论文部分内容阅读
目的:探讨延迟缺血预处理(delayed ischemic preconditioning,DIPC)对急性心肌梗死(AMI)大鼠远期的心肌保护及其促进小动脉再生的作用。方法:将54只SD大鼠随机分为4组,即①缺血预处理(IPC)+AMI组:于IPC后24 h,结扎冠状动脉建立AMI大鼠模型(n=24);②AMI组:开胸后,只穿线不进行IPC,于24 h后结扎冠脉建立AMI大鼠模型(n=24);③IPC组:只进行IPC不结扎冠脉(n=3);④假手术组:开胸后,既不进行IPC操作也不结扎冠状动脉(n=3)。前两组于模型建立后3 d、7 d和14 d,用免疫组化染色法检测梗死边缘区毛细血管新生及小动脉再生;后两组分别于IPC后及假手术后24 h,用免疫组化染色法检测梗死边缘区毛细血管新生及血管内皮生长因子(VEGF)、血小板源生长因子-B(PDGF-B)表达。14 d后采用小动物超声检测心功能,Masson’s Trichrome染色法测量心肌梗死(MI)面积。结果:IPC组于IPC后24 h,缺血区的心肌中可见毛细血管新生,VEGF及PDGF-B表达明显增加(与假手术组相比,P<0.05)。与AMI相比,IPC+AMI组于建模后3 d、7 d和14 d,梗死边缘区心肌中毛细血管的密度和小动脉的密度均明显增加(P<0.05),MI面积减小(P<0.05),心功能改善(与AMI组相比,左室短轴缩短率增高,P<0.05)。结论:DIPC可减小MI的面积,改善心功能,这一作用与其增加梗死边缘区中的小动脉再生有关;缺血区心肌中VEGF及PDGF-B表达的增加可能是小动脉再生的刺激因素。
Objective: To investigate the long-term myocardial protection of delayed ischemic preconditioning (DIPC) in rats with acute myocardial infarction (AMI) and its role in promoting arteriolar regeneration. Methods: Fifty-four SD rats were randomly divided into 4 groups: ① ischemic preconditioning (IPC) + AMI group: AMI rats were established by ligation of coronary arteries 24 h after IPC (n = 24); ② AMI group: After thoracotomy, the rats were anesthetized with IPC only, and the coronary artery was ligated after 24 h (n = 24). ③ IPC group: only IPC without coronary artery occlusion (n = 3); ④ Sham operation group: After thoracotomy, neither IPC nor ligation of the coronary arteries was performed (n = 3). In the first two groups, capillary angiogenesis and arteriolar regeneration were detected by immunohistochemistry 3 days, 7 days and 14 days after the model was established. The latter two groups were immunized with IPC The expression of angiogenesis, vascular endothelial growth factor (VEGF) and platelet derived growth factor-B (PDGF-B) were detected by histochemical staining in the marginal zone of infarction. Heart function was detected by small animal ultrasound 14 days later and myocardial infarction (MI) area was measured by Masson’s Trichrome staining. Results: Capillary neovascularization was observed in ischemic myocardium in IPC group at 24 h after IPC, and the expression of VEGF and PDGF-B were significantly increased (P <0.05 compared with sham operation group). Compared with AMI, capillary density and arteriolar density in IPC + AMI group were significantly increased (P <0.05) and MI area were decreased at 3 d, 7 d and 14 d after myocardial infarction P <0.05), cardiac function improved (compared with AMI group, shortening of left ventricular short axis increased, P <0.05). CONCLUSION: DIPC can reduce the area of MI and improve cardiac function, which is related to the increase of arteriolar regeneration in the marginal zone of infarction. Increased expression of VEGF and PDGF-B in ischemic myocardium may be the stimulus for arteriolar regeneration .