摘要
目的:探讨体外反搏保护缺血心肌的机制。方法:采用冠状动脉结扎法复制犬急性心肌缺血模型,检测缺血及外加反搏时缺血心肌肾素活性、血管紧张素Ⅱ(ANGⅡ)水平和血管紧张素转换酶(ACE)活性以及心肌细胞总、胞浆、胞膜蛋白激酶(PKC)活性,分析ANG Ⅱ与PKC之间的关系。结果:缺血能激活缺血区心肌肾素(0.97±0.19 vs 3.21±0.67)、ACE(13.7±5.2 vs 33.9±7.9)和ANGⅡ(20±3 vs 154±19),ECP能抑制三者(2.36±0.59,23.3±7.4,107±19)。缺血组细胞总、胞膜PKC活性明显高于假手术组(5.80±0.85 vs 7.76±0.92.3.43±0.76 vs6.59±1.06),胞浆PKC活性则明显低于假手术组(2.37±0.39 vs 1.16±0.29)。体外反搏对细胞总PKC无明显影响(7.15±0.64),使胞浆PKC恢复正常(2.67±0.52),对胞膜PKC(4.47±0.31)有一定抑制作用。ANGⅡ水平与胞膜PKC活性密切相关(r=0.873)。结论:体外反搏对缺血心肌局部肾素-血管紧张素系统有抑制作用,使PKC从胞浆移至胞膜,且ANGⅡ水平与胞膜PKC活性密切相关。提示体外反搏治疗心肌缺血时局部ANGⅡ可能通过PKC这一信号转导途径起作用。
Objective: To explore the signal transduction pathway of angiotensin Ⅱ during external counterpulastion treatment( ECP) in ischemic myocardium of dogs. Methods:18 dogs were divided into sham,MI,MI + ECP groups. Acute myocardial ischemia was induced by occluding the left anterior descending coronary artery of ischemic and ECP groups and ECP group also be treated by ECP 1 h after MI. The local renin activity, angiotensin ( ANG Ⅱ ) level,ACE activity in ischemic myocardium were tested and protein kinase C(PKC) activity of total cell,cytosol and membrane were assayed separately. Results:ECP could reduce cardical renin activity, ANG Ⅱ level and ACE activity,which were activated by ischemia. PKC activity of total cell and membrane increased, but that of cytosol decreased. ECP showed no markedly effect on PKC of total cell,reduced that of cytosol to normal level,suppressed that of membrane. And there was close relationship between membranous PKC activity and ANG Ⅱlevel. Conclusion: ECP can depress the local RAS, activate PKC, make it translocate and bound to membrane. There is close relationship between membranous PKC activity and ANG Ⅱ level in ischemic myocardium. Those suggest that local ANG Ⅱ work by PKC signal transduction pathway during ECP protecting ischemic myocardium.
出处
《广州医学院学报》
2003年第2期32-34,49,共4页
Academic Journal of Guangzhou Medical College
