犬急性心肌缺血后左室功能变化与心肌细胞凋亡

目的观察犬急性心肌缺血后左心室壁动度、射血功能、细胞凋亡与心肌组织中caspase3活性的变化。方法犬30只随机分为实验组15只及对照组15只,实验组结扎左冠状动脉前降支近端,结扎时间分别为10min、30min、60min,每一时间点5只,对照组游离左冠状动脉前降支近端,不结扎。心肌组织行三苯四氮唑(TTC)染色,梗死区为黄白色,非梗死区为砖红色。超声心动图测定左室前壁增厚率及左心室射血分数,原位末端脱氧核苷酸转移酶介导的生物素脱氧尿嘧啶核苷酸缺口末端标记法(TUNEL)检测梗死区心肌组织凋亡细胞数,行caspase3活性测定。结果TTC染色示左室前壁及部分前间隔染色为黄白色,其余区域为砖红色。实验组冠脉结扎后10min,左室前壁增厚率降低,与对照组比较有显著性差异(P<0.05)。左心室射血分数未发生明显改变,与对照组比较无显著性差异(P>0.05)。冠脉结扎后30min至60min,前壁增厚率降低与左心室射血分数进一步下降,与对照组比较有非常显著性差异(P<0.01)。实验组冠脉结扎后10min,梗死区心肌TUNEL阳性细胞数与对照组比较无显著性差异;冠脉结扎后30min至60min,梗死区心肌TUNEL阳性细胞数明显增加,与对照组比较有非常显著性差异(P<0.01)。实验组冠脉结扎后10min,梗死区心肌caspase3荧光值升高,与对照组比较有显著性差异(P<0.05)。30min至60min梗死区心肌caspase3荧光值明显升高,与对照组比较有非常显著性差异(P<0.01)。结论急性心肌缺血后早期,促凋亡基因caspase3激活,缺血心肌细胞凋亡可能为急性心肌缺血的早期病理改变,并且与心肌室壁动度与左室收缩功能降低有一定关系。

Changes of cell apoptosis , caspase 3 activity , left ventricular function in experimental acute myocardial ischemia dogs

Objective To investigate the changes of apoptosis and caspase 3 activity, left ventricular ejection function, and regional myocardial dysfunction following acute ischemia in dogs. Methods Thirty dogs were divided into experiment and control groups. Dogs in experiment group were studied at 10, 30 or 60 min following left anterior descending coronary artery were occluded. Triphenyltetrazolium chlorde (TTC) staining was used to identify ischemia myocardial. The left ventricular ejection fraction and the degree of the increase in left ventricular wall thickness were detected by echocardiography. The percentage of apoptosis in regional left myocardial dysfunction was detected by terminal deoxynucleotidyl transferease-mediated biotinylated deoxyuridine triphosphate nick end labeling (TUNEL). Caspase 3 activity assay was employed to detect caspase 3 activity. Results Anterior wall of left ventricule and regional interventricular septum in experiment group were ischemic. The degree of the increase in left ventricular wall thickness in experiment group decreased at 10 min after coronary artery occlusion (P<0.05). The left ventricular ejection fraction in experiment group had no change at 10 min after coronary artery occlusion. The left ventricular ejection fraction and the degree of the increase in left ventricular wall thickness decreased at 30 min after coronary artery occlusion in experiment group. The positive cells of TUNEL detected in infarcted myocardial had no difference between experiment and control groups at 10 min, and increased in experiment groups at 30 min after coronary artery occlusion (P<0.01), caspase 3 activity in experiment group increased at 10min, and reached its peak at 30, 60min after coronary artery occlusion. Conclusion Caspase 3 activated and cell apoptosis may be the early pathologic changes following acute ischemia in dogs, which are related to the left decrease in left ventricular ejection fraction and in left ventricular wall systolic thichness.