Effects of ketamine on renal nerve activity, arterial pressure and heart rate in rats.

Effects of ketamine on renal nerve activity, arterial pressure and heart rate in rats.
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氯胺酮对大鼠肾神经活动、动脉压和心率的影响。

DOI:
10.2170/jjphysiol.33.391
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发表时间:
1983
期刊:
The Japanese Journal of Physiology
影响因子:
--
通讯作者:
I. Ninomiya
I. Ninomiya
中科院分区:
--
文献类型:
--
作者:
M. Shirahata;Y. Okada;I. Ninomiya

文献摘要

被引文献

相似文献

在24只N2 O麻醉的Wister大鼠上,记录肾神经活动(RNA)、动脉压(AP)和心率(HR),观察氯胺酮对交感神经活动和心血管动力学的影响。在19只大鼠中研究了对四个分级剂量的氯胺酮(1,5,10,25 mg/kg)的反应的幅度和时程。RNA呈双相反应,1、5、10和25 mg/kg剂量下,最初呈剂量依赖性降低至最小值,分别为对照组的89 +/- 4.4、77 +/- 8.2、54 +/- 5.2和17 +/- 3.7%,然后呈剂量依赖性增加至对照组以上。AP表现为双相反应。HR首先呈剂量依赖性降低,但随后略有升高。在其余5只大鼠中,我们比较了氯胺酮5 mg/kg对手术压力感受器去神经前和去神经后RNA、AP和HR的影响。去神经支配突然增加RNA,AP和HR。氯胺酮减少RNA,AP和HR在去神经支配状态下,并将其恢复到氯胺酮前的值,而没有过冲。在神经完整状态下,氯胺酮产生特征性的RNA双相反应的发现可以通过以下机制来解释:(1)氯胺酮抑制血管中枢,导致RNA的初始减少;(2)氯胺酮抑制压力感受性反射的抑制作用,导致RNA的连续增加。AP的双相变化可能部分归因于RNA对氯胺酮的双相反应。
We recorded renal nerve activity (RNA) together with arterial pressure (AP) and heart rate (HR) in 24 Wister rats anesthetized with nitrous oxide to investigate the effects of ketamine on the sympathetic nerve activity and the cardiovascular dynamics. The magnitude and time course of the responses to four graded doses of ketamine (1, 5, 10, 25 mg/kg) were studied in 19 rats. RNA responded biphasically, initially decreasing dose-dependently to minimal values of 89 +/- 4.4, 77 +/- 8.2, 54 +/- 5.2, and 17 +/- 3.7% of control for 1, 5, 10, and 25 mg/kg, respectively, and then increasing above control dose-independently. AP showed a biphasic response. HR first decreased dose-dependently but then increased slightly. In the remaining five rats, we compared the effects of ketamine 5 mg/kg on RNA, AP, and HR before surgical baroceptor denervation with those after the denervation. The denervation abruptly increased RNA, AP, and HR. Ketamine decreased RNA, AP, and HR in the denervated state and returned them to pre-ketamine values without overshoot. The finding that in the nerve intact state ketamine produced the characteristically biphasic response of RNA could be explained by the following mechanisms: (1) ketamine depresses the vasomotor center causing the initial decrease in RNA; (2) ketamine depresses the inhibitory effects of baroreflex causing the successive increase in RNA. The biphasic change in AP could be partly attributed to biphasic responses of RNA to ketamine.