Matsubara S, Omori T
Jpn J Physiol. 1985;35(2):335-41. doi: 10.2170/jjphysiol.35.335.
Rapid cooling contracture (RCC) was observed in frog toe muscles pretreated with caffeine, chlorpromazine (CPZ), or haloperidol (HPD). During rapid cooling contracture in the presence of caffeine (caffeine-RCC) tension developed to more than 0.8 of the maximum tetanic tension (P0). CPZ inhibited twitch but induced rapid cooling contracture (CPZ-RCC) between 50 and 150 microM; the tension saturated at the level of 0.75 P0 at 100 microM. HPD also inhibited twitch and induced rapid cooling contracture (HPD-RCC) at concentrations greater than 25 microM; the maximum tension was 0.25 P0. In the presence of dantrolene (10 microM), the tension during CPZ-RCC was reduced by 40%. Procaine (0.25%) reduced the CPZ-RCC tension by as much as 60%. These results suggest that CPZ and HPD induced rapid cooling contracture by reducing Ca2+-accumulation in sarcoplasmic reticulum.
在预先用咖啡因、氯丙嗪(CPZ)或氟哌啶醇(HPD)处理过的青蛙趾肌中观察到快速冷却挛缩(RCC)。在咖啡因存在下的快速冷却挛缩(咖啡因-RCC)过程中,张力发展到最大强直张力(P0)的0.8以上。CPZ在50至150微摩尔之间抑制抽搐但诱导快速冷却挛缩(CPZ-RCC);在100微摩尔时,张力在0.75 P0水平达到饱和。HPD在浓度大于25微摩尔时也抑制抽搐并诱导快速冷却挛缩(HPD-RCC);最大张力为0.25 P0。在丹曲林(10微摩尔)存在下,CPZ-RCC期间的张力降低了40%。普鲁卡因(0.25%)使CPZ-RCC张力降低多达60%。这些结果表明,CPZ和HPD通过减少肌浆网中Ca2+的积累诱导快速冷却挛缩。