| Myocardial infarction (MI) is the death of myocardium for lack of blood, it is on the foundation in coronary artery pathological changes,and the coronary artery blood provide sharply decreases or breaks off. With the result of that, it makes the corresponding myocardium to get a severity lack of blood. In clinical, the performance is the violent ache of back of the breastbone, having fever, the increasing of the count of white cell and serum myocardial enzyme, and the change of electrocardiogram; it may leads to cardiac arrhythmia, shock or heart failure, MI is the severity type of coronary heart diease. Myocardial cell will be dead with the blood supply break off for about 30 min, so opening the criminal blood vessel in time and resuming the myocardial blood supply are as very importance means for saving myocardium. In clinical there have three kinds of method to solve the acute myocardial infarction (AMI) reason by coronary atherosclerotic, which are medicine treatment, surgical operation treatment and PCI treatment. The opening of the criminal blood vessel after AMI can obviously decrease the myocardial harm degree and improve the prognosis. But the death of myocardial cell, abnormal of hypodynamics, myocardial ischemia reperfusion injury (MIRI), no-reflo -w and the abnormal secretion of cytokine can have importance influence for the ventricular remodeling in the days to come inevitably.Ventricular remodeling is one of the basic mechanisms which cause the occurrence and development of heart failure. It changes the structure and function of heart through a series complications mechanism of member and cell. These varieties include myocardial cells fatty big,apoptosis, and outside of the myocardial cells. The occurrence and development of majority cardiovascular dieases accompanies with ventricular remodeling. It takes seriously influence on the patient's heart function and prognosis, and is the independence dangerous factor of the cardiovascular disease mortality. So more and more experiment research try to improve heart function and prognosis through restricting ventricular remodeling.Along with the occurrence mechanism research of ventricular remodeling, more and more medicine to improve the ventricular remodeling is positive extensive of application in clinical, and obtained good curative effect. In recent time, what we are familiar with include ACEI,β-receptor blocker, CCB, et. They all can effectively repress and prevent the remodeling of ventricular. But these medicine can't have complete repression on the ventricular remodeling with complication mechanism, so to look for a kind of medicine which can improve ventricular remodeling completely is very urgent. This experiment aim to give atorvastatin in rats of acute myocardial ischemia and reperfusion, observe the influence of atorvastatin for ventricular remodeling, and try to study it possibility mechanism.Objective: To investigate the effect and mechanism of atorvastatin on ventricular remodeling in rats of acute myocardial ischemia and reperfusion.Methods: Thirty-four healthy Wistar rats (half male and half female) randomly divided into same-operated group (n=10, normal saline 10ml/kg/d),MIR group (n=12, normal saline 10ml/kg/d),MIR+atorvastatin group (n=12, atorvastatin 2mg/kg/d). After myocardial ischemia and reperfusion, the atorcastatin group were treated with atorvastatin for 4 weeks, than measured the changes of hemodynamics, histopathologics of myocardical cells, the left ventricle weight index (LVWI), the right ventricle weight index (RVWI) and the thickness of ventricular septal to reflect the level of ventricular remodeling. At the same time, observed the content of SOD, MDA, NO, ET, IL-6 and TNF-а.Results: Compared with I/R group, atorvastatin group got better hymodynamics (P<0.05), and LVWI,RVWI and the thickness of ventricler septal were significantly lower (P<0.01), and histopathologics of myocardical cells are much better, increased the activity of SOD and the content of NO (P<0.05), decreased the content of MDA, ET, IL-6 and TNF-а(P<0.05).Conclusion: Atorvastatin can lighten the level of ventricular remodeling in rats of acute myocardial ischemia and reperfusion. The mechanism is mediated by having better hypodynamics, enhancing the release of NO, SOD and decreasing the content of MDA, ET, IL-6 and TNF-а. |
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