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实验性心脏肥大的生化方面

Biochemical aspects of experimental cardiac hypertrophy.

作者信息

Matsushita S

出版信息

Jpn Circ J. 1976 Oct;40(10):1147-52. doi: 10.1253/jcj.40.1147.

Abstract

In experimental cardiac hypertrophy induced by aortic constriction of rats, the hypertrophy was established after 5-7 days. The basic biochemical changes for increasing tissue mass; increases in protein, nucleic acid, and polyamine synthesis started to occur between 2 and 8 hours followed by an increase in uridine nucleotide pools via predominance of "salvage" pathway. Although the precise coupling mechanism between mechanical stress and biochemical changes is still obscure, an interval between increased load and DNA transcription may be quite short. Some of the key enzymes regulating these processes showed a biphasic response the reason of which is not clear. The established hypertrophied heart muscle showed a decrease in velocity of isotonic shortening and an increase in resting tension. The former alteration is referred to a decrease in myosin ATPase activity and an disorder in excitation-contraction coupling mechanism, and the latter is supposed to be due to an increase in collagen in heart muscle.

摘要

在大鼠主动脉缩窄诱导的实验性心脏肥大中,5-7天后建立起肥大模型。增加组织质量的基本生化变化,即蛋白质、核酸和多胺合成增加,在2至8小时之间开始出现,随后通过“补救”途径占主导地位导致尿苷核苷酸池增加。尽管机械应力与生化变化之间的确切耦合机制仍不清楚,但负荷增加与DNA转录之间的间隔可能相当短。调节这些过程的一些关键酶表现出双相反应,其原因尚不清楚。已建立的肥大心肌表现为等张收缩速度降低和静息张力增加。前一种改变归因于肌球蛋白ATP酶活性降低和兴奋-收缩偶联机制紊乱,后一种改变据推测是由于心肌中胶原蛋白增加所致。

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