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骨骼肌中的钙悖论:生理学和微观观察

Calcium paradox in skeletal muscles: physiologic and microscopic observations.

作者信息

Soza M, Karpati G, Carpenter S

出版信息

Muscle Nerve. 1986 Mar-Apr;9(3):222-32. doi: 10.1002/mus.880090306.

DOI:10.1002/mus.880090306
PMID:3084970
Abstract

Immersion of rat hemidiaphragms in Ca2+-free Krebs solution (KS) containing Ca2+ chelator in vitro leads to separation of basal lamina from the plasma membrane, as well as transient contracture and rapid loss of twitch response [calcium paradox (CP) phase 1]. Subsequent immersion in regular KS results in necrosis of muscle fibers accompanied by slowly increasing contracture (CP phase 2). This contracture could be prevented or reduced by using either Ca2+-free KS or calcium channel blockers, but not by dantrolene sodium, implying that after drastic reduction of extracellular and sarcolemmal Ca2+ during CP phase 1, the sarcolemma has lost its ability to control normal Ca2+ fluxes. Contracture did not develop at 21 degrees C. CP is a convenient model to study calcium-induced muscle cell death and the role of Ca2+ in maintaining sarcolemmal integrity.

摘要

将大鼠半膈肌在体外浸入含有钙离子螯合剂的无钙Krebs溶液(KS)中,会导致基膜与质膜分离,以及短暂挛缩和抽搐反应迅速丧失[钙反常(CP)第1阶段]。随后浸入常规KS中会导致肌纤维坏死,并伴有挛缩缓慢增加(CP第2阶段)。使用无钙KS或钙通道阻滞剂可预防或减轻这种挛缩,但丹曲林钠则无效,这意味着在CP第1阶段细胞外和肌膜钙离子急剧减少后,肌膜已失去控制正常钙离子通量的能力。在21摄氏度时未发生挛缩。CP是研究钙诱导的肌肉细胞死亡以及钙离子在维持肌膜完整性中的作用的便捷模型。

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