Storella R J, Keykhah M M, Rosenberg H
Department of Anesthesiology, Hahnemann University, Philadelphia, Pennsylvania 19102.
Anesthesiology. 1993 Dec;79(6):1261-5. doi: 10.1097/00000542-199312000-00017.
The agonist actions of succinylcholine (SCh) have recently come under study because of their involvement in the clinical problem of masseter muscle rigidity, and their possible involvement in malignant hyperthermia. The authors investigated factors affecting SCh-induced contractures in an animal preparation.
Rats were anesthetized with either halothane (1-2%) or pentobarbital. Resting and twitch isometric tension were measured from the jaw muscles. Succinylcholine (500 or 750 micrograms/kg) was administered intravenously, producing increases in resting tension (i.e., contractures). Jaw muscle temperature was controlled by radiant heat.
Succinylcholine increased jaw muscle tension for several seconds. These contractures exhibited tachyphylaxis, and were antagonized by vecuronium (0.8-1.5 mg/kg), indicating mediation by acetylcholine receptors (AChR). In the presence of 2% halothane, contractures were tenfold greater at a rectal temperature of 41 degrees C than at 37 degrees C. In contrast, under 50 mg/kg intraperitoneal pentobarbital anesthesia, contractures were not affected by rectal temperature. Neither the half-decay time of contracture nor twitch tension (0.2 Hz, preceding SCh) were increased in the presence of halothane at 41 degrees C. In a set of experiments in which rectal temperature was maintained at 37 degrees C but jaw temperature was varied between 36-41 degrees C, there was a significant regression of SCh-induced jaw contracture on temperature in the presence of halothane. In contrast, there was no significant relationship between jaw temperature and contracture in the presence of pentobarbital.
These results in the rat demonstrate a temperature-dependent interaction between halothane and SCh that has not previously been described.
由于琥珀酰胆碱(SCh)的激动剂作用与咬肌痉挛的临床问题有关,且可能与恶性高热有关,最近对其进行了研究。作者在动物实验中研究了影响SCh诱导挛缩的因素。
用氟烷(1-2%)或戊巴比妥麻醉大鼠。测量下颌肌肉的静息和抽搐等长张力。静脉注射琥珀酰胆碱(500或750微克/千克),导致静息张力增加(即挛缩)。通过辐射热控制下颌肌肉温度。
琥珀酰胆碱使下颌肌肉张力增加数秒。这些挛缩表现出快速耐受,并被维库溴铵(0.8-1.5毫克/千克)拮抗,表明由乙酰胆碱受体(AChR)介导。在2%氟烷存在下,直肠温度为41摄氏度时的挛缩比37摄氏度时大10倍。相比之下,在50毫克/千克腹腔注射戊巴比妥麻醉下,挛缩不受直肠温度影响。在41摄氏度的氟烷存在下,挛缩的半衰期和抽搐张力(0.2赫兹,SCh之前)均未增加。在一组实验中,直肠温度保持在37摄氏度,但下颌温度在36-41摄氏度之间变化,在氟烷存在下,SCh诱导的下颌挛缩与温度呈显著回归关系。相比之下,在戊巴比妥存在下,下颌温度与挛缩之间无显著关系。
大鼠实验结果表明氟烷和SCh之间存在温度依赖性相互作用,这是以前未描述过的。