Takaki M, Nakahara H, Kawatani Y, Utsumi K, Suga H
Department of Physiology II, Okayama University Medical School, Japan.
Jpn J Physiol. 1997 Feb;47(1):87-92. doi: 10.2170/jjphysiol.47.87.
Pentobarbital sodium is a widely used anesthetic for animal experiments. We have already reported that a high dose of pentobarbital sodium (100 mg/kg i.p., twice the usual anesthetic dose) depresses myocardial mechanoenergetics in the canine heart. Furthermore, it has been reported that a high concentration of pentobarbital sodium inhibits myocardial contractility and mitochondrial electron transport and energy transfer. Therefore, we were afraid that the mitochondrial respiratory function would be impaired by pentobarbital anesthesia and that pentobarbital sodium would be an inappropriate anesthetic for cardiac mechanoenergetic studies. In this study, we investigated the respiratory function of mitochondria isolated from the hearts of anesthetized rats with high-dose pentobarbital sodium. We examined the mitochondrial respiratory function by the ADP/O ratio, respiratory control index (RCI), oxygen consumption rate in state III (State III O2) by oximetry, and membrane potential using a fluorescent dye, 3,3'-dipropylthiodicarbocyanine iodide (diS-C3-(5). The ADP/O ratio, RCI, and State III O2 values and changes in membrane potential induced by various respiratory substances were not significantly different between the rats with and without anesthesia. These results indicate that the respiratory function is not suppressed in the isolated myocardial mitochondria of rat hearts after high-dose pentobarbital anesthesia, although the pentobarbital sodium blood concentration was of the same order as that which exerts mitochondrial uncoupling in rat isolated mitochondrial preparation. Therefore, pentobarbital sodium anesthesia up to 100 mg/kg i.p. is applicable for mechanoenergetic studies of excised rat hearts, at least from the energetic aspect.
戊巴比妥钠是动物实验中广泛使用的麻醉剂。我们已经报道，高剂量的戊巴比妥钠（腹腔注射100mg/kg，为常用麻醉剂量的两倍）会抑制犬心脏的心肌机械能量学。此外，有报道称高浓度的戊巴比妥钠会抑制心肌收缩力以及线粒体电子传递和能量转移。因此，我们担心戊巴比妥麻醉会损害线粒体呼吸功能，并且戊巴比妥钠对于心脏机械能量学研究而言是一种不合适的麻醉剂。在本研究中，我们调查了用高剂量戊巴比妥钠麻醉的大鼠心脏分离出的线粒体的呼吸功能。我们通过ADP/O比值、呼吸控制指数（RCI）、用血氧测定法测量的状态III下的氧消耗率（状态III O2）以及使用荧光染料3,3'-二丙基硫代二碳菁碘化物（diS-C3-(5)）测量膜电位来检测线粒体呼吸功能。麻醉和未麻醉大鼠之间，ADP/O比值、RCI和状态III O2值以及各种呼吸物质诱导的膜电位变化没有显著差异。这些结果表明，尽管戊巴比妥钠血药浓度与在大鼠离体线粒体制备中产生线粒体解偶联的浓度处于同一水平，但高剂量戊巴比妥麻醉后大鼠心脏分离出的心肌线粒体的呼吸功能并未受到抑制。因此，腹腔注射高达100mg/kg的戊巴比妥钠麻醉至少从能量方面适用于离体大鼠心脏的机械能量学研究。
