Mori T, Nishikawa K, Terai T, Yukioka H, Asada A
Department of Anesthesiology and Intensive Care Medicine, Osaka City University Medical School, Osaka, Japan.
Anesthesiology. 1998 Jun;88(6):1558-65. doi: 10.1097/00000542-199806000-00020.
Epidural morphine yields postoperative pain relief and hemodynamic stability. However, the effects of epidural morphine on sympathetic tone are unclear. This study was designed to elucidate the effects of epidural morphine on cardiac (CSNA) and renal (RSNA) sympathetic nerve activity by direct measurement in anesthetized cats.
Thirty mongrel cats anesthetized with alpha-chloralose were randomly assigned to one of the following five groups: control (0.2 ml/kg thoracic epidural normal saline; n=5); thoracic epidural morphine (n=9); lumbar epidural morphine (n=6); vagotomized, sinoaortic denervated, thoracic epidural morphine (n=5); or intravenous morphine (n=5). Mean arterial pressure (MAP), heart rate (HR), CSNA, and RSNA were measured 0, 15, 30, 60, 90, and 120 min after saline or morphine (200 microg/kg) administration and 15 min after reversal with 200 microg naloxone given intravenously.
In the control group, no changes in measured variables were found after either thoracic epidural saline or intravenous naloxone. Thoracic and lumbar epidural morphine both significantly reduced MAP, HR, CSNA, and RSNA 30 through 120 min after morphine administration (P < 0.05). These changes were reversed by intravenous naloxone. Changes after thoracic epidural morphine administration in vagotomized, baroreceptor-denervated cats were similar to those in intact cats. Intravenous morphine produced no significant changes except for a decrease in MAP, which was reversed by intravenous naloxone.
In contrast to intravenous morphine, thoracic and lumbar epidural morphine both inhibited cardiac and renal sympathetic nerve activity and consequently reduced MAP and HR in alpha-chloralose anesthetized cats.
硬膜外注射吗啡可缓解术后疼痛并维持血流动力学稳定。然而,硬膜外注射吗啡对交感神经张力的影响尚不清楚。本研究旨在通过直接测量麻醉猫的交感神经活动,阐明硬膜外注射吗啡对心脏(CSNA)和肾脏(RSNA)交感神经活动的影响。
30只用α-氯醛糖麻醉的杂种猫被随机分为以下五组之一:对照组(0.2 ml/kg胸段硬膜外注射生理盐水;n = 5);胸段硬膜外注射吗啡组(n = 9);腰段硬膜外注射吗啡组(n = 6);迷走神经切断、窦主动脉去神经支配、胸段硬膜外注射吗啡组(n = 5);或静脉注射吗啡组(n = 5)。在给予生理盐水或吗啡(200 μg/kg)后0、15、30、60、90和120分钟以及静脉注射200 μg纳洛酮逆转后15分钟,测量平均动脉压(MAP)、心率(HR)、CSNA和RSNA。
在对照组中,胸段硬膜外注射生理盐水或静脉注射纳洛酮后,测量变量均无变化。胸段和腰段硬膜外注射吗啡均在给药后30至120分钟显著降低MAP、HR、CSNA和RSNA(P < 0.05)。这些变化可被静脉注射纳洛酮逆转。迷走神经切断、压力感受器去神经支配的猫在胸段硬膜外注射吗啡后的变化与完整猫相似。静脉注射吗啡除MAP降低外无显著变化,该变化可被静脉注射纳洛酮逆转。
与静脉注射吗啡不同,胸段和腰段硬膜外注射吗啡均抑制了α-氯醛糖麻醉猫的心脏和肾脏交感神经活动,从而降低了MAP和HR。