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脓毒症大鼠心脏中微血管负电荷丧失并伴有间质水肿。

Loss of microvascular negative charges accompanied by interstitial edema in septic rats' heart.

作者信息

Gotloib L, Shostak A, Galdi P, Jaichenko J, Fudin R

机构信息

Department of Nephrology, Central Emek Hospital, Afula, Israel.

出版信息

Circ Shock. 1992 Jan;36(1):45-56.

PMID:1372536
Abstract

We studied the effect of Gram-negative sepsis on negative charges of heart capillaries and myocardial cells. We used a rat model of multiorgan failure, with ruthenium red (RR) and polyethyleneimine (PEI) as cationic binding tracers. Twenty-four hours after induction of sepsis, negative charges had decreased in glycocalyx and basement membrane of myocardial capillary endothelial cells. There were substantial amounts of interstitial edema. Density of anionic charges in the sarcolemmal glycocalyx complex of cardiac cells was markedly reduced. Myocardial cells' mitochondria consistently showed morphologic changes, whose severity ranged between stages II and IV C of Trump. Thirteen days after induction of sepsis, capillary endothelial and myocardial cells had recovered almost completely and showed no intracellular edema. Gram-negative sepsis caused a significant reduction in negative charges normally present in the microvascular wall as well as on myocardial cells. Consequently, several membranes limiting the various compartments of heart tissue lost their structural integrity. This morphometric data could explain the development of protein-rich interstitial edema and defective cell volume regulation observed in cardiac muscle of endotoxin-shocked animals. This myocardial edema may be at the origin of the cardiac dysfunction observed in both experimental and human septic shock.

摘要

我们研究了革兰氏阴性菌败血症对心脏毛细血管和心肌细胞负电荷的影响。我们使用多器官衰竭大鼠模型,以钌红(RR)和聚乙烯亚胺(PEI)作为阳离子结合示踪剂。败血症诱导后24小时,心肌毛细血管内皮细胞糖萼和基底膜中的负电荷减少。出现大量间质水肿。心肌细胞肌膜糖萼复合物中阴离子电荷密度明显降低。心肌细胞的线粒体持续出现形态学变化,其严重程度介于特朗普分类的II期和IV C期之间。败血症诱导后13天,毛细血管内皮细胞和心肌细胞几乎完全恢复,未出现细胞内水肿。革兰氏阴性菌败血症导致微血管壁以及心肌细胞中正常存在的负电荷显著减少。因此,限制心脏组织各个腔室的几层膜失去了结构完整性。这些形态计量学数据可以解释在内毒素休克动物的心肌中观察到的富含蛋白质的间质水肿的发展以及细胞体积调节缺陷。这种心肌水肿可能是实验性和人类脓毒性休克中观察到的心脏功能障碍的根源。

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