title: 3.5% hypertonic saline produces sympathetic activation in hemorrhaged rabbits.
abstract: 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.
authors.affiliation: Department of Anesthesiology and Emergency Medicine, School of Medicine, Kagawa Medical University, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Seki
authors.forename: M
authors.initials: M
authors.lastname: Aibiki
authors.forename: S
authors.initials: S
authors.lastname: Ogura
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D003714:Denervation; D006470:Hemorrhage / Q000503:physiopathology*; D007668:Kidney / Q000294:innervation*; D009994:Osmolar Concentration; D011817:Rabbits; D012462:Saline Solution, Hypertonic / Q000494:pharmacology*; D012850:Sinus of Valsalva / Q000294:innervation; D013564:Sympathetic Nervous System / Q000187:drug effects* / Q000503:physiopathology*; D014628:Vagotomy
chemical_list: D012462:Saline Solution, Hypertonic