Korostyshevskaia I M, Maksimov V F
Arkh Anat Gistol Embriol. 1990 Jan;98(1):15-20.
Ultrastructure of cardiomyocytes of the left ventricle has been studied in dogs during the experiments, performed with a general external cooling, prolonged circulatory arrest, as well as during long term periods after the operation. In the experiment without cooling it is not possible to restore hemodynamics after 30 min of total ischemia. In cardiomyocytes severe, sometimes irreversible lytic lesions are registered. Opposite to this, by the end of one hour's cardiac arrest under total cooling up to 24-22 degrees C, changes in ultrastructure of cardiomyocytes are minimal. This is proved by a stabilizing action of hypothermia to membranous, fibrillar and even labile granular cellular components. More manifested changes occur in cells after restoration of the cardiac activity and worming, though even at this stage certain morphological signs of partial restoration of synthetic processes are noted. By the third day after the operation ultrastructure of cardiomyocytes is fully normalized at an essential hypertrophy and hyperplasia of protein synthesis organels and lysosomes. Thus, under conditions of aperfusional hypothermia (24-22 degrees C) and cardiac arrest, produced with pharmacological cooling, cardiomyocytes safely survive one hour's total ischemia, presenting their ability to intracellular regeneration in full.
在实验过程中,对犬左心室心肌细胞的超微结构进行了研究,实验采用全身外部降温、长时间循环骤停以及术后长期观察。在无降温的实验中,完全缺血30分钟后无法恢复血流动力学。在心肌细胞中,可观察到严重的、有时是不可逆的溶解损伤。与此相反,在全身冷却至24 - 22摄氏度的情况下,心脏骤停一小时结束时,心肌细胞超微结构的变化最小。这通过低温对膜性、纤维状甚至不稳定颗粒状细胞成分的稳定作用得到证明。心脏活动恢复和复温后,细胞中出现更明显的变化,不过即使在这个阶段,也注意到了合成过程部分恢复的某些形态学迹象。术后第三天,心肌细胞超微结构完全恢复正常,同时蛋白质合成细胞器和溶酶体出现明显肥大和增生。因此,在灌注性低温(24 - 22摄氏度)和药物降温导致心脏骤停的条件下,心肌细胞能够安全度过一小时的完全缺血,充分展现其细胞内再生能力。