Sudo R T, Zapata G, Suarez-Kurtz G
Can J Physiol Pharmacol. 1987 Apr;65(4):697-703. doi: 10.1139/y87-115.
The characteristics of transient contractures elicited by rapid cooling of frog or mouse muscles perfused in vitro with solutions equilibrated with 0.5-2.0% halothane are reviewed. The data indicate that these halothane-cooling contractures are dose dependent and reproducible, and their amplitude is larger in muscles containing predominantly slow-twitch type fibers, such as the mouse soleus, than in muscles in which fast-twitch fibers predominate, such as the mouse extensor digitorum longus. The halothane-cooling contractures are potentiated in muscles exposed to succinylcholine. The effects of Ca2+-free solutions, of the local anesthetics procaine, procainamide, and lidocaine, and of the muscle relaxant dantrolene on the halothane-cooling contractures are consistent with the proposal that the halothane-cooling contractures result from synergistic effects of halothane and low temperature on Ca sequestration by the sarcoplasmic reticulum. Preliminary results from skinned rabbit muscle fibers support this proposal. The halothane concentrations required for the halothane-cooling contractures of isolated frog or mouse muscles are comparable with those observed in serum of patients during general anesthesia. Accordingly, fascicles dissected from muscle biopsies of patients under halothane anesthesia for programmed surgery develop large contractures when rapidly cooled. The amplitude of these halothane-cooling contractures declined with the time of perfusion of the muscle fascicles in vitro with halothane-free physiological solutions. It is suggested that the halothane-cooling contractures could be used as a simple experimental model for the investigation of the effects of halothane on Ca homeostasis and contractility in skeletal muscle and for study of drugs of potential use in the management of the contractures associated with the halothane-induced malignant hyperthermia syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)
本文综述了用含0.5 - 2.0%氟烷平衡的溶液对青蛙或小鼠肌肉进行体外灌注时,快速冷却所引发的短暂挛缩的特征。数据表明,这些氟烷冷却性挛缩具有剂量依赖性且可重复,在主要含有慢肌纤维类型的肌肉(如小鼠比目鱼肌)中,其幅度大于以快肌纤维为主的肌肉(如小鼠趾长伸肌)。在接触琥珀酰胆碱的肌肉中,氟烷冷却性挛缩会增强。无钙溶液、局部麻醉药普鲁卡因、普鲁卡因酰胺和利多卡因以及肌肉松弛剂丹曲林对氟烷冷却性挛缩的影响与以下观点一致:氟烷冷却性挛缩是氟烷和低温对肌浆网钙摄取的协同作用所致。去皮兔肌纤维的初步结果支持这一观点。分离的青蛙或小鼠肌肉产生氟烷冷却性挛缩所需的氟烷浓度与全身麻醉期间患者血清中观察到的浓度相当。因此,在氟烷麻醉下接受程控手术的患者肌肉活检中取出的肌束,快速冷却时会产生较大的挛缩。这些氟烷冷却性挛缩的幅度会随着肌束在无氟烷生理溶液中体外灌注时间的延长而下降。有人提出,氟烷冷却性挛缩可作为一种简单的实验模型,用于研究氟烷对骨骼肌钙稳态和收缩性的影响,以及研究可能用于治疗与氟烷诱导的恶性高热综合征相关挛缩的药物。(摘要截短于250字)