Suppr超能文献

[运动减少和体力负荷对心肌细胞超微结构的影响]

[Effect of hypokinesia and physical loading on the ultrastructure of cardiac myocytes].

作者信息

Karupu V Ia, Ferents A I

出版信息

Arkh Anat Gistol Embriol. 1978 Jan;74(1):28-37.

PMID:626595
Abstract

The experiments were carried out in rabbits and rats during 1--7.5 months. They demonstrated increasing disturbances in ultrastructure of the protein synthesizing myocardiocyte apparatus. The major and most dangerous disorder is the deficiency in the myocardial apparatus, which is, evidently, the main cause in the reduction of the cardiac functional reserves. Externally, similar reaction of the organism in response to loading (treadmill)--deep fatigue--produces diverse ultrastructural changes in the myocardium depending on the initial adaptive level to motor activity. In rabbits, having satisfactory adaptation to motor activity, the loading (treadmill) results, mainly, in exhaustion of their energy storage. In disadapted animals it produces dangerous lesions in the contractile apparatus of the cardial myocytes.

摘要

实验在兔子和大鼠身上进行,为期1至7.5个月。实验表明,蛋白质合成心肌细胞装置的超微结构紊乱不断加剧。主要且最危险的紊乱是心肌装置缺乏,这显然是心脏功能储备降低的主要原因。从外部来看,机体对负荷(跑步机运动)的类似反应——深度疲劳——会根据对运动活动的初始适应水平,在心肌中产生不同的超微结构变化。在对运动活动有良好适应的兔子中,负荷(跑步机运动)主要导致其能量储备耗尽。在适应不良的动物中,它会在心肌细胞的收缩装置中产生危险损伤。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验