Research

Vasopressin in septic shock: effects on pancreatic, renal, and hepatic blood flow

Vladimir Krejci¹ , Luzius B Hiltebrand² , Stephan M Jakob³ , Jukka Takala³ and Gisli H Sigurdsson⁴

¹Department of Anesthesiology, Washington University School of Medicine, Campus Box 8054, St. Louis, MO 63110, USA

²Department of Anesthesiology, University of Bern, Inselspital, CH-3010 Bern, Switzerland

³Department of Intensive Care Medicine, University of Bern, Inselspital, CH-3010 Bern, Switzerland

⁴Department of Anesthesia & Intensive Care Medicine, Landspitali University Hospital, Hringbraut, IS 101 Reykjavik, Iceland, and University of Iceland, Reykjavik, Iceland

author email corresponding author email

Critical Care 2007, 11:R129doi:10.1186/cc6197

Published:	13 December 2007

Abstract

Introduction

Vasopressin has been shown to increase blood pressure in catecholamine-resistant septic shock. The aim of this study was to measure the effects of low-dose vasopressin on regional (hepato-splanchnic and renal) and microcirculatory (liver, pancreas, and kidney) blood flow in septic shock.

Methods

Thirty-two pigs were anesthetized, mechanically ventilated, and randomly assigned to one of four groups (n = 8 in each). Group S (sepsis) and group SV (sepsis/vasopressin) were exposed to fecal peritonitis. Group C and group V were non-septic controls. After 240 minutes, both septic groups were resuscitated with intravenous fluids. After 300 minutes, groups V and SV received intravenous vasopressin 0.06 IU/kg per hour. Regional blood flow was measured in the hepatic and renal arteries, the portal vein, and the celiac trunk by means of ultrasonic transit time flowmetry. Microcirculatory blood flow was measured in the liver, kidney, and pancreas by means of laser Doppler flowmetry.

Results

In septic shock, vasopressin markedly decreased blood flow in the portal vein, by 58% after 1 hour and by 45% after 3 hours (p < 0.01), whereas flow remained virtually unchanged in the hepatic artery and increased in the celiac trunk. Microcirculatory blood flow decreased in the pancreas by 45% (p < 0.01) and in the kidney by 16% (p < 0.01) but remained unchanged in the liver.

Conclusion

Vasopressin caused marked redistribution of splanchnic regional and microcirculatory blood flow, including a significant decrease in portal, pancreatic, and renal blood flows, whereas hepatic artery flow remained virtually unchanged. This study also showed that increased urine output does not necessarily reflect increased renal blood flow.