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氢离子诱导犬心脏浦肯野纤维的膜去极化。

H+-induced membrane depolarization in canine cardiac Purkinje fibers.

作者信息

Lauer M R, Rusy B F, Davis L D

出版信息

Am J Physiol. 1984 Aug;247(2 Pt 2):H312-21. doi: 10.1152/ajpheart.1984.247.2.H312.

Abstract

The H+-induced membrane depolarization in canine cardiac Purkinje cells in false tendons was studied. In some electrically paced Purkinje cells ("sensitive" cells), exposure to a pH 6.0 superfusate produced a large membrane depolarization [44.5 +/- 6.7 (SD) mV], whereas other Purkinje cells ("resistant" cells) developed only a small depolarization (9.8 +/- 5.6 mV) even after 60 min of exposure to the low-pH superfusate. Cs+, Ba2+, tetraethylammonium, 9-aminoacridine, verapamil, or exposure to Ca2+- or K+-deficient or hypertonic solutions were capable of converting resistant cells to sensitive cells. Increasing extracellular K+ concentration [( K+]) or rapid electrical pacing failed to convert resistant cells to sensitive cells. Membrane depolarizations of approximately equal magnitude produced in Purkinje cells by either increasing [K+] to 18.2 mM, decreasing [K+] to 0.5 mM, reducing extracellular pH to 4.1, or ouabain administration were associated with membrane resistances of approximately 45, 377, 386, or 45%, respectively, of the membrane resistances in the control solution. The results suggest that the H+-induced membrane depolarization in sensitive Purkinje cells is caused by a mechanism similar to that responsible for a low [K+]-induced depolarization.

摘要

研究了犬类心脏假腱索中浦肯野细胞的H⁺诱导的膜去极化。在一些电刺激的浦肯野细胞(“敏感”细胞)中,暴露于pH 6.0的灌流液会产生较大的膜去极化[44.5±6.7(标准差)mV],而其他浦肯野细胞(“抗性”细胞)即使在暴露于低pH灌流液60分钟后也仅产生较小的去极化(9.8±5.6 mV)。Cs⁺、Ba²⁺、四乙铵、9-氨基吖啶、维拉帕米,或暴露于缺钙或钾的溶液或高渗溶液能够将抗性细胞转化为敏感细胞。增加细胞外钾离子浓度[(K⁺)]或快速电刺激未能将抗性细胞转化为敏感细胞。通过将[K⁺]增加到18.2 mM、将[K⁺]降低到0.5 mM、将细胞外pH降低到4.1或给予哇巴因在浦肯野细胞中产生的大致相等幅度的膜去极化分别与对照溶液中膜电阻的约45%、377%、386%或45%相关。结果表明,敏感浦肯野细胞中H⁺诱导的膜去极化是由一种类似于低[K⁺]诱导的去极化的机制引起的。

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