生理学报
生理學報
생이학보
ACTA PHYSIOLOGICA SINICA
1999年
2期
153-160
,共8页
骨骼肌%钙释放通道%咖啡因%高钾%挛缩
骨骼肌%鈣釋放通道%咖啡因%高鉀%攣縮
골격기%개석방통도%가배인%고갑%련축
skeletal muscle%ryanodine receptor%caffeine%high potassium%contracture
用蛙胫前肌小束为材料, 研究了提高胞外钾[K+]O对咖啡因挛缩的作用.[K+]O从2 mmol/L提高到10或25 mmol/L, 由3 mmol/L咖啡因引起的挛缩明显增强.以PKC/PC (PKC和PC分别为在高钾和正常钾条件下的咖啡因挛缩)表示的咖啡因挛缩增强, 依赖[K+]O和高钾作用时间.随着10 mmol/L [K+]O作用时间延长, 直至10 min, 增强逐渐增加.但是, 25 mmol/L [K+]O作用1 min时增强达到最大, 然后下降到对照.PKC/PC变化时程不能用高钾引起的去极化解释, 而与由相似[K+]O引起的胞浆自由钙变化时程相符.提示, 至少在蛙骨骼肌, 高钾引起的咖啡因挛缩增强主要是由胞浆自由钙升高引起的.
用蛙脛前肌小束為材料, 研究瞭提高胞外鉀[K+]O對咖啡因攣縮的作用.[K+]O從2 mmol/L提高到10或25 mmol/L, 由3 mmol/L咖啡因引起的攣縮明顯增彊.以PKC/PC (PKC和PC分彆為在高鉀和正常鉀條件下的咖啡因攣縮)錶示的咖啡因攣縮增彊, 依賴[K+]O和高鉀作用時間.隨著10 mmol/L [K+]O作用時間延長, 直至10 min, 增彊逐漸增加.但是, 25 mmol/L [K+]O作用1 min時增彊達到最大, 然後下降到對照.PKC/PC變化時程不能用高鉀引起的去極化解釋, 而與由相似[K+]O引起的胞漿自由鈣變化時程相符.提示, 至少在蛙骨骼肌, 高鉀引起的咖啡因攣縮增彊主要是由胞漿自由鈣升高引起的.
용와경전기소속위재료, 연구료제고포외갑[K+]O대가배인련축적작용.[K+]O종2 mmol/L제고도10혹25 mmol/L, 유3 mmol/L가배인인기적련축명현증강.이PKC/PC (PKC화PC분별위재고갑화정상갑조건하적가배인련축)표시적가배인련축증강, 의뢰[K+]O화고갑작용시간.수착10 mmol/L [K+]O작용시간연장, 직지10 min, 증강축점증가.단시, 25 mmol/L [K+]O작용1 min시증강체도최대, 연후하강도대조.PKC/PC변화시정불능용고갑인기적거겁화해석, 이여유상사[K+]O인기적포장자유개변화시정상부.제시, 지소재와골격기, 고갑인기적가배인련축증강주요시유포장자유개승고인기적.
The effect of raising extracellular potassium ([K+]O) on caffeine contracture was inves～tigated, using small bundles dissected from frog anterior tibialis muscle. Elevating [K+]O from the control of 2 mmol/L to 10 or 25 mmol/L significantly potentiated the contracture induced by 3 mmol/L caffeine. The potentiation represented by PKC/PC, where PKC and PC are the peak tension of the caffeine contracture evoked in high and normal [K+]O respectively, was dependent on [K+]O and the duration of conditioning high K+ exposure. With 10 mmol/L [K+]O, the potentiation was gradually increased by prolonging conditioning exposure up to 10 min. On the contrary, with 25 mmol/L [K+]O the potentiation reached a maximum within only 1 min, and then subsided to the control. These different time courses of PKC/PC could not be accounted for by high K+ induced depolarization, but were in general consistence with the time courses of the change in myoplasmic free calcium induced by corresponding high [K+]O[10]. It is suggested that, at least in frog skeletal muscle, the high [K+]O induced potentiation of caffeine contracture is mainly due to an increase of myoplasmic free calcium.
