Racemic Ketamine Decreases Muscle Sympathetic Activity but Maintains the Neural Response to Hypotensive Challenges in Humans
Racemic Ketamine Decreases Muscle Sympathetic Activity but Maintains the Neural Response to Hypotensive Challenges in Humans
复制标题
外消旋氯胺酮可降低人类肌肉交感神经活动，但维持对低血压挑战的神经反应
DOI：
10.1097/00000542-200001000-00019
复制
发表时间：
2000
期刊：
影响因子：
8.8
通讯作者：
J. Peters
中科院分区：
文献类型：
--
作者：
P. Kienbaum;T. Heuter;M. Michel;J. Peters
背景在各种实验模型中，氯胺酮麻醉期间心血管刺激和儿茶酚胺血浆浓度增加归因于中枢交感神经活性增加以及儿茶酚胺再摄取抑制。然而，传出交感神经活动的直接记录尚未在人类中进行。作者检验了外消旋氯胺酮增加传出肌肉交感神经活性（MSA）并维持肌肉交感神经对兴奋性刺激的反应的假设。方法6名健康受试者在氯胺酮（2 mg/kg静脉注射+30 g · kg-1 · min-1）麻醉前和麻醉过程中，用显微神经电图记录腓总神经的交感神经活动。还测定了血浆儿茶酚胺浓度、心率和血压。在氯胺酮麻醉前和麻醉过程中，通过注射硝普钠（2-10 g/kg）来评估肌肉交感神经对兴奋性激发的反应。在最后一步中，通过硝普钠输注（1-6 g · kg−1 · min−1）将氯胺酮麻醉期间观察到的动脉压升高调整至麻醉前基线。结果氯胺酮显着降低了MSA爆发频率（平均值± SD，18 ± 9次/min至9 ± 8次/min）和爆发发生率（26 ± 11次/100次心跳至9 ± 6次/100次心跳）。然而，当通过硝普钠将升高的平均动脉压（85 ± 8 mmHg至121 ± 20 mmHg）标准化至清醒基线时，MSA恢复（25 ± 18次/min; 23 ± 14次/100次心跳）。氯胺酮麻醉期间，肾上腺素（15 ± 10 pg/ml至256 ± 193 pg/ml）和去甲肾上腺素（250 ± 105 pg/ml至570 ± 270 pg/ml）血浆浓度显著升高，心率也显著升高（67 ± 13次/min至113 ± 15次/min）。在清醒状态和氯胺酮麻醉期间，低血压挑战同样增加了MSA。结论在氯胺酮引起的动脉血压升高过程中，交感神经对肌肉血管的放电减少，同时血浆去甲肾上腺素浓度增加。当这种动脉血压升高逆转时，氯胺酮期间的MSA与前氯胺酮基线记录相比没有变化。最后，强迫性的挑战仍然引起不变的交感神经反射反应。因此，我们的研究结果不支持氯胺酮麻醉以广义的方式增加交感神经活动的假设。
Background Cardiovascular stimulation and increased catecholamine plasma concentrations during ketamine anesthesia have been attributed to increased central sympathetic activity as well as catecholamine reuptake inhibition in various experimental models. However, direct recordings of efferent sympathetic nerve activity have not been performed in humans. The authors tested the hypothesis that racemic ketamine increases efferent muscle sympathetic activity (MSA) and maintains the muscle sympathetic response to hypotensive challenges. Methods Muscle sympathetic activity was recorded by microneurography in the peroneal nerve of six healthy subjects before and during anesthesia with racemic ketamine (2 mg/kg intravenously plus 30 &mgr;g · kg−1 · min−1). Catecholamine plasma concentrations, heart rate, and blood pressure were also determined. Muscle sympathetic neural responses to a hypotensive challenge were assessed by injection of sodium nitroprusside (2–10 &mgr;g/kg) before and during ketamine anesthesia. In the final step, increased arterial pressure observed during ketamine anesthesia was adjusted to preanesthetic baseline by sodium nitroprusside infusion (1–6 &mgr;g · kg−1 · min−1). Results Ketamine significantly decreased MSA burst frequency (mean ± SD, 18 ± 9 bursts/min to 9 ± 8 bursts/min) and burst incidence (26 ± 11 bursts/100 heart beats to 9 ± 6 bursts/100 heart beats). However, when increased mean arterial pressure (85 ± 8 mmHg to 121 ± 20 mmHg) was normalized to the awake baseline by sodium nitroprusside, MSA recovered (25 ± 18 bursts/min; 23 ± 14 bursts/100 heart beats). During ketamine anesthesia, both epinephrine (15 ± 10 pg/ml to 256 ± 193 pg/ml) and norepinephrine (250 ± 105 pg/ml to 570 ± 270 pg/ml) plasma concentrations significantly increased, as did heart rate (67 ± 13 beats/min to 113 ± 15 beats/min). Hypotensive challenges similarly increased MSA both in the awake state and during ketamine anesthesia. Conclusions During increased arterial blood pressure associated with ketamine, sympathetic discharge to muscle blood vessels decreases at the same time that plasma concentrations of norepinephrine increase. When this increase in arterial blood pressure is reversed, MSA during ketamine is not changed from preketamine baseline recordings. Finally, hypotensive challenges still evoke an unchanged sympathetic reflex response. Thus, our results do not support the assumption that ketamine anesthesia increases sympathetic nerve activity in a generalized fashion.
影响因子：
9.8
作者：
WHITE, PF;SCHUTTLER, J;TREVOR, AJ
通讯作者：
TREVOR, AJ
主动脉压力反射在低血压期间调节交感神经反应中的重要性。
影响因子：
37.8
作者：
Sanders,JS;Mark,AL;Ferguson,DW
通讯作者：
Ferguson,DW