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不同脊椎动物物种心肌在高碳酸血症性酸中毒状态下的细胞内pH值、收缩性和钙平衡

pHi, contractility and Ca-balance under hypercapnic acidosis in the myocardium of different vertebrate species.

作者信息

Gesser H, Jørgensen E

出版信息

J Exp Biol. 1982 Feb;96:405-12. doi: 10.1242/jeb.96.1.405.

Abstract

The influence of hypercapnic acidosis upon the heart was examined in four vertebrate species. The CO2 in the tissue bath was increased from 2.7 to 15% at 12 degrees C for flounder (Platichthys flesus) and cod (Gadus morhua) and from 3 to 13% at 22 degrees C for turtle (Pseudemys scripta) and rainbow trout (Salmo gairdneri). During hypercapnia, as previously described, there was a decline and recovery of contractility in heart strips of flounder and turtle, and a sustained decrease in cod and rainbow trout. At high CO2 the increase in contractile force following increases in the extracellular Ca-concentration were smaller for the cod myocardium than for the other myocardia. The intracellular pH (pHi), measured with the DMO method, in heart strips of turtle and trout was significantly lower at high than at low CO2. This acidifying effect expressed as the increase in the intracellular concentration of hydrogen ions was larger in the turtle than in the trout myocardium. Intracellular Ca-activity, measured by efflux of 45Ca from preloaded heart strips, was unaffected by high CO2 in trout, but was raised in the other three species. Thus the ability to counteract the negative inotropic effect of hypercapnia is apparently not due to cellular buffering or extrusion of hydrogen ions. More probably it involves (a) a release of intracellular Ca; (b) a positive inotropic effect of an increase in intracellular Ca-activity.

摘要

在四种脊椎动物中研究了高碳酸血症酸中毒对心脏的影响。在12摄氏度时,将比目鱼(欧洲比目鱼)和鳕鱼(大西洋鳕鱼)组织浴中的二氧化碳从2.7%提高到15%,在22摄氏度时,将乌龟(伪彩龟)和虹鳟鱼(吉氏虹鳟)组织浴中的二氧化碳从3%提高到13%。如前所述,在高碳酸血症期间,比目鱼和乌龟心脏条带的收缩力下降并恢复,而鳕鱼和虹鳟鱼则持续下降。在高二氧化碳浓度下,鳕鱼心肌细胞外钙浓度升高后收缩力的增加幅度小于其他心肌。用二甲基氧苯测定的乌龟和虹鳟鱼心脏条带中的细胞内pH值(pHi)在高二氧化碳浓度下显著低于低二氧化碳浓度。这种以细胞内氢离子浓度增加表示的酸化作用在乌龟心肌中比在虹鳟鱼心肌中更大。通过预加载心脏条带中45Ca的流出量测量的细胞内钙活性在虹鳟鱼中不受高二氧化碳的影响,但在其他三种物种中升高。因此,抵消高碳酸血症负性肌力作用的能力显然不是由于细胞缓冲或氢离子的排出。更有可能涉及(a)细胞内钙的释放;(b)细胞内钙活性增加的正性肌力作用。

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