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犬浦肯野纤维中的锰与电生现象。

Manganese amd electrogenic phenomena in canine Purkinje fibers.

作者信息

Hogan P M, Spitzer K W

出版信息

Circ Res. 1975 Mar;36(3):377-91. doi: 10.1161/01.res.36.3.377.

Abstract

Studies were performed on canine cardiac Purkinje fibers to evaluate the effects of manganese on membrane electrogenesis. The results indicate that manganese has a calciumlike effect on the excitatory sodium current and inhibitory effects on potassium conductance and slow inward current. The calciumlike effect of manganese on sodium current was reflected through a leftward (toward less negative potentials) and downward shift in the curve relating maximum upstroke velocity to membrane potential. The inhibitory action of manganese on potassium conductance was suggested by the following observations. (1) Manganese caused an initial increase in action potential duration largely due to a lengthening of the plateau and decreases in the rates of phase 3 and terminal repolarization. (2) Manganese increased the rate of diastolic depolarization. (3) Manganes blocked the initial fall in maximum diastolic potential accompanying rapid stimulation. (4) Manganese in high concentrations caused generalized depolarization which was reversed by rapid stimulation and by increased extracellular potassium concentrations. The action of manganese to block slow inward current was indicated by the eventual shortening of the plateau and by the elimination of responses initiated from low levels of membrane potential (less than minus 55 mv). In addition to these effects, manganese also reduced membrane excitability, eliminated arrhythmic beats occurring during low-frequency electrical stimulation, and caused membrane hyperpolarization which was blocked by tetrodotoxin.

摘要

对犬心脏浦肯野纤维进行了研究,以评估锰对膜电活动的影响。结果表明,锰对兴奋性钠电流有类似钙的作用,对钾电导和缓慢内向电流有抑制作用。锰对钠电流的类似钙的作用通过最大上升速度与膜电位关系曲线向左(向较不负极化方向)和向下移动得以体现。锰对钾电导的抑制作用由以下观察结果表明。(1)锰导致动作电位持续时间最初增加,这主要是由于平台期延长以及第3相和终末复极化速率降低。(2)锰增加了舒张期去极化速率。(3)锰阻止了快速刺激时伴随的最大舒张电位的初始下降。(4)高浓度的锰导致广泛的去极化,快速刺激和增加细胞外钾浓度可使其逆转。锰阻断缓慢内向电流的作用表现为平台期最终缩短以及消除了由低水平膜电位(小于 -55 mV)引发的反应。除了这些作用外,锰还降低了膜兴奋性,消除了低频电刺激期间出现的心律失常搏动,并导致膜超极化,这种超极化被河豚毒素阻断。

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