实验性肌强直的能量代谢和疲劳。

B U Ramírez
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引用次数: 0

摘要

用2,4-二氯苯氧乙酸(2,4- d)诱导大鼠实验性肌强直。治疗4 ~ 24小时后,胫骨前肌在低频(30 Hz)神经刺激下疲劳增加,但在高频(100 Hz)刺激下张力恢复正常。糖原含量、糖原磷酸化酶、乳酸脱氢酶和苹果酸脱氢酶活性均正常。在肌强直的实验模型中,疲劳和能量代谢之间缺乏相关性,表明兴奋-收缩耦合功能障碍。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Energetic metabolism and fatigability in experimental myotonia.

Experimental myotonia was induced in rats by 2,4-dichloro-phenoxyacetic acid (2,4-D). After 4 to 24 h of treatment, the anterior tibialis muscles exhibited increased fatigue at low frequency (30 Hz) nerve stimulation, but they developed normal tension at high-frequency (100 Hz) stimulation. Glycogen content and the activities of glycogen phosphorylase, lactate dehydrogenase and malate dehydrogenase remained normal. The absence of correlation between fatigability and energetic metabolism in this experimental model of myotonia suggests a dysfunction in excitation-contraction coupling.

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