The Protective Effect And Mechanism Of FG On Acute Myocardial Infarct In Rats

The CHD have become one of the heavy disease of threatenning mankind's health.The rate of incidence become higher and higher, basing on the atherosclerosis occurrence coronary artery convulsion, inflammation,and occlusion of a coronary artery caused either by bacteria clot or by a blood clot, the hemorheology of coronary artery all can cause myocardial ischemia.The pathologic foundation of myocardial infarction is because of the unbalance of tissue's of the heart metabolism and constituents and oxygen supply, make myocardial severity ischemia can cause irreversible necrosis of the myocardial. myocardial ischemia cause pathologic physiology change,such as the material metabolism changes, the oxygen free radicals increases, the calcium overloads, line grain body structure and function change etc., cause various cardiovascular system diseases, end make the heart comfortable function lower, even take place myocardial cell apoptosis, necrosis.Under normal condition, oxyradical can be eliminate by endogenous free radical scavenging agent, such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px), which can protect cells against oxyradical-induced toxicity damage. During rhagiocrine cell ischemia, hypoxia, function of oxyradical scavenging system degrade or loss, but activity of generating system reinforcement can make oxyradical generated highly and accumulated rapidly, could cause cells acute or chronic injury. So SOD can reflect the ability of which organism eliminate oxyradical indirectly. Moreover, MDA is the end product of the process which oxyradical induce lipid peroxidation reaction, whose value reflect the level of organism histiocyte damaged by free radical indirectly.As the energy resources from FFA is the main consumption of normal myocardium, FFA comsuption increased during myocardium aerobic metabolism dysbolism with ischemia and hypoxia. With myocardial ischemia, CAT released heavy in vivo induced adipolysis augment, generated too much FFA. At the same time, process of FFA oxidated of was locked, FFA re-esterificated reduced,and so on, all can cause continuous increase of FFA, Hypsi-FFA-emia. Moreover Hypsi-FFA-emia can cause myocardial consumption of oxygen (MCO2) and then aggravate ischemia of myocardium, enlarge the extent of ischemic or infarct. Thereby there are parallel relationship between extent of MIS and level of FFA in serum.During acute myocardial infarction, as hypoxia caused by ischemic, furthermore promote ET releasing heavy, which lead aeteria coronaria anastole to contract continuously and vigorously, even cause blood flow in aeteria coronaria cease. ET can promote myocardium and vascular smooth muscle synthesis release Ang II, at the same time, Ang II can act on blood vessel or endocardium endotheliocyte, increasing ET release. Interaction within the two factors can cause cells hyperplasy, myocardial hypertrophy and vascular remodeling, further aggravate damage of Cardiovascular system.Myocardial ischemia can cause not only increase of oxyradical but also calcium overload, damage of architecture and function of mitochondrionwhich can further induce apoptosis of cadiocyte. According to the research, besides death, in the processes of myocardial hypertrophy and cardia failure induced by ischemic/ reperfusion injury and increase of pressure load, apoptosis of cadiocyte accur. Intervention with medicamentous can change the destiny of cells, so seeking medicine against apoptotic has a important significance on curatio of cardiovascular disease and explore medicine function target.Ginkgo leaf total flavonoids (FG) is active component extracted from ginkgo leaf (Egb). In vitro test certificate flavanoid has function of dilat blood vessel, decrease serum cholesterol and increase coronary blood flow, and so on. It can eliminate superoxide anion, hydroxy radical, lipid peroxylradicals, and also can step down the formation process of atherosclerotic,antagonism apoptosis induced with ischemic orig.In current experiment we research the protection effect of FG on model rats with acute miocardial infarction, simulated by ligating left anterior descending of coronary artery of awake rats, and its mechanism through several different techniques such as miocardial infarction size (MIS), cardiac muscle enzymology, oxygen free radical, cellular apoptosis and Hematoxylin-Eosin (HE) staining of pathologic tissue. The results show that FG can significantly decrease the MIS of rats with acute miocardial infarction, decrease the activity of lactate dehydrogenase (LDH) and the content of malondialdehyde (MDA), increase the activity of superoxide dismutase (SOD), decrease the content of free fatty acid (FFA), lower the level of ET and Angâ…¡in blood, relieve the cellular apoptosis of rats with acute miocardial infarction. So it suggests that FG has some protection effects on the cardiac muscle with acute ischemia of rats. The mechanism may be the synthesis effect through antagonizing the damnification to cellular membrane of cardiac muscle caused by oxygen-derived free radicals, increasing the power to clean out oxygen-derived free radicals, relieving the damnification to cellular membrane lipid caused by peroxidation, protecting the structure and function of mitochondria, suppressing the apoptosis of cardiac muscle cells.