| Objective:To explore the protective effects and mechanism of Nimodiping,a kind of calcium channel bloker,in acute myocardial ischemia(AMI)injury in rats and its influence on apoptosis of cardiomyocytes through duplicating the AMI modle and caculating the myocardium infarct size and the±dp/dtmaxof left ventriular.Methods: Seventy Wistar rats were included in the study,among which,forty were divided randomly into 4 groups:group A(n=10,normal control group),group B(n=10,acute myocardial ischemia),group C(n=10,nimodiping 0.2mg/kg),and group D(n=10, nimodiping 0.5mg/kg).Thirty Wistar rats were used to calculate myocardial infarct size,with 10 in each group(B,C and D).The rat model of AM was established by tying and untying the left anterior descending branch(LAD)of rat coronary.The animals were then sacrificed and hearts were harvested for the determination of myocardial infarct size by using 1%TTC.The expression of apoptosis cells were observed by immunohistochemical technique.Results:After ligating the left anterior descending branch,the ST segment of group c elevated obviously comparing with group d;The ST segment of group C and group D all dropped and the ECG data have a statistical significance compared with the acute myocardial ischemia group separetly;The myocardium infarct size was smaller in group D than that in group B(P<0.01). Nimodiping could depress human AMI apoptosis.The expression of apoptosis increased significantly as compared with that in group A(P<0.01).Conclusions:Nimodiping can protect myocardium from AMIR injury by inhibiting the apoptosis of cardiomyocytes induced by Nimodiping. |