缺血再灌注损伤Ischemia-Reperfusion injury.ppt
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1、Ischemia-Reperfusion injury,Ischemia,Anesthesiologist: MI, peripheral vascular insufficiency, stroke, and hypovolemic shock Restoration of blood flow to an ischemic organ is essential to prevent irreversible cellular injury Reperfusion may augment tissue injury,Ischemia-Reperfusion,Thrombolytic ther
2、apy, organ transplantation, coronary angioplasty, aortic cross-clamping, or cardiopulmonary bypass Severe: systemic inflammatory response syndrome (SISS) or multiple organ dysfunction syndrome (MODS) Account for 3040% of the mortality in tertiary referral ICU,Cellular change during Ischemia,Altered
3、membrane potential Altered ion distribution (+ intracellular Ca/Na) Cellular swelling Cytoskeletal disorgnization Increased hypoxanthine Decreased ATP Decreased phosphocreatinine Cellular acidosis,Cellular Effects of Ischemia,Decreased ATP Intracellular accumulation of hypoxanthine Toxic reactive ox
4、ygen species (ROS) during reperfusion,Ischemia at Endothelium,Express certain proinflammatory gene products(leukocyte adhesion molecules, cytokines) bioactive agents (endothelin, thromboxane A2) Repressing other “protective” gene products (constitutive nitric oxide synthase, thrombomodulin) and bioa
5、ctive agents ( prostacyclin, nitric oxide).,Role of Reactive Oxygen Species,Including (O2), (OH), (HOCl), (H2O2), and nitric oxidederived peroxynitrite Directly damage cellular membranes by lipid peroxidation. Stimulate leukocyte activation and chemotaxis by activating plasma membrane phospholipase
6、A2 to form arachidonic acid (thromboxane A2 and leukotriene B4) Increase leukocyte activation, chemotaxis, and leukocyteendothelial adherence after I-R,Role of Complement,I/R results in complement activation and the formation of several proinflammatory mediators that alter vascular homeostasis C3a,
7、C5a, iC3b, C5b9 Most potent is C5a complement may compromise blood flow to an ischemic organ by altering vascular homeostasis and increasing leukocyteendothelial adherence.,Role of Leukocytes,I/R results in leukocyte activation, chemotaxis, leukocyteendothelial cell adhesion, and transmigration mech
8、anical obstruction activated leukocytes release toxic ROS, proteases, and elastases, resulting in increased microvascular permeability, edema, thrombosis, and parenchymal cell death,Manifestations of I/R injury,Vascular Injury and the “No Reflow” Phenomenon Myocardial Stunning Reperfusion Arrhythmia
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- 缺血再灌注损伤Ischemia-Reperfusion injury 缺血 灌注 损伤 Ischemia Reperfusion
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