Rentero N, Bruandet N, Viale J P, Quintin L
Department of Physiology, School of Medicine, Lyon, France.
Synapse. 1998 Oct;30(2):130-9. doi: 10.1002/(SICI)1098-2396(199810)30:2<130::AID-SYN2>3.0.CO;2-D.
The rostral ventrolateral medulla (RVLM) controls the vascular system. It may contribute to postoperative hypertension observed upon emergence from anesthesia. This structure contains adrenergic cardiovascular neurons. Therefore, one question was addressed: does a change in RVLM catechol activity occur upon emergence from anesthesia? Halothane-anesthetized, paralyzed rats had their ventilatory, circulatory, and acid-base stability controlled. All pressure points and incisions were infiltrated with local anesthetic. With in vivo electrochemistry, a catechol signal was recorded in the RVLM in the following circumstances: (1) under stable halothane anesthesia for 120 minutes (halothane group), (2) during 120 minutes after halothane discontinuation (saline-emergence group), (3) during 60 minutes after halothane discontinuation followed by 60 minutes after halothane readministration (readministration group), (4) emergence in rats treated with atenolol and nitroprusside to hold blood pressure as close as possible to baseline, (5) emergence after morphine 1 mg.kg(-1) i.v., (6) emergence after decerebration, and (7) emergence upon recording in the mid-brain dopaminergic A10 area. Stable halothane anesthesia (n = 6) led to no change in mean arterial pressure (MAP), heart rate (HR), and catechol signal (CAOC). During emergence from anesthesia (n = 6), MAP, HR, and catechol signal increased and did not return to baseline. By contrast, a return of MAP, HR, and catechol signal to baseline was observed upon readministration of halothane (n = 6). Whereas blood pressure and heart rate were maintained as closely as possible to baseline, a large catechol activation (n = 5) was observed upon emergence from anesthesia. A catechol activation from a lowered baseline was observed upon emergence following morphine administration (n = 5). A minor circulatory activation without RVLM catechol activation was observed upon emergence following decerebration (n = 5). Recordings in the A10 area revealed no increase in the catechol signal following emergence (n = 5). Adrenergic RVLM neurons appear to be responsive upon emergence from anesthesia, possibly being activated by suprapontine afferents impinging on the RVLM.
延髓头端腹外侧区（RVLM）控制着血管系统。它可能与麻醉苏醒时出现的术后高血压有关。该结构包含肾上腺素能心血管神经元。因此，研究人员提出了一个问题：麻醉苏醒时RVLM中的儿茶酚活性是否会发生变化？对氟烷麻醉、麻痹的大鼠的通气、循环和酸碱平衡进行控制。所有的压力点和切口都用局部麻醉剂浸润。采用体内电化学方法，在以下情况下记录RVLM中的儿茶酚信号：（1）在氟烷稳定麻醉120分钟期间（氟烷组），（2）氟烷停用后的120分钟内（生理盐水苏醒组），（3）氟烷停用60分钟后再给予氟烷60分钟期间（再给药组），（4）用阿替洛尔和硝普钠治疗使血压尽可能接近基线水平的大鼠苏醒时，（5）静脉注射1mg.kg(-1)吗啡后的苏醒，（6）大脑切除后的苏醒，以及（7）在中脑多巴胺能A10区记录时的苏醒。稳定的氟烷麻醉（n = 6）导致平均动脉压（MAP）、心率（HR）和儿茶酚信号（CAOC）无变化。在麻醉苏醒期间（n = 6），MAP、HR和儿茶酚信号增加且未恢复到基线水平。相比之下，再次给予氟烷后，MAP、HR和儿茶酚信号恢复到了基线水平（n = 6）。尽管血压和心率尽可能维持在基线水平，但在麻醉苏醒时观察到大量儿茶酚激活（n = 5）。吗啡给药后苏醒时，观察到儿茶酚从较低基线水平开始激活（n = 5）。大脑切除后苏醒时，观察到轻微的循环激活但无RVLM儿茶酚激活（n = 5）。在A10区的记录显示苏醒后儿茶酚信号无增加（n = 5）。肾上腺素能RVLM神经元在麻醉苏醒时似乎有反应，可能是由撞击RVLM的脑桥上段传入神经激活的。
