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目的 缺血预适应是指心肌短暂缺血再灌注后 ,使心肌产生适应性反应 ,对随后持续缺血的耐受能力明显增强 ,使持续缺血造成的心肌梗塞范围缩小 ,减轻缺血再灌注心律失常和心功能异常。我们用在体兔心脏缺血预适应模型 ,初步观察了预适应心脏保护的电生理基础 ,探讨其在减少恶性心律失常中的可能作用。方法 将 30只健康家兔随机分成对照组、缺血组、预适应组 ,运用Franz心外膜MAP探针记录技术 ,观察约 40分钟稳定的心电图和MAP图形 ,此后行程序期前刺激测定心室肌有效不应期。结果 缺血组缺血 1分钟内 ,即出现心肌细胞MAPA和dv dtmax明显下降 (P <0 0 1)。此后 ,随缺血时间延长 ,MAP形态逐渐变小。分别于再灌注 5、10和 2 0分钟 ,MAPD5 0 、MAPA和dv dtmax才逐渐恢复接近正常 (P >0 0 5 )。缺血组持续缺血前 5分钟和整个再灌注期 ,MAPD90 和基础值比较变化不大 (P >0 0 5 ) ,而持续缺血 5～ 2 0分钟 ,才发现MAPD90 明显缩短。持续缺血早期 ,ST段逐渐升高 ,但随缺血时间的进一步延长 ,至缺血 15分钟后 ,ST段反而下降。在上述参数动态变化过程中 ,预适应可明显减轻缺血造成的MAPA、dv dtmax下降程度 ,相对延长MAPD5 0 和MAPD90 ,减少ST段升高幅度。各实验组ERP MAPD90 分别为 :C组 1 0 5± 0 0 3;IS组
Objective Ischemic preconditioning refers to the myocardial ischemic reperfusion, the myocardial adaptive response, followed by persistent ischemic tolerance was significantly enhanced, so that the scope of sustained ischemia caused by myocardial infarction, reduce ischemia reperfusion Arrhythmia and cardiac dysfunction. We used preconditioning model of rabbit heart ischemia to preliminarily observe the electrophysiological basis of preconditioning cardioprotection and explore its possible role in reducing malignant arrhythmia. Methods Thirty healthy rabbits were randomly divided into control group, ischemic group and preconditioning group. Franz epicardial MAP probe recording technique was used to observe stable electrocardiogram and MAP pattern in about 40 minutes. Muscle effective refractory period. Results Within 1 minute of ischemic ischemia, myocardial MAPK and dv dtmax were significantly decreased (P <0.01). Since then, with the prolonged ischemia, MAP morphological gradually smaller. At 5, 10 and 20 minutes after reperfusion, MAPD50, MAPA and dv dtmax gradually returned to normal (P> 0.05). MAPD90 and basal values of MAPK90 did not change much (P> 0.05) in the ischemic group 5 minutes before ischemia and during the whole reperfusion period. However, MAPD90 was found to be shortened obviously after continuous ischemia for 5-20 minutes. In the early stage of persistent ischemia, the ST segment gradually increased, but with the further extension of the ischemic time, the ST segment decreased after 15 minutes of ischemia. In the process of dynamic changes of parameters mentioned above, preconditioning can obviously reduce the decrease of MAPv and dv dtmax induced by ischemia, and prolong the MAPD50 and MAPD90 and decrease the increase of ST segment. The ERP MAPD90 in each experimental group were: C group 105 ± 0 0 3; IS group