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[在钙离子通道被锰离子阻断的情况下,高频刺激后青蛙心室心肌纤维的挛缩]

[Contracture of the myocardial fibers of the frog ventricle after high frequency stimulation while the calcium channels were blocked by manganese ions].

作者信息

Zakharov S I, Undrovinas A I, Rozenshtraukh L V

出版信息

Biull Eksp Biol Med. 1978 Apr;85(4):407-10.

PMID:306840
Abstract

The contractile force of the myocardial strip of the frog ventricle stimulated by impulses of 0.5 Hz was diminished to 3--5% of the initial value when perfused with Ringer's solution containing 2.5 mM manganese. Under this condition the action potential duration was significantly decreased. An increase in frequency of stimulation up to 5 Hz leads to the development of contracture. The amplitude of contracture was about 30% of the initial contractile force in normal perfusion solution. The amplitude of contracture was more than doubled under the effect of ouabain (2 X X 10(-6) g/ml). Similar experiments with lanthanum failed to discover contracture produced by the increase of the stimulation frequency. In these experiments ouabain was also ineffective. It is supposed that contracture observed in the presence of manganese was caused by nonelectrogenic calcium transport into the muscle fibers.

摘要

当用含2.5 mM锰的林格氏液灌注时,由0.5 Hz冲动刺激的青蛙心室心肌条的收缩力降至初始值的3 - 5%。在此条件下,动作电位持续时间显著缩短。刺激频率增加到5 Hz会导致挛缩的发生。在正常灌注液中,挛缩幅度约为初始收缩力的30%。在哇巴因(2×10⁻⁶ g/ml)作用下,挛缩幅度增加了一倍多。用镧进行的类似实验未发现因刺激频率增加而产生的挛缩。在这些实验中,哇巴因也无效。据推测,在锰存在的情况下观察到的挛缩是由非电致钙转运到肌纤维中引起的。

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