摘要
目的 :探讨卡托普利预处理对家兔实验性心肌梗塞范围及心肌细胞凋亡的影响。方法 :健康家兔 ,分为 (1)假手术对照组 (sham -operatedcontrolgroup) ,(2 )急性心梗组 (acuteinfarctgroup) ,(3)卡托普利预处理组 (capto prilgroup ,2 5mg·kg- 1 ·d- 1 ,喂饲 1周 )。结扎冠状动脉左旋支造成急性心肌梗塞模型。测结扎前、结扎后 15、30、6 0min的心功能。结扎前及结扎后 1h的全血粘度与血球压积。结扎后 6h取心脏 ,以缺血区重 左室重比为缺血范围 ,梗塞区重 缺血区重比为梗塞范围。TUNEL法染色检测细胞凋亡 ,以心肌凋亡阳性细胞数占总心肌细胞数的百分比作为心肌细胞凋亡指数。结果 :(1)卡托普利预处理组梗塞范围显著小于心梗组 (16 6 0 %± 0 94%比 36 2 4%±1 94% ,P <0 0 5 ) ,并改变左室功能及血粘度。 (2 )梗塞周围可见凋亡心肌细胞 ,卡托普利预处理该区心肌细胞凋亡指数明显小于急性心梗组 (2 6 37%± 0 71%比 42 44 %± 2 32 % ,P <0 0 5 )。结论 :卡托普利预处理可明显减少梗塞范围及心肌细胞凋亡程度 ,改善心功能。
AIM: To investigate the effects of pretreatment of captopril on the infarct size and myocardial cell apoptosis in rabbits. METHODS: Rabbits were randomly divided into sham-operated control group (SO), acute infarct group (AI) and captopril pretreatment group (CP). The rabbits of CP group were treated with captopril (25 mg·kg -1 .d -1 ) for 1 week before harvest. The left circumflex branch of coronary (LCX) was ligated to develop acute ischemic model. The systolic and diastolic function of left ventricle(LV) was measured before and at 15, 30, 60 min after ligating LCX, and the blood viscosity and hematocrit before and at 60 min after ligating LCX were measured also. 6 hours later LCX ligation, the hearts were harvested for determining the infarction size, which was expressed as the ratio of infarct area to the total ischemic area, and evaluating apoptosis index expressed as the percentage of myocardial cells with TUNEL positive staining. RESULTS: 1.Compared with AI group, captopril pretreatment significantly reduced the infarction size (16 60%±0.94% vs 36.24%±1.94%, P<0.05 ), and improved the LV function and viscosity of blood. 2. Apoptosis of myocardial cell was found in the myocardium surrounding to the infarction area, however, the apoptosis index of CP group was significantly lower than that of AI group (26.30%±0.71% vs 42.44%±2.32%, P<0.05 ).CONCLUSION: Apoptosis of myocardial cell exists in the area surrounding the infarction. Captopril pretreatment can reduce infarction size and myocardial apoptosis index, and improve the LV function as well as blood viscosity in this acute ischemic model.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2001年第4期319-322,共4页
Chinese Journal of Pathophysiology
基金
江西省自然科学基金!资助 (No .970 6 0 1)