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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 purpose of this paper is to observe the effect of RBMI on the local myocardium with awake rabbit repeat myocardial ischemia (RBMI) model. Each ischemia for 3 minutes, 10 consecutive times, the results did not cause significant changes in myocardial ultrastructure and cumulative changes in ECG changes, but can cause local myocardial capillary density increased (P <0.001, X ± SD) and mitochondrial transverse (0.5302 ± 0.1060 VS 0.5923 ± 0.1305 (μm ~ 2), P <0.05). The mortality of animals undergoing RBMI in the fourth hour of myocardial ischemia (1/9 Vs 9/17, P <0.001, Square test). The frequency of occurrence of Q wave was significantly lower in IS range (33.23 ± 2.82 vs 56.61 ± 8.01,% in necrotic area / ischemic area, P <0.001) and ST elevation Blood group, while plasma NAGase activity was significantly increased in both groups, but there was no difference between the two groups. The above shows that RBMI not only does not accumulate damage to the myocardium of rabbits, but also reduces the damage of myocardium under severe ischemia. The mechanism may be related to the opening or reconstruction of collateral circulation. The significance of mitochondrial cross-sectional area is worth noting .