Sharov V G
Kardiologiia. 1975 Dec;15(12):73-9.
The ultrastructure of the left ventricle was studied in 10 rats, 5 of whom were subjected to partial ligation of the aortic isthmus 9 months prior to the procurement of the material. In 3 of the operated rats cardiac insufficiency was induced by means of additional exercises. Three normal rats could swim for 5 hours running before they got exhausted, 2 rats were intact. The operated animals with signs of cardiac insufficiency exhibited highly distinct ultrastructural changes that did not differ qualitatively from those observed in the acute phase of myocardial hypertrophy. No alterations were noted in the mitochondria, which does not permit to interpret the disorders in the energy balance of the cell as the leading cause of chronic cardiac insufficiency. In chronic cardiac insufficiency the myocardial cells seem to develop physiological disturbances undetectable by electron microscopy that may be the cause of cardiac failure. This is supported by the appearance of gross changes in the myocardium on the advanced stages of hypertrophy even after insignificant additional exercises.
对10只大鼠的左心室超微结构进行了研究,其中5只在取材前9个月接受了主动脉峡部部分结扎。在3只手术大鼠中,通过额外运动诱发了心脏功能不全。3只正常大鼠在精疲力竭前能游5小时,2只大鼠未作处理。有心脏功能不全迹象的手术动物表现出高度明显的超微结构变化,在质量上与心肌肥大急性期观察到的变化没有差异。线粒体未发现改变,这使得无法将细胞能量平衡紊乱解释为慢性心脏功能不全的主要原因。在慢性心脏功能不全中,心肌细胞似乎出现了电子显微镜无法检测到的生理紊乱,这可能是心力衰竭的原因。即使在进行微不足道的额外运动后,肥大晚期心肌出现的明显变化也支持了这一点。