Umehara Shino, Tanaka Makoto, Nishikawa Toshiaki
Department of Anesthesia, Akita University School of Medicine, Akita-city, Japan.
Anesth Analg. 2006 Jan;102(1):38-44. doi: 10.1213/01.ane.0000183651.10514.9a.
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.
七氟醚会降低心迷走压力反射增益（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，研究了七氟醚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。通过将颈部腔室压力（施加在双侧颈动脉窦上的外部压力）增加至40 mmHg并持续5个心跳周期，然后在屏气期间以15 mmHg的幅度逐次递减至-65 mmHg来诱发颈动脉-心脏压力反射反应。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%（呼气末）七氟醚麻醉期间、在使用和未使用去氧肾上腺素输注以维持清醒状态下的动脉血压时，以及麻醉苏醒后30、60、120和180分钟时，测定范围、最大增益和工作点（静息设定点在整个压力反射反应曲线中的相对位置）。七氟醚麻醉显著降低了反射关系的最大增益（从3.84±0.99降至1.04±0.40 ms/mmHg [平均值±标准差]；P<0.001）和范围（从207±43降至52±19 ms；P<0.001），两者在苏醒后120和180分钟时恢复。去氧肾上腺素输注仅部分恢复了这些变量。在整个研究过程中工作点未发生变化。我们的结果表明，在七氟醚麻醉期间，对缓冲血流动力学扰动的最大心迷走代偿反应受到抑制。七氟醚诱导的低血压导致迷走神经撤离，但在抑制心迷走反射功能方面未发挥重要作用。
