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通过急性降低灌注介质的pH值导致心脏收缩力丧失和严重形态学改变:脂肪酸的保护作用

Loss of cardiac contractility and severe morphologic changes by acutely lowering the pH of the perfusion medium: protection by fatty acids.

作者信息

Hülsmann W C, de Wit L E, Schneydenberg C, Verkleij A J

机构信息

Thorax Centre, Erasmus University Rotterdam, The Netherlands.

出版信息

Biochim Biophys Acta. 1990 Feb 26;1033(2):214-8. doi: 10.1016/0304-4165(90)90016-p.

Abstract

When the pH of the perfusion medium of rat Langendorff heart, paced at a rate of 300 beats/min, is abruptly lowered from pH 7.5 to 7.0, the hearts stop beating within 6 min in more than half of the cases. Reperfusion with pH 7.5 medium after 10 min pH 7.0 perfusion does not cause contractility to resume within 5 min. The causative factor is intracellular acidosis, resulting in severe morphological alterations of plasma membrane and mitochondria. It is probably initiated by the loss of membrane-bound calcium. Oleate, complexed with albumin included in the perfusion media, protects the hearts. This may be explained by maintenance of capillary flow and limitation of cellular acidosis.

摘要

当以300次/分钟的速率起搏的大鼠Langendorff心脏的灌注介质pH值从7.5突然降至7.0时,超过半数的心脏会在6分钟内停止跳动。在pH值为7.0的介质中灌注10分钟后,再用pH值为7.5的介质进行再灌注,并不会使心脏收缩力在5分钟内恢复。致病因素是细胞内酸中毒,导致质膜和线粒体发生严重的形态学改变。这可能是由膜结合钙的丢失引发的。灌注介质中与白蛋白结合的油酸可保护心脏。这可能是通过维持毛细血管血流和限制细胞酸中毒来解释的。

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