Anzai Y, Nishikawa T, Namiki A
Department of Anaesthesiology, Sapporo Medical College and Hospital, Japan.
Can J Anaesth. 1990 Mar;37(2):245-9. doi: 10.1007/BF03005477.
The purpose of this study was to determine whether centrally mediated sympathetic tone exerts compensatory effects on nitrous oxide-induced myocardial depression during high-dose fentanyl anaesthesia. The cardiovascular responses to 60 minutes of nitrous oxide administration after fentanyl, 100 micrograms.kg-1, were examined in 18 dogs with or without autonomic blockade induced by hexamethonium. Decreases of cardiac output and left ventricular stroke work were significantly greater in dogs with autonomic blockade (n = 9) by about 20 per cent of baseline values than in dogs without autonomic blockade (n = 9) at 30, 45, and 60 min. Similarly, left ventricular dP/dt was reduced more in dogs with autonomic blockade than in dogs without autonomic blockade, but this difference was only significant at the 60-min period. It is concluded that the sympathetic nervous system provides partial compensation for myocardial depression induced by nitrous oxide in the presence of high-dose fentanyl, suggesting that large doses of fentanyl do not ablate the centrally mediated sympathomimetic effects of nitrous oxide.
本研究的目的是确定在高剂量芬太尼麻醉期间,中枢介导的交感神经张力是否对氧化亚氮诱导的心肌抑制发挥代偿作用。对18只犬给予100微克/千克芬太尼后,观察其在有或没有六甲铵诱导的自主神经阻滞情况下,吸入氧化亚氮60分钟的心血管反应。在30、45和60分钟时,有自主神经阻滞的犬(n = 9)心输出量和左心室每搏功的降低比无自主神经阻滞的犬(n = 9)显著大,约为基线值的20%。同样,有自主神经阻滞的犬左心室dp/dt降低比无自主神经阻滞的犬更多,但这种差异仅在60分钟时显著。结论是,在高剂量芬太尼存在的情况下,交感神经系统对氧化亚氮诱导的心肌抑制提供了部分代偿,这表明大剂量芬太尼并未消除氧化亚氮的中枢介导的拟交感神经效应。