• Surprisingly, Txnip-KO hearts had greater recovery of cardiac function after an ischemia-reperfusion insult. (jci.org)
  • Cardiac function and injury were determined by microcirculation, electrocardiography, and infarct size. (ntnu.edu.tw)
  • α-TOH significantly reduced infarct size, restored cardiac function as measured by ejection fraction, fractional shortening, cardiac output, and stroke volume, and prevented pathological changes as assessed by state-of-the-art strain and strain-rate analysis. (tocotrienolresearch.org)
  • Overall, α-TOH inhibits ischemia/reperfusion injury-induced oxidative and inflammatory responses, and ultimately preserves cardiac function. (tocotrienolresearch.org)
  • This augmented adverse remodelling after I/R and led to an increased infarct size and deterioration of cardiac function. (elifesciences.org)
  • Cardiac function, histology, and infarct size were assessed, and inflammatory markers quantified by RT-PCR. (biomedcentral.com)
  • Recent data suggested that microRNA-101a (miR-101a) exerted anti-fibrotic effects in post-infarct cardiac remodeling and improved cardiac function. (cyberleninka.org)
  • When AICAR is given 24 hours prior to reperfusion, it prevents post ischemic leukocyte-endothelial cell adhesive interactions with increased NO production. (wikipedia.org)
  • AICAR also increases AMPK-dependent glucose uptake through translocation of GLUT-4 which is beneficial for the heart during post-ischemic reperfusion. (wikipedia.org)
  • Empagliflozin also enhanced cardiac robustness by maintaining intracellular ATP levels and the recovery capacity in the infarcted area during ischemic-reperfusion. (nature.com)
  • In addition, several studies have demonstrated the beneficial effects of empagliflozin on myocardial infarction (MI) in diabetic animal models 10 , 11 , prompting us to investigate the real-time ATP change in cardiac energy production in an ischemic-reperfusion model of MI. (nature.com)
  • Numerous apoptotic cardiomyocytes were found in ischemic fields in ischemia-reperfusion groups and werent observed in the sham-operated group. (ac.ir)
  • Although ideally positioned for immediate response to ischemic stroke (IS) and reperfusion, their progressive morphological transformation into activated cells has not been quantified. (biomedcentral.com)
  • CD11b expression, but not iNOS expression, was increased in regions of hyper- and de-ramified microglia during the course of ischemic stroke and 24 h of reperfusion. (biomedcentral.com)
  • Results Coronary arterial ischemia/reperfusion depressed cardiac microcirculation, induced ST-segment elevation and increased infarct size in non-PTP and PTP rats. (ntnu.edu.tw)
  • Wistar rats underwent 30 min of ischemia by ligation of the left anterior descending coronary artery, followed by administration of hAFS cells and 2 h of reperfusion. (ox.ac.uk)
  • 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)
  • Methods and Results: Two weeks following coronary artery occlusion in rats, the expression levels of both TGFpi and TGFpRI were increased, but the expression of miR-101a was decreased at the site of the infarct and along its border. (cyberleninka.org)
  • We suggest PTP might efficiently diminish cardiac ischemia/reperfusion-induced apoptosis and autophagy injury. (ntnu.edu.tw)
  • 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)
  • We measured the cardiac O 2 - amount in vivo in response to left anterior descending coronary artery ligation for 2 hours and reperfusion for 3 hours. (ntnu.edu.tw)
  • The preclinical work focuses on animal models of myocardial ischemia-reperfusion injury, which is an experimental model for STEMI, as well as ex-vivo models of myocardial ischemia. (gu.se)
  • 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)
  • Murine models of Matrigel plug and hindlimb ischemia were employed as in vivo angiogenic assays. (biomedcentral.com)
  • 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)
  • The drug is a potential first-in-class agent for prevention of reperfusion injury in CABG surgery. (wikipedia.org)
  • Conclusions PTP significantly reduced cardiac ischemia/reperfusion injury by upregulating antioxidant, antiapoptotic, and antiautophagic mechanisms. (ntnu.edu.tw)
  • Chien, CY , Chien, CT & Wang, SS 2014, ' Progressive thermopreconditioning attenuates rat cardiac ischemia/reperfusion injury by mitochondria-mediated antioxidant and antiapoptotic mechanisms ', Journal of Thoracic and Cardiovascular Surgery , 卷 148, 編號 2, 頁 705-713. (ntnu.edu.tw)
  • Short-term cardiac stress, induced by ischemia-reperfusion (I/R) injury resulted in impaired left ventricular (LV) recovery and increased infarct size in heterozygous Hmox1-deficient (Hmox1 +/− ) mice [ 55 ]. (springer.com)
  • We applied alpha- tocopherol (α-TOH), the strongest anti-oxidant form of vitamin E, in murine cardiac ischemia/reperfusion injury induced by ligation of the left anterior descending coronary artery for 60 min. (tocotrienolresearch.org)
  • Despite extensive research, our understanding of the precise role of different subsets of macrophages in ischemia/reperfusion injury remains incomplete. (elifesciences.org)
  • 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)
  • In summary, resident macrophages orchestrate inflammatory responses improving cardiac remodelling, while recruited macrophages determine infarct size after I/R injury. (elifesciences.org)
  • Using state-of-the-art fate-mapping models and genetic and pharmacological targeting approaches, the authors provide solid evidence that the absence of resident macrophages do not influence infarct size but instead alter the immune cell crosstalk in response to injury. (elifesciences.org)
  • Acute kidney injury (AKI) can result from a variety of etiologies (e.g., ischemia, toxicity, and sepsis) and is characterized by high rates of morbidity and mortality. (biolifesas.org)
  • 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)
  • 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)
  • 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)
  • Recent studies have shown that ferroptosis is closely related to the pathophysiological processes of many diseases, such as tumors, nervous system diseases, ischemia-reperfusion injury, kidney injury, and blood diseases. (nature.com)
  • Ferroptosis plays an important regulatory role in the occurrence and development of many diseases, such as tumors, neurological diseases, acute kidney injury, ischemia/reperfusion, etc. (nature.com)
  • As such, the dichotomous nature of these cells continues to confound our understanding of microglia-mediated injury after IS and reperfusion. (biomedcentral.com)
  • The purpose of this study was to quantitatively characterize the spatiotemporal pattern of microglia morphology during the evolution of cerebral injury after IS and reperfusion. (biomedcentral.com)
  • Quantitative analysis reveals a significant spatiotemporal relationship between microglia morphology and evolving cerebral injury in the ipsilateral hemisphere after IS and reperfusion. (biomedcentral.com)
  • Importantly, quantitative analyses of microglial morphology and activity are feasible and, in future studies, would assist in the comprehensive identification and stratification of their dichotomous contribution toward cerebral injury and recovery during IS and reperfusion. (biomedcentral.com)
  • Hmox1 knockout (Hmox1 −/− ) and wild-type (WT, Hmox1 +/+ ) mice were subjected to a permanent ligation of the left anterior descending coronary artery. (springer.com)
  • The progression of cardiovascular diseases is usually associated with numerous stimuli, including ischemia, inflammation, and pressure or volume overload, all of which may induce cardiac fibrosis. (cyberleninka.org)
  • Live cell morphology and process activity were measured from movies acquired in acute brain slices from GFP-CX3CR1 transgenic mice after IS and 24-h reperfusion. (biomedcentral.com)
  • Given the central role that mitochondria play during hypoxia, we hypothesized that Txnip deletion would enhance ischemia-reperfusion damage. (jci.org)
  • Similarly, cardiomyocyte-specific Txnip deletion reduced infarct size after reversible coronary ligation. (jci.org)
  • this change was not completely reversible during the 10-minute reperfusion period. (curehunter.com)
  • AICAR has been shown to precondition the heart shortly before or during ischemia. (wikipedia.org)
  • As a result, AICAR reduces the frequency and size of myocardial infarcts up to 25% in humans allowing improved blood flow to the heart. (wikipedia.org)
  • While high levels of overall cardiac sympathetic drive are a negative prognostic indicator of mortality following MI and during heart failure, β-adrenergic receptor stimulation in the infarct border zone reduced spatially heterogeneous alternans, and prevented conduction block and propagation of extrasystoles. (frontiersin.org)
  • The main therapeutic measures in AMI are aimed at myocardial reperfusion as soon as possible with the restoration of blood flow by percutaneous coronary intervention (PCI) followed by guideline-directed medical therapy to prevent secondary events and progression to heart failure (HF). (biomedcentral.com)
  • 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)
  • The increase in glucose during AICAR preconditioning lengthens the period for preconditioning up to 2 hours in rabbits and 40 minutes in humans undergoing coronary ligation. (wikipedia.org)
  • The extension of the necrotic core into the penumbra is influenced by additional factors such as regional differences in the composition of brain tissue, the vulnerability of different cell types to ischemia, residual tissue perfusion and additional events such as reperfusion [ 2 - 4 ]. (biomedcentral.com)
  • It increases AMPK-dependent recruitment of ATP-sensitive K channels to the sarcolemma causing the action potential duration to shorten, and preventing calcium overload during reperfusion. (wikipedia.org)
  • Furthermore, M2 polarization and angiogenesis were induced upon the administration of exosomes in mouse Matrigel plug and hindlimb ischemia (HLI) models. (biomedcentral.com)
  • Co-registered 3D rendered ultrasound (greyscale) and color Doppler (red and blue) coronal image of a mouse brain during ligation of the right common carotid artery. (visualsonics.com)
  • More than 6 million of those deaths are attributed to direct tobacco use, while around 890,000 deaths are the result of non-smokers being exposed to second-hand smoke ( http://www.who.int/mediacentre/factsheets/fs339/en/ ). (biomedcentral.com)
  • Ten cigarettes were smoked twice daily for 2 weeks followed by MI and then 1 additional week post permanent LAD ligation. (biomedcentral.com)
  • 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)
  • MI is also associated with remodeling of the sympathetic innervation in the infarct border zone, although how this influences arrhythmogenesis is controversial. (frontiersin.org)
  • This is exacerbated by changes in the expression of membrane ion channels and under-expression and reorganization of gap junctions ( Luke and Saffitz, 1991 ) in the infarct border zone also slowing conduction ( Tse, 2016 ). (frontiersin.org)