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[脂质过氧化在心脏肥大消退中的作用]

[Involvement of lipid peroxidation in regression of heart hypertrophy].

作者信息

Arkhipenko Iu V, Shimkovich M V

出版信息

Biull Eksp Biol Med. 1989 Nov;108(11):556-8.

PMID:2534472
Abstract

The regression of hypertrophied heart presupposes disassembling of all cardiomyocyte components including membrane structures. The involvement of free radical oxidation of membrane phospholipids was studied in the cardiac regression. Altitude hypertrophy was developed in barocamera (7000 m, 6 hours daily). 3 weeks of periodical hypoxia leads to 1.5-fold increase of heart weight (right ventricle weight was 2-fold increased). In 7-10 days after adaptation the heart weight reduced to normal. Both, the development and regression of myocardial hypertrophy was accompanied by changes in Mb and Hb organ concentration proportional to weight changes. In lipid extraction of maximal hypertrophied heart, the 30% decrease of lipid peroxidation product (diene conjugates) regularly occurred. The rate of regression had negative correlation with peroxidation products accumulation. Intraperitoneal injection of free radical scavenger BHT attenuate the regression rate. The results suggest that unlike the common knowledge about the membrane injury effect, lipid peroxidation can play positive role in disassembling of superfluous cell membrane structures.

摘要

肥大心脏的消退以包括膜结构在内的所有心肌细胞成分的分解为前提。在心脏消退过程中研究了膜磷脂的自由基氧化作用。在气压舱中诱导海拔性肥大(7000米,每天6小时)。3周的周期性缺氧导致心脏重量增加1.5倍(右心室重量增加2倍)。适应后7-10天,心脏重量恢复正常。心肌肥大的发展和消退均伴随着肌红蛋白(Mb)和血红蛋白(Hb)器官浓度的变化,且与重量变化成比例。在最大程度肥大心脏的脂质提取中,脂质过氧化产物(二烯共轭物)经常出现30%的下降。消退速率与过氧化产物的积累呈负相关。腹腔注射自由基清除剂丁基羟基甲苯(BHT)会减缓消退速率。结果表明,与关于膜损伤作用的常识不同,脂质过氧化在多余细胞膜结构的分解中可能发挥积极作用。

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