• Myocardial ischemia-reperfusion (I/R) injury is an important health concern in myocardial infarction and situations such as angioplasty and cardiac surgeries. (usask.ca)
  • GRh2 reduced the area of myocardial infarction and the histological changes in the myocardium and improved cardiac functions. (spandidos-publications.com)
  • The administration of bone marrow-derived mesenchymal stem cells (BMSCs) is emerging as a promising approach for I/R injury-induced myocardial infarction due to its multiple differentiation potential(7, 8). (researchsquare.com)
  • B. Rosiglitazone, a peroxisome proliferator-activated receptor-gamma ligand, reduces infarction volume and neurological deficits in an embolic model of stroke. (ac.ir)
  • Result: Compared with the experimental group, Salvia miltiorrhiza injection ameliorated myocardial ischemia-reperfusion injury, and decreased the infarction area seen in Evans/TTC staining. (archive.org)
  • This timing makes postconditioning relevant from the clinical perspective, in which limitation of irreversible myocardial damage following a coronary thrombosis and ST-elevation myocardial infarction remains a major objective [3]. (justia.com)
  • 4] disclose in Cardiovasc Drugs Ther (2007) 21:253-256, that GLP-1 alone did not decrease myocardial infarction but in combination with the GLP-1 breakdown inhibitor valine pyrrolidide (VP) a significant reduction in myocardial infarction occurred. (justia.com)
  • The areas of myocardial ischemia and myocardial infarction are also calculated. (dpi-journals.com)
  • Schisandra chinensis is a commonly used traditional Chinese medicine, which has been widely used in the treatment of acute myocardial infarction in China. (frontiersin.org)
  • Cardiovascular disease, including atherosclerosis, myocardial infarction, heart failure and stroke, is the leading cause of morbidity and mortality in developed nations. (frontiersin.org)
  • Cardiovascular diseases (CVDs) encompass all pathologies of the heart or circulatory system, including coronary artery disease (CAD), myocardial infarction (MI), heart failure and peripheral vascular disease. (encyclopedia.pub)
  • A significant amount of myocardial damage during a myocardial infarction (MI) occurs during the reperfusion stage, termed ischaemia/reperfusion (I/R) injury, and accounts for up to 50% of total infarcted tissue post-MI. (ucl.ac.uk)
  • Stroke and myocardial infarction are among the most common causes of mortality and disability in the world. (cdc.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)
  • However, whether GRh2 has a protective effect on ischaemia/reperfusion (I/R) in the myocardium has yet to be elucidated. (spandidos-publications.com)
  • 2002 - defended ahead of time his PhD thesis in Pathologic Physiology entitled «Comparative evaluation of the cardioprotective efficacy of local and distant ischemic adaptation of the myocardium» dedicated to myocardial protection against ischemia injury in the experiment. (almazovcentre.ru)
  • 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)
  • â'£For HE staining, the myocardium tissue of rats in SHAM Group shows no obvious pathological change. (dpi-journals.com)
  • Both ischemic and reperfused rat myocardium can undergo apoptotic cell death, however the myocardium, which is subjected to ischemia followed by reperfusion, undergoes accelerated apoptosis [ 3 ]. (ac.ir)
  • These pleiotropic effects thus have a major role in protecting the myocardium against ischemic injury. (ac.ir)
  • We hypothesize that SAHA protects the myocardium by maintaining mitochondrial homeostasis and reducing reactive oxygen species (ROS) production during I/R injury. (wustl.edu)
  • and is an intrinsic process through which repeated short episodes of ischemia are instituted to protect the myocardium against subsequent ischemic insults [ 7 ]. (biomedcentral.com)
  • 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)
  • Effects of three types of bariatric interventions on myocardial infarct size and vascular function in rats with type 2 diabetes mellitus. (almazovcentre.ru)
  • Our results showed that pretreatment with CDDPs decreased the level of serum myocardial enzymes and infarct size in rats after IR. (bvsalud.org)
  • Interrupting reperfusion as a stroke therapy: ischemic postconditioning reduces infarct size after focal ischemia in rats. (ac.ir)
  • 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)
  • 10. Allahtavakoli M, Jarrott B. Sigma-1 receptor ligand PRE-084 reduced infarct volume, neurological deficits, pro-inflammatory cytokines and enhanced anti-inflammatory cytokines after embolic stroke in rats. (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)
  • These findings were further confirmed when HIF-1 stabilization in the rat and murine heart resulted in smaller myocardial infarct sizes (both in vivo and ex vivo), decreased mitochondrial oxidative stress, and inhibited MPTP opening following IRI, effects which were also found to be dependent on HKII. (ox.ac.uk)
  • MG53 KO mice lack IPC-mediated cardioprotection as evidenced by a failure of IPC to reduce IR-induced myocardial infarct size. (biomedcentral.com)
  • MC-3 receptor and the inflammatory mechanisms activated in acute myocardial infarct. (ox.ac.uk)
  • Dexmedetomidine pretreatment can obviously relieve myocardial ischemia-reperfusion injury and cardiomyocyte apoptosis in rats probably by activating the Janus kinase 2/signal transducers and activators of transcription 3 signaling pathway. (ijpsonline.com)
  • All of these factors are known to result in myocardial apoptosis(5) and the acceleration of allograft rejection or chronic allograft dysfunction. (researchsquare.com)
  • 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)
  • Observe and count:â' The Amount of Apoptosis Positive Cell Nucleus, Total Cell Nucleus, and rate of myocardial cell apoptosis. (dpi-journals.com)
  • 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)
  • Mitochondrial dysfunction and oxidative damage are major contributors to myocardial apoptosis during I/R injury. (wustl.edu)
  • During the reperfusion phase, a complex interplay of multiple pathways and mechanisms is activated, which ultimately leads to cell death, primarily through apoptosis. (ucl.ac.uk)
  • 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)
  • Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. (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)
  • METHODS AND RESULTS: Stabilization of myocardial HIF-1 was achieved by pharmacological inhibition of prolyl hydroxylase (PHD) domain-containing enzyme using GSK360A or using cardiac-specific ablation of von Hippel-Lindau protein (VHL(fl/fl)) in mice. (ox.ac.uk)
  • 0.0417dl · g -1, Cp=0.2663 cal/(g · °C). The hepatoprotective effect of ACN2a was evaluated using a mouse model of hepatic injury that was induced by Propionibacterium acnes (P. acnes) and lipopolysaccharide (LPS). (simpsonbiotech-usa.com)
  • Hydrogen gas can reduce ROS and alleviate cerebral, myocardial, and hepatic ischemia/reperfusion injuries. (molecularhydrogenstudies.com)
  • This study aimed to evaluate the effects of TQ on spatial memory and hippocampal long-term potentiation (LTP) in rats with thioacetamide (TAA)-induced liver injury and hepatic encephalopathy. (magiran.com)
  • 2014): Changes in ADMA/DDAH pathway after hepatic ischemia/reperfusion injury in rats: the role of bile. (ankara.edu.tr)
  • Hypercholesterolemia causes endothelial and myocardial dysfunction, as well as aggravates ischemia/reperfusion (I/R)-induced myocardial injury. (nih.gov)
  • A wealth of studies now confirm that PQQ's cell-signaling activity translates into substantial protection against degenerative and age-related conditions, such as mitochondrial dysfunction, 1 heart degeneration, 18-20 brain injury, and cognitive decline. (lifeextension.com)
  • 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)
  • 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)
  • Blood platelets dysfunction was induced after myocardial ischemia-reperfusion, and the level of PECAM-1 increased. (archive.org)
  • 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)
  • Conclusions: SAHA prevents I/R induced-mitochondrial dysfunction and loss, and reduces myocardial ROS production when given before or after the ischemia. (wustl.edu)
  • 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)
  • 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)
  • 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)
  • 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)
  • This study aims to explore the protective effects of sufentanil-postconditioning on myocardial cells in rats. (dpi-journals.com)
  • AIMS: Hypoxia-inducible factor-1 (HIF-1) has been reported to promote tolerance against acute myocardial ischaemia-reperfusion injury (IRI). (ox.ac.uk)
  • Endogenous cardioprotective mechanisms against I/R are impaired in hyperlipidemic and hyperglycemic in vivo animal models. (nih.gov)
  • 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 vivo, administration of the melanocortin agonist MTII (10 microg per mouse equivalent to 9.3 nmol) 30 min prior to ischemia (25 min) attenuated mouse heart 2 h reperfusion injury by approximately 40%, an effect prevented by the mixed MC3/4-R antagonist SHU9119 but not by the selective MC4-R antagonist HS204. (ox.ac.uk)
  • Meanwhile, CDDPs pretreatment increased myocardial autophagic flux, with upregulation of LC3B, downregulation of p62, and increased autophagosomes and autolysosomes . (bvsalud.org)
  • 50% loss of mtDNA content in the border zones of mouse hearts, but SAHA pretreatment and reperfusion treatment alone reverted mtDNA content and mitochondrial mass to control levels. (wustl.edu)
  • Aims: The FDA-approved histone deacetylase (HDAC) inhibitor, suberoylanilide hydroxamic acid (SAHA, Vorinostat) has been shown to induce cardiomyocyte autophagy and blunt ischemia/reperfusion (I/R) injury when administered at the time of reperfusion. (wustl.edu)
  • Twenty-four male Sprague-Dawley rats weighing 240-280 g and aged 7 weeks were housed individually in an animal resources facility in a room at a controlled temperature (20-22.8°C) and under a 12 h light/dark cycle. (hindawi.com)
  • A total of 40 male Sprague‑Dawley rats were divided into the following four groups: The sham group, the I/R group, the I/R+GRh2 (10 mg/kg) group and the I/R+GRh2 (20 mg/kg) group. (spandidos-publications.com)
  • Here, we determined the effects of CDDPs in Sprague-Dawley rats with the IR model. (bvsalud.org)
  • Neonatal rat cardiomyocytes were also used to evaluate the protective effect of GRh2 on hypoxia/reoxygenation (H/R)‑induced myocardial injury in vitro. (spandidos-publications.com)
  • This study describes the enhanced pathogenic effect of purified IgG derived from patients with lupus and/or the antiphospholipid syndrome in a cardiomyocyte H/R in vitro model. (ucl.ac.uk)
  • This was shown to be inhibited using a recombinant human peptide of domain I of β2GPI in the fluid phase, suggesting that the pathogenic anti-β2GPI antibodies in this in vitro model target this domain. (ucl.ac.uk)
  • Cardiac ischemia is modelled in vitro through the application of hypoxic and oxidative stress. (biomedcentral.com)
  • 2001): Melatonin inhibits spontaneous and oxytocin-induced contractions of rat myometrium in vitro. (ankara.edu.tr)
  • Focus areas: mechanisms of myocardial protection against ischemia-reperfusion injury, development of targeted drug delivery using nanocarriers. (almazovcentre.ru)
  • The objectives of this study were to 1) determine the extent to which ascorbate or catechin alone at levels which could be in blood after dietary supplementation, can protect myocardial tissue in the reperfusion phase of I/R injury, and 2) evaluate the possible cooperative or synergistic protective effect of ascorbate and catechin when given together. (usask.ca)
  • During myocardial ischemia (lack of blood flow to the muscle tissue of the heart, commonly referred to as a "heart attack"), blood flow is interrupted because of damage to one or more of the coronary blood vessels that irrigate the heart. (prohealth.com)
  • In many cases, damage to heart tissue by reperfusion injury is greater than the damage done by the interruption of blood flow. (prohealth.com)
  • However, accumulating evidence suggests that MG53 has a potentially protective role in heart tissue, including in ischemia/reperfusion injury of the heart, cardiomyocyte membrane injury repair, and atrial fibrosis. (biomedcentral.com)
  • The 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)
  • but reperfusion may introduce additional harm to the tissue through a process known as ischemia/reperfusion injury. (cdc.gov)
  • 14. Bederson JB, Pitts LH, Tsuji M, Nishimura MC, Davis RL, Bartkowski H. Rat middle cerebral artery occlusion: evaluation of the model and development of a neurologic examination. (ac.ir)
  • This results in a considerable improvement in injury caused by oxidative stress produced by different ischemia of cerebral areas of brain. (healthandhydrogen.com)
  • Method: Male Wistar rats were used for establishment of myocardial ischemia-reperfusion model. (archive.org)
  • Male Wistar rats were randomized into four groups: Control Group (CG), Exposure to Smoke Group (ESG), Antioxidant Group (AG) and Exposure to Smoke plus Antioxidant Group (ESAG). (bvsalud.org)
  • 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)
  • 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)
  • In addition to its function in skeletal muscle, MG53 has been shown to have protective effects on various forms of cardiac muscle injury. (biomedcentral.com)
  • 2008. Protective effects of amlodipine on ischemia-reperfusion injury of rat ovary: biochemical and histopathologic evaluation. (ankara.edu.tr)
  • Ischemia/reperfusion (I/R) in mouse hearts and hypoxia/oxidative stress in neonatal rat cardiomyocytes have been associated with a downregulation of MG53. (biomedcentral.com)
  • To evaluate the effects of dexmedetomidine on myocardial ischemia-reperfusion injury in rats and its anti-apoptotic role, as well as the mechanism by which it regulates Janus kinase 2/signal transducers and activators of transcription 3 signal. (ijpsonline.com)
  • It was discovered in 2007 that inhaled hydrogen had genuine protection against brain damage caused by ischemia and reperfusion because of its anti-inflammatory and anti-apoptotic properties (Fukuda et al. (healthandhydrogen.com)
  • The left anterior descending coronary artery was ligated to construct the model of myocardial ischemia-reperfusion. (ijpsonline.com)
  • 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)
  • Conclusion: Post-treatment with sufentanil alleviates myocardial ischemia-reperfusion injury in rats. (dpi-journals.com)
  • 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)
  • Abstract Compound Danshen Dripping Pills (CDDPs) have been used in clinical treatment to protect the heart from ischemia / reperfusion (IR) injury for many years. (bvsalud.org)
  • Several other promising scientific studies now show that lipoic acid has a beneficial effect on a number of the factors involved in metabolic syndrome: it reduces triglyceride levels, lowers cholesterol, improves fasting plasma glucose, and causes weight loss in rodent models of obesity. (lifeextension.com)
  • Recently, the role of inflammation in the central nervous system, particularly the hypothalamus in diet-induced IR progress, has been noted in rodent models and human (Posey et al. (deepdyve.com)
  • 1998): The effects of twisted ischemic adnexa managed by detorsion on ovarian viability and histology: an ischemia-reperfusion rodent model. (ankara.edu.tr)
  • 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)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
  • Methods: Mouse and cultured cardiomyocytes (neonatal rat ventricular myocytes and human embryonic stem cell-derived cardiomyocytes) I/R models were used to investigate the effects of SAHA on mitochondria. (wustl.edu)
  • Since cardiomyocytes are terminally differentiated cells with limited self-renewal capacity, and membrane rupture is a major cause of cardiomyocyte cell death following injury, membrane repair is a necessary process for preserving cardiomyocyte viability [ 6 ]. (biomedcentral.com)
  • KKAy mice, a genetically susceptible model of type II diabetes mellitus, were administered intra-cerebroventricularly with IKK2 inhibitor (IMD-0354) and were exposed to either concentrated PM2.5 or filtered air (FA) for 4 weeks simultaneously via a versatile aerosol concentration exposure system. (deepdyve.com)
  • The phenomenon may be modelled in an experimental setting, in this case on an isolated rat heart. (justia.com)
  • While studies using various materials to overcome ischemia-reperfusion (IR) injury are becoming increasingly common, studies on the effects of botulinum toxin A (BoTA) on IR injury in musculocutaneous flaps are still limited. (hindawi.com)
  • Research done in animals shows that treatment with NAD+ precursors like NMN have cardioprotective effects against ischemia/reperfusion injury (4). (prohealth.com)
  • The authors carried out tests on an animal model to investigate the individual and combined effects of melatonin and NMN on myocardial function, mitochondrial activity, and oxidative stress status following ischemia/reperfusion injury in aged rat hearts. (prohealth.com)
  • Statins are known to improve pulmonary arterial hypertension (PAH) by their anti-inflammatory and anti-proliferative effects in animal models. (escardio.org)
  • Bone marrow mesenchymal stem cells (BMSCs) have been reported to attenuate myocardial I/R injury via their paracrine effects, which can be enhanced by hypoxic preconditioning. (researchsquare.com)
  • Moreover, the autophagic flux inhibitor chloroquine could increase IR injury , while CDDPs could partially reverse the effects. (bvsalud.org)
  • A number of animal and cell models are used to study cardiac function within the division of experimental cardiology, including intervention studies to investigate the effects of (new) drugs on cardiac function in disease models, and examining the role of specific genes in the development of cardiac diseases. (gcure.nl)
  • Over the past three decades, clinical and pharmacological studies have accumulated a body of evidence that not only demonstrated these therapeutic effects, but also provided significant insights into the pharmacokinetic behavior, therapeutic profile, and mode of action of scutellarin in humans and animal models. (cdc.gov)
  • Each group was then subjected to simulated ischemia/reperfusion (SI/R) or corresponding normoxic condition, respectively. (nih.gov)
  • Normoxic CM and hypoxic CM were isolated from rat BMSCs cultured under normoxic (20% O 2 ) or hypoxic (1% O 2 ) condition. (researchsquare.com)
  • This figure outlines the time course for normoxic (A) and ischemia-reperfusion (B) experiments. (justia.com)
  • Abouzaki NA, Christopher S, Trankle C, Van Tassell BW, Carbone S, Mauro AG, Buckley L, Toldo S and Abbate A: Inhibiting the inflammatory injury after myocardial ischemia reperfusion with plasma-derived Alpha-1 Antitrypsin: A post hoc analysis of the VCU-α1RT study. (spandidos-publications.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)
  • Rats were randomly assigned into sham, model, experimental and control groups. (ijpsonline.com)
  • At 1 h before operation, 5.0 μg/kg dexmedetomidine and 5.0 μg/kg Janus kinase 2/signal transducers and activators of transcription 3 signaling pathway agonist SC-39100 were intraperitoneally injected into experimental and control groups, respectively, while the same dose of normal saline was injected into sham and model groups. (ijpsonline.com)
  • 12. Allahtavakoli M, Shabanzadeh A, Roohbakhsh A, Pourshanazari A. Combination therapy of rosiglitazone, a peroxisome proliferator-activated receptor-gamma ligand, and NMDA receptor antagonist (MK-801) on experimental embolic stroke in rats. (ac.ir)
  • The rats were randomly assigned to four groups: experimental group, low dose group (Salvia miltiorrhiza injection, 10 mL/kg/day), moderate dose group (Salvia miltiorrhiza injection, 20 mL/kg/day) and high dose group (Salvia miltiorrhiza injection, 40 mL/kg/day). (archive.org)
  • HIF-1 reduces ischaemia-reperfusion injury in the heart by targeting the mitochondrial permeability transition pore. (ox.ac.uk)
  • Cardiac function can be analysed using a number of techniques in our animal models. (gcure.nl)
  • In conclusion, this study showed strong protection by ascorbate, which could be used in clinically relevant situations, and is the first to report the protection by catechin at this dose under conditions of myocardial ischemia-reperfusion injury. (usask.ca)
  • Conclusion: Salvia miltiorrhiza injection maintains normal function of blood platelets and ameliorates myocardial ischemia-reperfusion injury by decreasing expression of PECAM-1. (archive.org)
  • In conclusion, this study has highlighted a previously unrecognized protective role for MC3-R activation on acute and delayed heart reperfusion injury. (ox.ac.uk)
  • Many studies have tried to discover pharmacologic or surgical interventions that may alleviate IR flap injuries [ 2 - 13 ]. (hindawi.com)
  • The toxin appears to not only have a positive effect on muscle circulation and vessels [ 20 - 23 ] but also apparently have the ability to alleviate IR injury in muscle flaps [ 6 , 24 ]. (hindawi.com)
  • Methods: Choosing 80 healthy rats, all was established in Myocardial Ischemia-reperfusion Model. (dpi-journals.com)
  • [ 3 , 4 ] Further refinements in CPB hardware and techniques, perfusion methods, myocardial and brain protection over the past seven decades contributed to improved outcomes of surgical treatment of CHD. (medscape.com)
  • 18. Wang CX, Yang T, Shuaib A. An improved version of embolic model of brain ischemic injury in the rat. (ac.ir)
  • Comparative evaluation of metformin and liraglutide cardioprotective effect in rats with impaired glucose tolerance. (almazovcentre.ru)
  • Our findings evidenced the cardioprotective effect of trans- resveratrol in rats exposed to cigarette smoke. (bvsalud.org)
  • 2003): Effect of melatonin on estrogen and progesterone receptors in relation to uterine contraction in rats. (ankara.edu.tr)
  • 1996): Oxidative damage in the liver induced by ischemia-reperfusion: protection by melatonin. (ankara.edu.tr)
  • The GRh2 pre‑treatment reduced the I/R‑ or H/R‑induced release of myocardial enzymes and the production of IL‑1β, IL‑18 and TNF‑α. (spandidos-publications.com)
  • As such, new drugs that would complement reperfusion by providing neural and cardiovascular protection and by targeting multiple abnormalities in ischemia are receiving increased attention. (cdc.gov)
  • Five asthma outcomes-two quality and three morbidity measures-were modeled using generalized estimating equations with a logit link function. (cdc.gov)
  • 2007 - Head of Research Laboratory of Myocardial Metabolism, Almazov Federal Heart, Blood and Endocrinology Centre (Almazov National Medical Research Centre). (almazovcentre.ru)
  • It was shown that functional Fas system contributes to apoptotic myocardial cell death in response to ischemia/reperfusion injury [ 4 , 5 ]. (ac.ir)
  • Importantly, delayed myocardial damage as measured 24 h post-reperfusion was equally protected by administration of 10 microg MTII. (ox.ac.uk)
  • A comparison of IR hearts with two controls, sham (perfused for a 15 min stabilization period) and continuous perfusion (perfused for 135 min), showed in most but not all measurements that this was a suitable model of IR injury. (usask.ca)
  • 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)