Chen B B, Nyhan D P, Goll H M, Clougherty P W, Fehr D M, Murray P A
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.
Am J Physiol. 1988 Sep;255(3 Pt 2):H569-76. doi: 10.1152/ajpheart.1988.255.3.H569.
Our objectives were 1) to investigate the extent to which the pulmonary vascular response to increasing cardiac index after a period of hypotension and hypoperfusion (defined as reperfusion) measured in conscious dogs is altered during pentobarbital sodium anesthesia, and 2) to determine whether pentobarbital anesthesia modifies autonomic nervous system (ANS) regulation of the pulmonary circulation during reperfusion. Base-line and reperfusion pulmonary vascular pressure-cardiac index (P/Q) plots were generated by stepwise inflation and deflation, respectively, of an inferior vena caval occluder to vary Q in conscious and pentobarbital-anesthetized (30 mg/kg iv) dogs. During pentobarbital anesthesia, controlled ventilation (without positive end-expiratory pressure) allowed matching of systemic arterial and mixed venous blood gases to conscious values. Marked pulmonary vasoconstriction (P less than 0.01) was observed during reperfusion in pentobarbital-anesthetized but not in conscious dogs. Both sympathetic alpha-adrenergic receptor block and total ANS ganglionic block attenuated, but did not abolish, the pulmonary vasoconstriction during reperfusion in pentobarbital-anesthetized dogs. Neither sympathetic beta-adrenergic receptor block nor cholinergic receptor block enhanced the magnitude of the pulmonary vasoconstrictor response to reperfusion during pentobarbital anesthesia. Thus, in contrast to the conscious state, the pulmonary vascular response to reperfusion is characterized by active, non-flow-dependent pulmonary vasoconstriction during pentobarbital anesthesia. This response is primarily, but not exclusively, mediated by sympathetic alpha-adrenergic vasoconstriction and is not offset by either sympathetic beta-adrenergic or cholinergic vasodilation. These results indicate, that, compared with the conscious state, pentobarbital anesthesia modifies pulmonary vasoregulation, during reperfusion following hypotension and hypoperfusion.(ABSTRACT TRUNCATED AT 250 WORDS)
1)研究在戊巴比妥钠麻醉期间,清醒犬在经历一段时间的低血压和低灌注(定义为再灌注)后,肺血管对心指数增加的反应程度是否发生改变;2)确定戊巴比妥麻醉是否会在再灌注期间改变自主神经系统(ANS)对肺循环的调节。通过分别逐步充气和放气下腔静脉阻塞器以改变清醒和戊巴比妥麻醉(静脉注射30mg/kg)犬的心指数,生成基线和再灌注时的肺血管压力-心指数(P/Q)图。在戊巴比妥麻醉期间,控制性通气(无呼气末正压)使体动脉和混合静脉血气与清醒时的值相匹配。在戊巴比妥麻醉的犬再灌注期间观察到明显的肺血管收缩(P<0.01),而清醒犬未观察到。交感α-肾上腺素能受体阻断和完全ANS神经节阻断均减弱但未消除戊巴比妥麻醉犬再灌注期间的肺血管收缩。在戊巴比妥麻醉期间,交感β-肾上腺素能受体阻断和胆碱能受体阻断均未增强肺血管对再灌注的收缩反应幅度。因此,与清醒状态相比,戊巴比妥麻醉期间肺血管对再灌注的反应特点是出现主动的、非流量依赖性肺血管收缩。这种反应主要但并非完全由交感α-肾上腺素能血管收缩介导,且未被交感β-肾上腺素能或胆碱能血管舒张抵消。这些结果表明,与清醒状态相比,戊巴比妥麻醉在低血压和低灌注后的再灌注期间改变了肺血管调节。(摘要截断于250字)