• Qingming Zhou, Dongliang Li, Zheng Zhang, Chunling Wang, and Xiufen Yang.
• Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2014 Jan 1;26(1):33-5.

ObjectiveTo investigate the vasopressin ( VP) response to increasing osmotic pressure in the late-phase of septic shock patients.MethodsThirty-seven septic shock patients hospitalized in intensive care unit ( ICU) of the First Hospital of Hebei Medical University from January 2012 to September 2013 were enrolled. All patients received 3% hypertonic saline solution infusion. Serum concentrations of VP and sodium were measured before and after hypertonic saline solution infusion. Patients with ratio of difference in VP and sodium before and after infusion of 3% hypertonic saline (ΔVP/ ΔNa) ≤ 0.5 pg/mmol were defined as nonresponders, and who >0.5 pg/mmol defined as responders, the age, acute physiological and chronic health evaluation II ( APACHE II) score, blood pressure, albumin level, vasoactive drug between the two groups were also analyzed.ResultsVP level in the nonresponsive group (n=20, 54.05 %) was markedly lowered before (ng/L: 10.41 ± 1.70 vs. 18.25 ± 5.90, t=5.29, P <0.01) and after (ng/L:11.36 ± 1.90 vs. 24.33 ±5.46, t=9.33, P <0.01) 3% hypertonic saline solution infusion, compared with that in the responsive group (n=17, 45.95%). All patients in the two groups were given dopamine (DA) or norepinephrine ( NE) for maintaining blood pressure, and the dose in the nonresponsive group were higher than those in the responsive group [DA (μg.Kg-1.min-1): 14.91 ± 3.78 vs. 8.64 ±1.69, t=-5.02, P <0.01; NE (μg.Kg-1.min-1): 1.03 ± 0.48 vs. 0.38 ±0.12, t=-3.12, P<0.01]. Three patients were given DA plus NE in the nonresponsive group while patients in the responsive group received only single drug therapy. The age, APACHE II score, blood pressure, albumin level, sodium level before and after hypertonic saline solution infusion between the two groups were not statistically different.ConclusionVP secretion to osmotic challenge was impaired and decreased in the late-phase of septic shock, prompting dysfunction in VP synthesis.

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