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疲劳刺激前后小鼠肌肉的钾和咖啡因挛缩

Potassium and caffeine contractures of mouse muscles before and after fatiguing stimulation.

作者信息

Pagala M, Ravindran K, Amaladevi B, Namba T, Grob D

机构信息

Department of Medicine, Maimonides Medical Center, Brooklyn, NY 11219.

出版信息

Muscle Nerve. 1994 Aug;17(8):852-9. doi: 10.1002/mus.880170804.

DOI:10.1002/mus.880170804
PMID:8041392
Abstract

To assess the impairment of muscle membrane excitation, excitation-contraction (E-C) coupling, and contractility during muscle fatigue, we monitored the contracture responses of resting and fatigued muscles on exposure to high potassium and caffeine. On exposure to 140 mmol/L potassium, mouse extensor digitorum longus (EDL) developed a contracture which was 15.7% of tetanic tension before fatigue and 31.7% after fatigue, while soleus developed 59.4% contracture before and 68.8% after fatigue. Potassium causes contractures by depolarizing the muscle fiber membrane. Hence, membrane excitation is reduced in fatigued EDL and soleus. On exposure to 32 mmol/L caffeine, the contracture was 7.1% in resting EDL, 8.5% in fatigued EDL, 50.1% in resting soleus, and 43.7% in fatigued soleus. On exposure to 1 mmol/L caffeine followed by rapid cooling, the contracture was 3.0% in resting EDL, 3.2% in fatigued EDL, 21.5% in resting soleus, and 10.3% in fatigued soleus. Caffeine causes contracture by releasing Ca++ from the sarcoplasmic reticulum. Our results indicate reduced E-C coupling attributable to reduced membrane excitation in fatigued EDL, and reduced contractility in fatigued soleus.

摘要

为了评估肌肉疲劳期间肌膜兴奋、兴奋-收缩(E-C)偶联和收缩性的损伤情况,我们监测了静息和疲劳肌肉在暴露于高钾和咖啡因时的挛缩反应。暴露于140 mmol/L钾时,小鼠趾长伸肌(EDL)出现挛缩,其在疲劳前为强直张力的15.7%,疲劳后为31.7%,而比目鱼肌在疲劳前出现59.4%的挛缩,疲劳后为68.8%。钾通过使肌纤维膜去极化而导致挛缩。因此,疲劳的EDL和比目鱼肌中的膜兴奋降低。暴露于32 mmol/L咖啡因时,静息EDL的挛缩率为7.1%,疲劳EDL为8.5%,静息比目鱼肌为50.1%,疲劳比目鱼肌为43.7%。暴露于1 mmol/L咖啡因后快速冷却时,静息EDL的挛缩率为3.0%,疲劳EDL为3.2%,静息比目鱼肌为21.5%,疲劳比目鱼肌为10.3%。咖啡因通过从肌浆网释放Ca++而导致挛缩。我们的结果表明,疲劳的EDL中由于膜兴奋降低导致E-C偶联减少,而疲劳的比目鱼肌中收缩性降低。

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