Effects of sevoflurane anesthesia on carotid-cardiac baroreflex responses in humans
Effects of sevoflurane anesthesia on carotid-cardiac baroreflex responses in humans
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DOI：
10.1213/01.ane.0000183651.10514.9a
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发表时间：
2006-01-01
影响因子：
5.7
通讯作者：
Nishikawa, T
中科院分区：
文献类型：
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作者：
Umehara, S;Tanaka, M;Nishikawa, T
七氟烷抑制心脏-迷走神经压力反射增益（迷走神经介导的R-R间期对动脉血压变化的反应能力）。我们通过检查整个刺激-反应压力反射关系来检查七氟烷麻醉对迷走神经介导的血流动力学控制的最大缓冲能力（压力反射范围）的影响。对11名健康志愿者进行心电图和有创动脉血压监测。颈动脉-心脏压力反射反应通过增加颈室压力（施加在双侧颈动脉窦上的外部压力）至40 mm Hg持续5次心跳，然后通过连续15 mm Hg R波触发的递减至-65 mm Hg来降低室压。将R-R间期绘制为先前颈动脉扩张压力的函数。在清醒基线、2%（潮气末）七氟烷麻醉期间、不输注和输注苯巴比妥以维持清醒动脉血压以及麻醉苏醒后30、60、120和180 min，确定范围、最大增益和操作点（整个压力反射反应曲线内静息设定点的相对位置）。七氟醚麻醉显著降低了反射关系的最大增益（从3.84 +/- 0.99到1.04 +/- 0.40 ms/mm Hg [平均值+/- SD]; P < 0.001）和范围（从207 +/- 43到52 +/- 19 ms; P < 0.001），这两个值在苏醒后120和180 min恢复。输注苯丙氨酸只能部分恢复这些变量。整个研究期间，操作点保持不变。我们的研究结果表明，最大心脏迷走神经代偿反应缓冲血流动力学扰动在七氟醚麻醉期间被抑制。七氟醚控制性降压引起迷走神经收缩，对抑制心-迷走神经反射功能无重要作用。
Sevoflurane depresses cardio-vagal baroreflex gain (ability of vagally mediated R-R interval response to arterial blood pressure change). We examined the effects of sevoflurane anesthesia on maximum buffering capacity of vagally mediated hemodynamic control (baroreflex range) by examining the entire stimulus-response baroreflex relation. Electrocardiogram and invasive arterial blood pressure were monitored in 11 healthy volunteers. Carotid-cardiac baroreflex responses were elicited by increasing neck chamber pressure (external pressure applied over the bilateral carotid sinuses) to 40 mm Hg for 5 heartbeats followed by decreasing chamber pressure by successive 15-mm Hg R-wave triggered decrements to -65 mm. Hg during held expiration. R-R intervals were plotted as functions of preceding carotid distending pressure. Range, maximum gain, and operational point (relative position of the resting set point within the entire baroreflex response curve) were determined at conscious baseline, during 2% (end-tidal) sevoflurane anesthesia, without and with phenylephrine infusion to maintain conscious arterial blood pressure, and at 30, 60, 120, and 180 min after emergence from anesthesia. Sevoflurane anesthesia significantly depressed maximum gain (from 3.84 +/- 0.99 to 1.04 +/- 0.40 ms/mm Hg [mean +/- SD]; P < 0.001) and range (from 207 +/- 43 to 52 +/- 19 ms; P < 0.001) of the reflex relation, both of which recovered at 120 and 180 min after emergence. Phenylephrine infusion only partially restored these variables. The operational point was unchanged throughout the study. Our results indicate that maximum cardio-vagal compensatory response to buffer hemodynamic perturbation is depressed during sevoflurane anesthesia. Sevoflurane-induced hypotension, which produced vagal withdrawal, did not play an important role in depressing cardio-vagal reflex function.