نتایج جستجو برای: ischemic reperfusion injury
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OBJECTIVE Matrix metalloproteinase-9 (MMP-9) activity is up regulated in the heart subjected to ischemic insult. Whether increased MMP-9 activity contributes to acute myocardial injury after ischemia-reperfusion remains unknown. To investigate the role of MMP-9 in myocardial infarction, we utilized a MMP-9 knockout mouse. METHODS AND RESULTS Standard homologous recombination in embryonic stem...
Background: Clinical studies have shown that disturbance of iron homeostasis in ischemic stroke influenced recovery and functional outcome following blood reperfusion of obstructed cerebral vessels, but the mechanism of iron-mediated toxicity in ischemic strokes has not been fully elucidated. Methods: A middle cerebral artery occlusion (MCAO) mouse model was established by introducing an embolu...
Reperfusion of ischemic tissue is associated with a characteristic pattern of cellular injury that can result in serious systemic and local effects. Ischemia-reperfusion syndrome (IRS) has been documented in a number of clinical situations, including the release of tense fascial compartments in the extremities. Although the lumbar paraspinal musculature is susceptible to fascial compartment syn...
Cerebral ischemia is a condition in which there is insufficient blood flow to the brain to meet metabolic demands. This leads to poor oxygen supply or cerebral hypoxia and thus leading to the death of brain tissues or cerebral infraction/ischemia stroke. It has been third most common cause of death in developed countries, Stroke can affect walking, talking, speech, vision, spatial awareness, sw...
Nonanticoagulant heparin inhibits NF-kappaB activation and attenuates myocardial reperfusion injury.
Heparin reduces ischemia-reperfusion injury to myocardium. This effect has been attributed to complement inhibition, but heparin also has other activities that might diminish ischemia-reperfusion. To further probe these mechanisms, we compared heparin or an o-desulfated nonanticoagulant heparin with greatly reduced anticomplement activity. When given at the time of coronary artery reperfusion i...
Several lines of evidence suggest that proteasomes are involved in multiple aspects of myocardial physiology and pathology, including myocardial ischemia-reperfusion injury. It is well established that the 26S proteasome is an ATP-dependent enzyme and that ischemic heart disease is associated with changes in the ATP content of the cardiomyocyte. A functional link between the 26S proteasome, myo...
The phenomenon of ischemic preconditioning has been recognized as one of the most potent mechanisms to protect against myocardial ischemic injury. In experimental animals and humans, a brief period of ischemia has been shown to protect the heart from more prolonged episodes of ischemia, reducing infarct size, attenuating the incidence, and severity of reperfusion-induced arrhythmias, and preven...
INTRODUCTION Ischemic postconditioning has been recognized as effective in the prevention of reperfusion injury in situations of ischemia and reperfusion in various organs and tissues. However, it remains unclear what would be the best way to accomplish it, since studies show great variation in the method of their application. OBJECTIVE To assess the protective effect of ischemic postconditio...
In the setting of acute myocardial infarction, reperfusion of ischemic myocardium carried out early after coronary occlusion can salvage reversibly injured, viable myocardium. Although still controversial, however, reperfusion itself may cause a population of reversibly injured cells to die, a phenomenon termed lethal reperfusion injury.1 A variety of pharmacological agents have been studied to...
Introduction: Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase-2 (Nox2) is one of the predominant sources of ROS production during myocardial ischemia-reperfusion and can be induced by angiotensin II. The evidence suggests that pharmacological blockers of renin-angiotensin system can exert direct tissue effects independent of their ability to regulate blood pressure. The mechanism...
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