Myocardial ischemia - reperfusion injury and myocardial ischemic preconditioning.doc

 PAGE \* MERGEFORMAT 23 Myocardial ischemia / reperfusion injury and myocardial ischemic preconditioning First, the metabolic features of myocardial The heart is a machine to power of organs, which determines that it has a high energy, high-oxygen, high metabolic rate characteristics. Myocardial oxygen uptake rate as high as 70%, when the myocardial oxygen consumption increases, further increases the potential for oxygen uptake rate is very small, to rely on expansion of coronary artery, increasing blood flow to increase the oxygen supply. Any resulting increase in cardiac oxygen consumption and / or oxygen supply to reduce the factors that affect cardiac work. Aerobic oxidation ability of myocardial hypoxia tolerance and the poor. Under normal circumstances, basically all myocardial aerobic metabolism. Metabolite (substrate) oxidation for myocardial performance continued to provide high-energy phosphate bonds; when the oxygen supply is limited, then by stimulating the anaerobic glycolytic capacity. Capacity place mainly in the mitochondria, energy-consuming process is mainly used for muscle actin and myosin combination as well as various ion pump activity. Second, myocardial ischemia caused by metabolic changes in (A) capacity reduction: myocardial ischemia and reduced oxygen supply to myocardial tissue, mitochondrial oxidative phosphorylation decreased, ATP is generated to reduce. Although anaerobic glycolysis enhanced, but production efficiency is low. Myocardial energy metabolism status and extent of myocardial ischemic injury is directly related to myocardial ischemia when the ATP levels in more than 35% of normal when the ischemic damage is reversible; when the ATP level dropped to 20% of normal, then the resulting irreversibility ischemic injury. (B) intracellular acidosis: Myocardial ischemia glycolysis strengthened, and lactate production increased; CO2 accumulation can be transformed into H2CO3; ATP produced during