摘要
为进一步确定短暂缺血预处理对缺血心肌在心肌梗塞面积、心律失常方面的保护作用,并对缺血区心室肌心电图及α_1受体激动剂对缺血心肌的影响和缺血预处理的可能机制进行初步探讨,本文对兔在体心脏施行5min短暂继以10min再灌注进行缺血预处理,在另一组中在给予兔5min低浓度α_1受体激动剂后继以10min无药再灌注,发现缺血预处理组兔心经历随后的30min持续缺血时,较未进行缺血预处理而直接给予30min缺血的对照组心肌梗塞面积减小(P<0.05)、心律失常发生率下降(P<0.05)、诱发心律失常的发生率下降(P<0.05)、缺血区心室肌心电图时限不比正常期延长(P>0.05),而对照组缺血期时限较正常期显著延长(P<O.05).在给予兔5min低浓度α_1受体激动剂继以10min无药再灌注时,在随后的持续性缺血后出现心梗面积减小,缺血区心室肌心电图时限与正常期无差别(P>0.O5).提示缺血预处理对心肌缺血性损伤具有保护作用,且这一保护作用可能与α_1受体兴奋有关.
To further determine the protection of transient ischemic preconditioning (IPC)to the ischemia myocardium on myocardial infarction size and arrythmia, as well as to study the electrocardiogram (ECG) of ischemic ventricular myocardium, the influence of aaaaaaaaaa1-receptor agonist on ischemic myocardium and the possible mechanisms' of IPC, 9 rabbits (PC group) underwent IPC with 5 min transient occlusion and then 10 min reperfusion, while another group (PE group, 9 rabbits) were treated with 5 min low density α1-receptor agonist then 10 min reperfusion without drug. It was discovered that, after another 30 min continuous ischemia, the infarction size and the incidence of arrythmia and the induced-arrythmia decreased in the PC group versus the control (9 rabbits) which were directly given 30 min ischemia without IPC (P<0. 05) ; the ECG time-limit of the ventricular myocardium in ischemic area was not longer than normal (P>0. 05) , however, the time-limit of control group had significantly prelonged than normal (P<0. 05). The infarction size of PE group declined, but the ECG time-limit had no significant difference from that of normal. The results indicated that IPC had protective effect on the ischemia injury of myocardium, which might be related to the excitation of α1-receptor.
出处
《中国心血管杂志》
1997年第2期76-78,111,共4页
Chinese Journal of Cardiovascular Medicine
基金
广东省医药卫生青年科学研究基金