Watkins L, Maixner W
Department of Pharmacology, University of North Carolina, Chapel Hill 27599-7455.
J Auton Nerv Syst. 1991 Nov;36(2):107-14. doi: 10.1016/0165-1838(91)90106-d.
This study determined the influence of pentobarbital anesthesia on the autonomic nervous system control of baroreceptor mediated reflex bradycardia in the rat. Reflex bradycardia was elicited by phenylephrine-induced hypertension in conscious and pentobarbital anesthetized (PA) rats before and after sympathetic blockade with the beta-1 receptor antagonist atenolol or parasympathetic blockade with the peripherally acting muscarinic receptor antagonist methyl-atropine. Reflex bradycardia was significantly decreased by pentobarbital anesthesia. Cardiosympathetic blockade produced equivalent relative decreases in baroreflex gain in conscious and PA rats. In contrast, parasympathetic nervous system blockade with methyl-atropine produced relatively less inhibition of baroreflex gain in the PA rat compared with the conscious rat. These results suggest that pentobarbital anesthesia decreases baroreflex gain by inhibiting vagally mediated reflex bradycardia.
本研究确定了戊巴比妥麻醉对大鼠压力感受器介导的反射性心动过缓的自主神经系统控制的影响。在用β-1受体拮抗剂阿替洛尔进行交感神经阻滞之前和之后，以及在用外周作用的毒蕈碱受体拮抗剂甲基阿托品进行副交感神经阻滞之前和之后，通过去氧肾上腺素诱导的高血压在清醒和戊巴比妥麻醉（PA）大鼠中引发反射性心动过缓。戊巴比妥麻醉显著降低了反射性心动过缓。心脏交感神经阻滞在清醒和PA大鼠中使压力反射增益产生同等程度的相对降低。相比之下，与清醒大鼠相比，用甲基阿托品进行副交感神经系统阻滞在PA大鼠中对压力反射增益的抑制相对较少。这些结果表明，戊巴比妥麻醉通过抑制迷走神经介导的反射性心动过缓来降低压力反射增益。
