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[严重实验性缺氧时肥厚心肌的超微结构变化。二磷酸硫胺素和维生素B1拮抗剂的作用(作者译)]

[Ultrastructural changes of hypertrophied myocardium in severe experimental hypoxia. Effects of diphosphothiamine and of an antagonist of the vitamin B1. (author's transl)].

作者信息

Marraro Carnazza M L, Alberghina M, Iannello A L

出版信息

G Ital Cardiol. 1975;5(3):372-81.

PMID:125212
Abstract

The ultrastructural changes occurring in hypertrophic heart cases during severe experimental hypoxia, conducted intermittently for 140 and 250 hours, are reported in the present study. For this purpose, serial right myocardial specimens of control and treated groups of animals were obtained and examined by electron-microscopy. Most areas of the individual myocardial tissue taken during prolonged degrees of exposures to normobaric hypoxia, showed an increased number of mitochondria, their prominent destructive changes, enlargement of cisternae of sarcoplasmic reticulum, reduction and derangement of the cristae and an increase of glycogen and lipif droplets cellular content. Different responses were associated with the various experimental designs which include simple hypoxia, hypoxia with administration of Diphosphothiamine (DPT, 30 mg/hie/Kg body weight) and hypoxia with administration of an antagonist of the vitamin B1, neopyrithiamine (PyTh, 20 mg/die/Kg body weight). Alterations in the fine structure of myocardial cells and cellular organelles could complement the increased glycolitic activity and phospholipid biosynthesis for the compensatory mechanism of the heart to hypoxic stimulus. These changes were most evident in the hypoxic animals treated with PyTh because of a large disturbance of energy production caused by the antivitamin. Most of ultrastructural and glycogen content changes disappeared when DPT was administered to the animals in hypoxia. However, the mitochondria were larger in size and their matrices had higher electron density than in the normal control animals. The significance of the morphological and biochemical findings are discussed.

摘要

本研究报告了在严重实验性缺氧期间,肥厚性心脏病患者心脏超微结构的变化,该实验间歇性进行了140和250小时。为此,获取了对照组和治疗组动物的右心肌连续标本,并通过电子显微镜进行检查。在长时间常压缺氧暴露过程中采集的个体心肌组织的大部分区域,线粒体数量增加,出现明显的破坏性变化,肌浆网池扩大,嵴减少和排列紊乱,细胞内糖原和脂滴含量增加。不同的反应与各种实验设计有关,包括单纯缺氧、给予二磷酸硫胺(DPT,30mg/hie/Kg体重)的缺氧以及给予维生素B1拮抗剂新吡硫胺(PyTh,20mg/die/Kg体重)的缺氧。心肌细胞和细胞器的精细结构变化可补充糖酵解活性和磷脂生物合成的增加,作为心脏对缺氧刺激的代偿机制。这些变化在用PyTh治疗的缺氧动物中最为明显,因为抗维生素导致能量产生的严重紊乱。当在缺氧动物中给予DPT时,大多数超微结构和糖原含量变化消失。然而,线粒体比正常对照动物更大,其基质具有更高的电子密度。讨论了形态学和生化研究结果的意义。

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