IODOACETATE-INDUCED SKELETAL-MUSCLE CONTRACTURE - CHANGES IN ADP, CALCIUM, PHOSPHATE, AND PH

被引:8
作者
RUFF, RL
WEISSMAN, J
机构
[1] CASE WESTERN RESERVE UNIV, SCH MED, CLEVELAND, OH 44106 USA
[2] EMORY UNIV, SCH MED, DEPT NEUROL, ATLANTA, GA 30322 USA
来源
AMERICAN JOURNAL OF PHYSIOLOGY-CELL PHYSIOLOGY | 1995年 / 268卷 / 02期
关键词
MUSCLE CRAMP; PATHOPHYSIOLOGY; METABOLISM; AND ENZYMOLOGY OF MUSCLES; MUSCULAR DISEASES; MCARDLES DISEASE; TAURIS DISEASE; PHOSPHORYLASE DEFICIENCY; IMPAIRED GLYCOLYSIS; IMPAIRED GLYCOGENOLYSIS; ADENOSINE 5'-DIPHOSPHATE;
D O I
10.1152/ajpcell.1995.268.2.C317
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
The effects of iodoacetic acid (IAA) and ischemic contraction were studied in rat extensor digitorum longus muscles. Ischemic stimulation of IAA-treated muscles produced contracture. We measured total muscle water content, distribution of water between intracellular and extracellular spaces, creatine concentration ([Cr]), creatine phosphate concentration ([PCr]), [ATP], [P-i], intracellular pH, and intracellular Ca2+ concentration ([Ca2+](i)) at the onset of contracture. [ADP] was calculated from the equilibrium of the creatine kinase reaction using the measured values of [ATP], [PCr], [Cr], and pH. At the onset of contracture there was a 75% reduction of [PCr], a 12-fold increase in [ADP], and an 11-fold increase in [Ca2+](i) compared with unstimulated IAA-treated muscles. [ATP] was not depleted at contracture compared with unstimulated IAA-treated muscles, and [P-i] increased less in muscles at contracture compared with stimulated control muscles. The persistent tension in contractures probably resulted from increased [Ca2+](i) combined with increased myofibrillar Ca2+ sensitivity due to elevated [ADP] and relatively reduced intracellular acidification and [P-i].
引用
收藏
页码:C317 / C322
页数:6
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