Abstract
IntroductionVasopressin 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.MethodsThirty-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.ResultsIn 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.ConclusionVasopressin 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.
Highlights
Vasopressin has been shown to increase blood pressure in catecholamine-resistant septic shock
Regional, and local parameters recorded during the development of septic shock and during fluid resuscitation but before t = 300 minutes are presented in Appendix 1
Administration of low-dose vasopressin in septic shock resulted in increased arterial blood pressure and decreased systemic blood flow
Summary
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. Smaller controlled studies of human subjects receiving low-dose vasopressin in septic shock have been rather encouraging, but adverse events, possibly related to the use of vasopressin, have been reported [3,4]. The effects of vasopressin were well documented in the 1970s and 1980s in human [9] and animal [1012] studies, but this was mostly in non-septic conditions and with doses significantly exceeding what today is considered to be a 'safe' range. Published results from animal studies have confirmed previous findings that high doses of vasopressin (greater than 0.1 units per minute) clearly redistribute regional blood flows and decrease tissue oxygenation [13,14].
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