Mechanisms of bronchoprotection by anesthetic induction agents -: Propofol versus ketamine
Mechanisms of bronchoprotection by anesthetic induction agents -: Propofol versus ketamine
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DOI：
10.1097/00000542-199903000-00025
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发表时间：
1999-03-01
期刊：
影响因子：
8.8
通讯作者：
Wagner, EM
中科院分区：
文献类型：
--
作者：
Brown, RH;Wagner, EM
背景：据称异丙酚和氯胺酮可减少麻醉诱导和插管期间的支气管收缩。它们是作用于气道平滑肌还是通过神经反射尚未确定。我们比较了异丙酚和氯胺酮减弱乙酰甲胆碱对 ah-way 平滑肌的直接激活作用和限制神经介导的支气管收缩（迷走神经刺激）。 方法：经机构审查委员会批准后，用戊巴比妥麻醉 8 只羊，进行麻痹和通气。左侧开胸后，支气管动脉插管灌注，随机顺序将5 mg/ml浓度的异丙酚、氯胺酮、硫喷妥钠分别以0.06、0.20、0.60 ml/min的速度注入支气管动脉，10 min后测量迷走神经刺激和经支气管动脉给予乙酰甲胆碱前后的气道阻力。数据以输注药物前基线反应的百分比表示，并通过方差分析进行分析，显着性设置为 P 小于或等于 0.05。 结果：全身血压不受任何药物的影响（P > 0.46）。三种药物之间（P = 0.56）或不同剂量（P = 0.96）的基线气道阻力没有差异。将异丙酚和氯胺酮输注到支气管动脉中，引起迷走神经刺激引起的支气管收缩呈剂量依赖性减弱，分别达到最大值的26 +/- 11%和8 +/- 2%（P < 0.0001）。此外，异丙酚在最高浓度时可使乙酰甲胆碱诱导的支气管收缩显着降低至最大值的 43 +/- 27%（P = 0.05）。结论：氯胺酮和异丙酚对气道的局部支气管保护作用是通过神经介导机制实现的。尽管高浓度时会对气道平滑肌产生直接影响，但这些不太可能具有主要的临床相关性。
Background: Propofol and ketamine have been purported to decrease bronchoconstriction during induction of anesthesia and intubation. Whether they act on airway smooth muscle or through neural reflexes has not been determined. We compared propofol and ketamine to attenuate the direct activation of ah-way smooth muscle by methacholine and Limit neurally mediated bronchoconstriction (vagal nerve stimulation).Methods: After approval from the institutional review board, eight sheep were anesthetized with pentobarbital, paralyzed, and ventilated. After left thoracotomy, the bronchial artery was cannulated and perfused, In random order, 5 mg/ml concentrations of propofol, ketamine, and thiopental were infused into the bronchial artery at rates of 0.06, 0.20, and 0.60 ml/min, After 10 min, airway resistance was measured before and after vagal nerve stimulation and methacholine given via the bronchial artery. Data were expressed as a percent of baseline response before infusion of drug and analyzed by analysis of variance with significance set at P less than or equal to 0.05.Results: Systemic blood pressure was not affected by any of the drugs (P > 0.46). Baseline airway resistance was not different among the three agents (P= 0.56) or by dose (P = 0.96). Infusion of propofol and ketamine into the bronchial artery caused a dose-dependent attenuation of the vagal nerve stimulation-induced bronchoconstriction to 26 +/- 11% and 8 +/- 2% of maximum, respectively (P < 0.0001). In addition, propofol caused a significant decrease in the methacholine-induced bronchoconstriction to 43 +/- 27% of maximum at the highest concentration (P = 0.05)Conclusions: The local bronchoprotective effects of ketamine and propofol on airways is through neurally mediated mechanisms. Although the direct effects on airway smooth muscle occur at high concentrations, these are unlikely to be of primary clinical relevance.