Seki K, Aibiki M, Ogura S
Department of Anesthesiology and Emergency Medicine, School of Medicine, Kagawa Medical University, Japan.
J Auton Nerv Syst. 1997 May 12;64(1):49-56. doi: 10.1016/s0165-1838(97)00016-7.
The neural mechanisms for pressor effects after hypertonic saline infusion are still unclear. Using direct measurement of the renal sympathetic nerve activity (RNA), we tested the hypothesis that the autonomic nervous system is involved in an acute blood pressure elevation produced by hypertonic saline (HTS) in anesthetized rabbits subjected to hemorrhage. Twenty urethane-anesthetized rabbits were ventilated mechanically after a tracheostomy and paralyzed with gallamine triethiodide. Heart rate (HR), mean blood pressure (MBP) and central venous pressure (CVP) were measured simultaneously with RNA. The animals were divided into the following four groups: (1) animals with intact baroreceptors that received HTS (intact HTS group, N = 5); (2) those with intact baroreceptors that received normal saline (intact NS group, N = 5); (3) those that underwent selective cervical vagotomy (vagotomy group, N = 5); (4) those with sino-aortic denervation (SAD group, N = 5). The last two groups were given HTS only. After inducing hemorrhagic hypotension to 40 mmHg over 10 min, 3.5% HTS at half the volume of shed blood was infused over approximately 120 s. In the intact HTS group, sympathetic activation, associated with tachycardia and pressor effects, developed. This enhancement of RNA was followed by a return to the pre-infusion level, but the increased blood pressure and tachycardia lasted until the end of the experiment. These levels of MBP and HR were significantly higher than those of the intact NS group. In the vagotomized animals, HTS resuscitation also increased RNA and systemic blood pressure. In contrast, in the SAD group, neither sympathetic activation nor an early phase increase in systemic blood pressure occurred. These results indicate that in hemorrhaged rabbits, 3.5% HTS produces sympathetic activation along with an acute pressor effect and that this is likely to be mediated through the sino-aortic nerves, possibly the peripheral chemoreceptors, but not through the vagal nerves.
高渗盐水输注后升压作用的神经机制仍不清楚。通过直接测量肾交感神经活动(RNA),我们检验了以下假设:自主神经系统参与了在出血的麻醉兔中由高渗盐水(HTS)引起的急性血压升高。20只经乌拉坦麻醉的兔在气管切开术后进行机械通气,并用三碘季铵酚使其麻痹。心率(HR)、平均血压(MBP)和中心静脉压(CVP)与RNA同时测量。动物被分为以下四组:(1)压力感受器完整且接受HTS的动物(完整HTS组,N = 5);(2)压力感受器完整且接受生理盐水的动物(完整NS组,N = 5);(3)接受选择性颈迷走神经切断术的动物(迷走神经切断术组,N = 5);(4)接受窦主动脉去神经支配的动物(SAD组,N = 5)。最后两组仅给予HTS。在10分钟内将出血性低血压诱导至40 mmHg后,以失血量一半的体积的3.5% HTS在约120秒内输注。在完整HTS组中,出现了与心动过速和升压作用相关的交感神经激活。这种RNA的增强随后恢复到输注前水平,但血压升高和心动过速持续到实验结束。这些MBP和HR水平显著高于完整NS组。在迷走神经切断的动物中,HTS复苏也增加了RNA和全身血压。相反,在SAD组中,既未发生交感神经激活,也未出现全身血压的早期升高。这些结果表明,在出血的兔中,3.5% HTS产生交感神经激活以及急性升压作用,并且这可能是通过窦主动脉神经介导的,可能是通过外周化学感受器,但不是通过迷走神经。