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

Krejci, Vladimir; Hiltebrand, Luzius B; Jakob, Stephan M; Takala, Jukka; Sigurdsson, Gisli H (2007). Vasopressin in septic shock: effects on pancreatic, renal, and hepatic blood flow. Critical care, 11(6), R129. London: BioMed Central 10.1186/cc6197

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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.

Item Type:

Journal Article (Original Article)

Division/Institute:

04 Faculty of Medicine > Department of Intensive Care, Emergency Medicine and Anaesthesiology (DINA) > Clinic and Policlinic for Anaesthesiology and Pain Therapy
04 Faculty of Medicine > Department of Intensive Care, Emergency Medicine and Anaesthesiology (DINA) > Clinic of Intensive Care

UniBE Contributor:

Krejci, Vladimir; Hiltebrand, Luzius; Jakob, Stephan and Takala, Jukka

ISSN:

1364-8535

ISBN:

18078508

Publisher:

BioMed Central

Language:

English

Submitter:

Jeannie Wurz

Date Deposited:

04 Oct 2013 14:55

Last Modified:

23 Jan 2018 12:17

Publisher DOI:

10.1186/cc6197

PubMed ID:

18078508

Web of Science ID:

000253286500013

BORIS DOI:

10.7892/boris.23275

URI:

https://boris.unibe.ch/id/eprint/23275 (FactScience: 40803)

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