摘要
本实验在离体灌流败血症休克大鼠心脏模型上,观察到晚期败血症休克时,心肌和心肌线粒体钙含量分别增加190和332(P0.01),~LCa摄入量增加208和178。(P0.01),心肌钙释放量无明显变化 用10mol/L降钙素基因相关肽(CGRP)或10mol/L心房钠尿肽(ANP)灌流离体心脏明显减轻休克时心肌和心肌线粒体的钙超负荷,体外实验观察线粒体摄钙储备的能力,休克时心肌线粒体最大摄钙量减少31.6,摄钙速率降低33％,(P0.01)结论认为,晚期败血症休克,心肌净钙流入量显著增加和线粒体钙转运能力降低导致其对胞浆钙缓冲能力减弱是心肌细胞钙超负荷发生的重要环节CGRP,ANP可显著减轻休克时心肌和线粒体钙超负荷,在休克过程中可能对细胞有保护意义。
On the isolated perfused heart model of septic rats, the present study showedthat: (1) Calcium content and ^(45)Ca--influx of myocardium increased 190%, 208%(P<0.01) and that of mitochondria elevated 332%, 178%; (P<0.01) respectivelywith no change of myocardial ^(45)Ca--release during sepsis. (2) 10^(-8) mol/L calcitoningene--related peptide (CGRP) or 10^(-7) mol/L atriopeptin (ANP) added into the Krebs-Henseleit solution could effectively reduce ^(45)Ca--influx to myocardium and mitocuondri-a with no effect on myocardial ^(45)Ca--release. (3) The calcium uptake reserve of mito-chondria evaluated in ritro showed that the maximal calcium uptake and uptake veloci-ty of mitochondria during sepsis were reduced 34.6%, 33.3% (P<0.01) respective-ly. The data suggested that the net increase of myocardial Ca^(2+) content resulted fromincrease of ^(45)Ca-influx with no change of ^(45)Ca--efflux and the reduction of mitochon-drial Ca^(2+) buffering capacity during sepeis were key events in the pathogenesis of intra-cellular Ca^(2+)-overload. CGRP and ANP could effectively all ievate Ca^(2+)-overload ofmyocardium and mitochondria. This may have some cellular protection action duringsepsis.
出处
《生理学报》
CAS
CSCD
北大核心
1993年第2期158-163,共6页
Acta Physiologica Sinica
关键词
败血症
休克
心肌
线粒体
钙
septic shock
myocardium
mitochondria
calcium
rat
regulatory peptide
