نتایج جستجو برای: myocardial ischemic reperfusion injury
تعداد نتایج: 520115 فیلتر نتایج به سال:
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...
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(s)...
Despite the latest advances in cardiovascular biology and medicine, myocardial infarction (MI) remains one of major causes deaths worldwide. While reperfusion myocardium is critical to limit ischemic damage typical a MI event, it detrimental morphological functional changes known as “reperfusion injury.” This complex scenario poorly represented currently available models ischemia/reperfusion in...
organ damage after reperfusion of previously viable ischemic tissues is defined as ischemia/reperfusion injury. the pathophysiology of ischemia/reperfusion injury involves cellular effect of ischemia, reactive oxygen species and inflammatory cascade. protection against ischemia/reperfusion injury may be achieved by preconditioning or postconditioning. in this review, we discuss basic mechanisms...
Myocardial ischemia/reperfusion injury affects not only the cardiomyocyte compartment but also all other cellular compartments, and the coronary circulation has a central role in it. Acute myocardial infarction most often arises from atherosclerotic plaque rupture/erosion with superimposed thrombosis (type 1 myocardial infarction). However, in the absence of coronary atherosclerosis, coronary v...
Background: Microvascular obstruction (MVO) and Intramyocardial hemorrhage (IMH) are associated with myocardial reperfusion injury and recognized as predictors of adverse left ventricular remodeling in acute myocardial infarction. The pathophysiology of reperfusion injury is characterized by release of reactive oxygen species and inflammation. We investigated whether post-ischemic reperfusion w...
Myocardial ischemia/reperfusion injury affects not only the cardiomyocyte compartment but also all other cellular compartments, and the coronary circulation has a central role in it. Acute myocardial infarction most often arises from atherosclerotic plaque rupture/erosion with superimposed thrombosis (type 1 myocardial infarction). However, in the absence of coronary atherosclerosis, coronary v...
Myocardial ischemia/reperfusion injury affects not only the cardiomyocyte compartment but also all other cellular compartments, and the coronary circulation has a central role in it. Acute myocardial infarction most often arises from atherosclerotic plaque rupture/erosion with superimposed thrombosis (type 1 myocardial infarction). However, in the absence of coronary atherosclerosis, coronary v...
the anti-apoptotic gene bcl-2 is located in mitochondria, but it is uncertain whether its expression affects hepatocyte survival in ischemia/reperfusion (i/r) injury. this experiment was designed to evaluate the role of folic acid in expression of bcl-2 in i/r in rat liver. eighteen wister rats were divided into sham-operated controlgroup (c) (n=6), i/r group (n=6), folic acid treated group whi...
Reperfusion of coronary arteries to limit myocardial ischemic injury and extent of myocardial necrosis is possible by either the use of fibrinolytic therapy, coronary angioplasty or coronary artery bypass surgery. The concept that early reperfusion may salvage jeopardized myocardium is derived from basic experimental studies which purported to demonstrate that the ultimate extent of irreversibl...
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