a decreased length of diastole compromises coronary flow, worsening myocardial ischemia. (medscape.com)
  • The aims of premedication are to minimize myocardial oxygen demands by reducing heart rate and systemic arterial pressure and to improve myocardial blood flow with vasodilators. (medscape.com)
  • For instance, functional magnetic resonance imaging monitors the blood oxygen level dependent (BOLD) contrast but is sensitive only to deoxygenated hemoglobin and the MRI machine is bulky. (lu.se)
  • In our studies, the feasibility of using PAI for estimating the spatial distribution of oxygen saturation is examined, in models of occlusion reperfusion and adrenalin-dependent vasoconstriction in humans. (lu.se)
Neuronal1
  • Not only can both produce symptoms that mimic ischemic stroke, but they can also aggravate ongoing neuronal ischemia. (medscape.com)
Ventricular tachycardia1
  • Pathological variants in TRPM4 gene have been linked to several cardiac phenotypes such as complete heart block (CHB), ventricular tachycardia, and Brugada syndrome (BrS). (frontiersin.org)
Therapeutic1
  • These studies may lead to thedevelopment of novel therapeutic strategies that protect the heart by promoting adaptive responses or bypreventing maladaptive responses. (grantome.com)
Arrhythmias1
  • Enhanced efferent sympathetic activity, increased concentrations of circulating catecholamines, and local release of catecholamines from nerve endings in the heart muscle itself have been proposed to play roles in the development of peri-infarction arrhythmias. (medscape.com)
Myocardial infarction3
Interventions1
  • In both cardiac surgical and cardiological settings, clinical interventions used to reperfuse the ischemic heart are associated with myocardial damage that is likely to influence long-term functional recovery. (mmu.ac.uk)
Role6
  • In this review, we summarized the mechanism of mitochondrial transfer in the cardiovascular system and outlined the fate and functional role of donor mitochondria. (frontiersin.org)
  • The role of PKA and PI3-K/Akt was investigated by the administration of the blockers Rp-8-CPT-cAMPs (16 μM) and wortmannin (100 nM) respectively, prior to RI or at the onset of reperfusion. (sun.ac.za)
  • In this proposal, we will investigate the role of HIF-1 and of proteinsencoded by HIF-1 target genes, such as EPO, in promoting protection against cardiac ischemia-reperfusioninjury. (grantome.com)
  • Aim 2 will investigate the role of HIF-1 in mediating adaptive responses to cardiac ischemiaand reperfusion. (grantome.com)
  • We discuss work by ourselves and others in these areas and also consider recent work describing the cellular signaling associated with the IGF-I receptor (IGF-IR) in the heart and its potential role in regulating excitation-contraction coupling. (mmu.ac.uk)
  • This review briefly summarizes relevant research and focuses on the role of signaling in heart-kidney crosstalk in the critical care setting. (biomedcentral.com)
Rats3
  • The hearts after transfection were heterotopically transplanted into the abdomens of recipient rats and excised on the fourth day after the surgery. (nii.ac.jp)
  • 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)
Infarction1
Circulation2
  • During ischemia, the comparative decrease in LAD stream and the comparative and overall reductions in subendocardial blood circulation were very similar in each group. (tam-receptor.com)
  • Desk 3 Hemodynamics, myocardial blood circulation, and LV systolic function Regional LV systolic function At baseline before ischemia, local LV systolic function in the anterior LV was very similar in all groupings as evaluated by fractional systolic region reduction (Desk 3) and by local exterior function (Fig. 3). (tam-receptor.com)
Significantly higher1
  • 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)
Receptor1
  • Secreted Frizzled Related Proteins (sFRPs) are a family of glycosylated Wnt antagonists that inhibit Wnt signaling, either by directly binding to Wnt proteins to prevent their binding to Frizzled (Fz) family receptor proteins or by forming non‐functional interactions with Frizzled receptors. (reliatech.de)
Left ventricle1
  • Coronary sinus, normally located between the LEFT ATRIUM and LEFT VENTRICLE on the posterior surface of the heart, can serve as an anatomical reference for cardiac procedures. (bvsalud.org)
Cardiovascular3
Increases1
  • They demonstrated that transferring functional mitochondria of bone marrow-derived stem cells to defective parenchymal cells increases the aerobic respiration capacity of recipient mitochondria ( 7 ). (frontiersin.org)
Organ1
  • The CRS classification system includes a vast array of acute or chronic conditions in these two important organs, where the primary failing organ can be either the heart or the kidneys. (biomedcentral.com)
Effects5
  • To study effects of ET-1 not related to coronary flow reduction, additional hearts were perfused under constant flow conditions (ET-1 0 or 400 pmol) during 15 min of control, 15 min of ischemia and 30 min of reperfusion. (ox.ac.uk)
  • When coronary flow was held constant, functional and energetic parameters were similar for untreated and ET-1 treated hearts during the entire protocol, i.e. the adverse effects of ET-1 on function and energy metabolism during ischemia/reperfusion were completely abolished. (ox.ac.uk)
  • However, the functional evaluation of resident macrophages is limited by potential off target effects in ∆FIRE mice. (elifesciences.org)
  • Steroid side effects can include an increased risk of a heart attack or stroke (inability to have a normal heart rate), hgh side effects0. (professionalwritingconnection.com)
  • Effects of treatment on manifestation of proinflammatory cytokines Having founded a functional good thing about treatment with troglitazone or -tocopherol, but not rosiglitazone, we wanted to determine whether these findings might be attributable to variations in inflammatory reactions and/or energy substrate rate of metabolism. (tam-receptor.com)
Reduction1
  • Infanger M, Baum E, Grimm D, Ertel W. Palmar Reduction And Internal Fixation For Displaced Intraarticular fractures of the radius with locking compression plate: Operative strategy leads to functional treatment J. Orthopaedics. (au.dk)
Global2
  • The cAMP analogue 8-Br-cAMP-AM (8-Br) confers marked protection against global ischaemia/reperfusion of isolated perfused heart. (mdpi.com)
  • The functional recovery from 30-min global ischemia was studied in the isolated hearts perfused in-vitro. (nii.ac.jp)
Function3
  • We hypothesized that the donor heart preservation with hypoxic conditioned medium derived from BMSCs (CM-BMSCs) would improve post-transplant graft function. (researchsquare.com)
  • Heart performance and kidney function are closely interconnected and communication between these organs occurs through a variety of bidirectional pathways. (biomedcentral.com)
  • We utilized a load-insensitive way of measuring contractile function, preload-adjusted local exterior work, to assess ramifications of test compounds on contractile function during ischemia and reperfusion. (tam-receptor.com)
Clinically1
  • It has been clinically applied for the treatment of heart failure and mental abnormalities, and gradually replaced agarwood in Mongolian medicine. (bvsalud.org)