Glucocorticoid-induced atrophy is not due to impaired excitability of rat muscle.
Glucocorticoid-induced atrophy is not due to impaired excitability of rat muscle.
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糖皮质激素引起的萎缩并不是由于大鼠肌肉的兴奋性受损所致。
DOI：
10.1152/ajpendo.1982.243.6.e512
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发表时间：
1982
期刊：
影响因子：
--
通讯作者：
Gordon,AM
中科院分区：
文献类型：
--
作者：
Ruff,RL;Martyn,D;Gordon,AM
我们探讨了糖皮质激素诱导的肌肉无力和萎缩是由于肌肉膜兴奋性受损的可能性。雄性Sprague-Dawley大鼠接受地塞米松、醋酸可的松（等效抗炎剂量）或生理盐水的肌内注射长达28天。在体外研究了伸趾长肌（EDL）、比目鱼肌（SOL）、肩胛舌骨肌（OMO）、尾股肌（CF）和胸锁乳突肌（仅膜电位）的肌肉质量、抽搐和强直张力、膜电位、电缆参数和兴奋性变化的时间模式。还在体内（戊巴比妥麻醉）研究了EDL纤维的膜性质。萎缩的相对严重程度为OMO大于CF大于EDL大于SOL。抽搐或强直张力的降低从未先于萎缩。抽搐和强直张力（每克肌肉）增加与糖皮质激素治疗。抽搐或强直的时间过程没有显著变化。地塞米松比醋酸可的松产生更严重的萎缩和力量减少。糖皮质激素治疗产生的EDL肌纤维的去极化在体外测量在23摄氏度，但这似乎没有生理意义，因为在体内研究的EDL纤维没有去极化，并有正常的动作电位振幅和阈值。糖皮质激素治疗没有改变膜电阻或电容。我们的结论是，糖皮质激素治疗并没有通过损害肌膜兴奋性或兴奋-收缩偶联产生肌无力，但肌无力是由肌肉萎缩引起的。
We explored the possibility that glucocorticoid-induced muscle weakness and atrophy resulted from impaired muscle membrane excitability. Male Sprague-Dawley rats received intramuscular injections of dexamethasone, cortisone acetate (equivalent anti-inflammatory doses), or saline for up to 28 days. Temporal patterns of change in muscle mass, twitch and tetanic tension, and membrane potential, cable parameters, and excitability were studied in vitro in the extensor digitorum longus (EDL), soleus (SOL), omohyoid (OMO), caudofemoralis (CF), and the sternomastoid muscles (membrane potential only). the membrane properties of EDL fibers were also studied in vivo (pentobarbital anesthesia). The relative severity of atrophy was OMO greater than CF greater than EDL greater than SOL. Reduction in twitch or tetanic tension never preceded atrophy. The twitch and tetanic tension (per g muscle) increased with glucocorticoid treatment. There were no significant changes in the time course of the twitch or tetanus. Dexamethasone produced more severe atrophy and force reduction than did cortisone acetate. Glucocorticoid treatment produced a depolarization of EDL muscle fibers measured in vitro at 23 degrees C, but this did not appear to be physiologically significant because EDL fibers studied in vivo were not depolarized and had normal action potential amplitudes and thresholds. Glucocorticoid treatment did not change the membrane resistance or capacitance. We conclude that glucocorticoid treatment did not produce muscle weakness by impairing sarcolemmal excitability or excitation-contraction coupling, but that the weakness resulted from muscle atrophy.
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DOI：
--
发表时间：
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期刊：
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影响因子：
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DOI：
--
发表时间：
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