Delle M, Ricksten S E, Thorén P
Department of Physiology, Sahlgrens Hospital, University of Gothenburg, Sweden.
Anesthesiology. 1989 Feb;70(2):309-17. doi: 10.1097/00000542-198902000-00022.
The study was undertaken to examine if endogenous opioid systems mediate the response of the sympathetic nervous system to halothane anesthesia. Steady state values of renal sympathetic nerve activity (rSNA), mean arterial pressure (MAP), and heart rate (HR) were continuously recorded in the conscious state and at three depths of halothane anesthesia (0.6%, 1.2%, and 2.4%) in rats. Halothane caused an inhibition of rSNA and hypotension and a decrease in HR at the three halothane concentrations. Repeated bolus doses of the opiate antagonist (-)naloxone given iv during 1.2% halothane anesthesia did not significantly increase any of the variables. However, pretreatment with (-)naloxone (2 or 15 mg.kg-1) induced an increase in rSNA at 0.6% halothane, and subsequently the rSNA inhibition was less pronounced at the two higher halothane concentrations compared with control. HR showed a similar pattern, whereas the hypotension was essentially unaffected. Pretreatment with the pharmacologically inactive compound (+)naloxone had no effect on the halothane-induced depression of rSNA. The ED50 halothane concentration concerning nociceptive aversive behavior was not significantly changed with (-)naloxone pretreatment (2 mg.kg-1). In order to determine if sympathoinhibitory bulbospinal serotonin pathways are activated during halothane anesthesia, rSNA, MAP, and HR were recorded in rats pretreated with the serotonin synthesis inhibitor parachlorophenylalanine (PCPA). However, PCPA pretreatment did not affect the rSNA response to halothane compared with control. These findings indicate that the halothane-induced inhibition of rSNA might partially result from a stereospecific activation of opioid receptors, whereas halothane analgesia does not seem to be mediated by opioid mechanisms.
本研究旨在探讨内源性阿片系统是否介导交感神经系统对氟烷麻醉的反应。在清醒状态以及大鼠氟烷麻醉的三个深度（0.6%、1.2%和2.4%）下，持续记录肾交感神经活动（rSNA）、平均动脉压（MAP）和心率（HR）的稳态值。在这三个氟烷浓度下，氟烷均导致rSNA抑制、低血压以及HR降低。在1.2%氟烷麻醉期间静脉注射重复推注剂量的阿片拮抗剂（-）纳洛酮，并未显著增加任何变量。然而，用（-）纳洛酮（2或15mg·kg-1）预处理可在0.6%氟烷时使rSNA增加，随后在两个较高氟烷浓度下，与对照组相比，rSNA抑制作用不那么明显。HR呈现类似模式，而低血压基本未受影响。用药理惰性化合物（+）纳洛酮预处理对氟烷诱导的rSNA抑制无影响。（-）纳洛酮预处理（2mg·kg-1）后，与伤害性厌恶行为相关的氟烷ED50浓度无显著变化。为了确定在氟烷麻醉期间交感抑制性延髓脊髓5-羟色胺通路是否被激活，在给予5-羟色胺合成抑制剂对氯苯丙氨酸（PCPA）预处理的大鼠中记录rSNA、MAP和HR。然而，与对照组相比，PCPA预处理并未影响rSNA对氟烷的反应。这些发现表明，氟烷诱导的rSNA抑制可能部分源于阿片受体的立体特异性激活，而氟烷镇痛似乎并非由阿片机制介导。
