摘要
本文旨在以清醒兔反复短阵心肌缺血(RBMI)模型,观察RBMI对局部心肌的影响。每24h缺血3分钟,连续10次,结果并不致心肌超微结构的明显改变及心电图的累积性损伤变化,但可致局部心肌毛细血管密度增加(P<0.001,X±SD)及线粒体横截面积增大(0.5302±0.1060 VS 0.5923±0.1305(μm^2),P<0.05);经历RBMI的动物在再次4h心肌缺血中的死亡率(1/9VS 9/17,P<0.001,卡方检验)、Q波出现的频率、梗塞范围(IS)(33.23±2.82 VS 56.61±8.01,坏死区/缺血区%,P<0.001)及ST段的抬高量均明显低于单纯4h缺血组,而两组血浆NAGase活性则明显增加,但组间比较并无差别。上述表明,RBMI不仅对兔心肌无累积性损伤,却能减少心肌严重缺血时的损伤,其机制可能与侧支循环的开放或重建有关;线粒体横截面积增大在其中的意义也值得重视。
The present study was designed to establish a model of repeated brief myocardial ischemia(RBMI)and investigate the effects of RBMI on regional myocardium in conscious rabbits(pure Strain of Japan). The results showed that there is no alteration of ultrastrueture and accumulative ECG injury, but a significant increase in capillary density(P<0.001)and mitochondrial cross section area(0.5302±0.1060 vs 0.5923±0.1305,P<0.05)in the regional myocardium after repeated 10 times of ischemia for periods of 3 min every 24 hours. The animals which have RBMI history when subjected to 4h severe ischemia revealed a small infarct size(33.23±2.82 vs 56.61±8.01, IS/RA% P<0.001), lower mortality(1/9 vs 9/17, P<0.001) and emerging frequency of Q wave and lower ST segment compared to the controls. The NAGase release after 4h ischemia increased dramatically in both groups, but no differences existed between two groups. These indicate that RBMI has no accumulative injury to local myocardium,but may prevent the infarcted myocardium from necrosis. The mechanism may be related to the development or opening of the collateral circulation. The increase in mitochondrial cross section area after RBMI should warrant attention.
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
1990年第6期464-467,共4页
Chinese Journal of Pathophysiology
关键词
兔
心肌梗塞
毛细血管
Rabbits
Myocardial infarction
Capillaries