Bhimji S, Godin D V, McNeill J H
Br J Exp Pathol. 1986 Dec;67(6):851-63.
The effects of left circumflex coronary artery occlusion (40 min) and subsequent reperfusion (60 min) on haemodynamics and myocardial ultrastructure were investigated in control and 10-week alloxan-diabetic rabbits. Before ligation, significant ultrastructural abnormalities, including mitochondrial swelling, disruption of cristae and deposition of lipids, were observed in hearts of diabetic animals. Occlusion of the coronary artery caused further worsening of the ultrastructural changes, including increased swelling and fragmentation of mitochondria, clumping and margination of nuclear chromatin and glycogen depletion in both control and diabetic animals. Following reperfusion, the ultrastructural alterations became even more marked, as characterized by disruption of mitochondria, hypercontraction of myofibrils and the presence of numerous amorphous electron-dense bodies. Paralleling these myocardial structural changes which were more prominent in the diabetic animals was a progressive worsening of haemodynamics, an increased incidence of arrhythmias (especially ventricular fibrillation) and cardiogenic shock in diabetic animals undergoing coronary artery ligation and reperfusion. Our studies indicate that reperfusion of the ischaemic diabetic myocardium accelerates tissue damage and is more detrimental than reperfusion in control animals.
在对照兔和经10周四氧嘧啶诱导的糖尿病兔中,研究了左旋冠状动脉闭塞(40分钟)及随后再灌注(60分钟)对血流动力学和心肌超微结构的影响。在结扎前,糖尿病动物心脏中观察到明显的超微结构异常,包括线粒体肿胀、嵴断裂和脂质沉积。冠状动脉闭塞导致超微结构变化进一步恶化,在对照兔和糖尿病兔中均表现为线粒体肿胀和碎片化增加、核染色质凝聚和边缘化以及糖原耗竭。再灌注后,超微结构改变更加明显,表现为线粒体破坏、肌原纤维过度收缩以及出现大量无定形电子致密体。与糖尿病动物中更显著的这些心肌结构变化相平行的是,在接受冠状动脉结扎和再灌注的糖尿病动物中,血流动力学逐渐恶化、心律失常(尤其是室颤)发生率增加以及心源性休克。我们的研究表明,缺血性糖尿病心肌的再灌注会加速组织损伤,且比对照动物的再灌注更具危害性。