重庆医科大学病理生理学缺血再灌注损伤的发病机制.pptxVIP

缺血-再灌注损伤的发病机制 Mechanism Underlying Ischemia-Reperfusion Injury;What is reperfusion injury? Why is it important?;;概念(Concept);;问题： 缺血-再灌注损伤？ 氧反常,钙反常,和pH反常？;缺血-再灌注损伤的发生机制 Mechanisms of I/R Injury ; 指在外层电子轨道含有一个或多个不配对电子的原子、原子团或分子。为表达不配对电子，常常在其分子式后方或上方加一个点（如R·）。;氧自由基（Oxygen Free Radicals）;脂性自由基:氧自由基与不饱和脂肪酸作用后生成的中间代谢产物. 烷自由基（L·） 烷氧自由基（LO·） 烷过氧自由基（LOO·）;;问题： 氧自由基？活性氧？ 超氧物岐化酶,过氧化氢酶,谷胱甘肽氧化酶催化何种反应? ;;;;;线粒体与活性氧 Mitochondria ROS;线粒体与活性氧 Mitochondria ROS;;Plasma membrane: lipoxygenases, cyclooxygenases, NADPH oxidase Mitochondria: electron transport system Cytosol: xanthine oxidase, hemoglobin, catecholamines, riboflavin, Transition metals (Fe2+/3+, Cu1+/2+) Peroxisome: oxidases, flavoproteins Endoplasmic reticulum: mixed-function oxidase cytochromes P-450 and b5;;问题： 氧自由基损伤发生的机制? ;;;钙超载引起缺血再灌注损伤的机制Mechanism of I/R Injury Induced by Calcium Overload ;问题： 钙超载发生的Na+/Ca2+交换机制? ;;Mechanisms Mediating Increased Leukocyte-Endothelial Adhesion;;;;Genesis of No-Flow Phenomenon;问题： 无复流现象及机制? ;;;;问题： 心肌顿抑的定义及发生机制？;;;;;;; The size of an infarct resulting from a 40-min occlusion of a branch of a dog’s coronary artery could be greatly reduced if the heart were subjected to 4 brief periods of 5 min of ischemia and 5 min of reperfusion prior to sustained ischemia. The heart adapted itself within minutes to become resistant to ischemia-induced infarction. Murry CE et al. Preconditioning with ischemia: a delay of lethal cell injury in ischemic myocardium. Circulation 74:1124–1136, 1986.;Acute preconditioning: (classical preconditioning) within ~2 h protein synthesis-independent Delayed preconditioning: (ischemic tolerance) 24 h - 72 h after the initial insult altered gene expression→synthesis of proteins (antioxidant enzymes, NO synthase, etc.).;Limit or spare infarct size Mitigate myocardial stunning Improve Arrhythmias; Blunt the impaired endothelial-dependent relaxation. Ameliorate capillary plugging, leukocyte adhesion, and emigration. Reduce venous p