Heterogeneity of the vasoconstrictor effect of vasopressin... : Critical Care Medicine (original) (raw)

Laboratory Investigations

Malay, Mary-Beth MD; Ashton, Jennifer L. MD; Dahl, Katherine MD; Savage, Edward B. MD; Burchell, Sherryl A. MD; Ashton, Robert C. Jr MD; Sciacca, Robert R. PhD; Oliver, Juan A. MD; Landry, Donald W. MD, PhD

From the Allegheny University of the Health Sciences (M-BM, JLA, EBS, SAB, RCA), Allegheny General Hospital, Division of General Surgery, Pittsburgh, PA; and Columbia University, Department of Medicine (KD, RRS, JAO, DWL), New York.

Supported, in part, by the Allegheny Singer Research Institute, Allegheny General Hospital, Pittsburgh, PA, and the 1998 Gambro Charitable Trust.

Address requests for reprints to: Juan A. Oliver, MD, Columbia University, Department of Medicine, 630 West 168th Street; New York, NY 10032. E-mail: [email protected]

Abstract

Objective:

To determine whether pressor doses of vasopressin impair organ blood flow in endotoxic shock.

Design:

Graded doses of vasopressin or phenylephrine, starting at the clinically recommended doses for pressure support in septic shock, were intravenously infused during endotoxic shock.

Setting:

University hospital surgical research laboratory.

Subjects:

Twelve random-bred female Yorkshire pigs.

Interventions:

We measured mean arterial pressure, cardiac output, heart rate, pulmonary artery occlusion pressure, and carotid, mesenteric, renal, and iliac blood flows.

Measurements and Main Results:

Low doses of vasopressin (typically used in the clinical management of septic shock) raised arterial pressure by increasing systemic vascular resistance without a significant preferential effect in the circulations measured. However, moderately greater doses of vasopressin had a very heterogeneous vasoconstrictor action; although there was no significant vasoconstriction in the carotid and iliac circulations, mesenteric and renal blood flows decreased markedly. Furthermore, at pressor doses vasopressin improved cerebral perfusion.

Conclusions:

The vasoconstrictor action of exogenous low-dose vasopressin in endotoxic shock does not impair blood flow to any of the vascular beds examined. However, moderately higher doses of vasopressin may induce ischemia in the mesenteric and renal circulations. The data indicate that the safe dose range for exogenous vasopressin in septic shock is narrow and support the current practice of fixed low-dose administration, generally 0.04 units/min and in no case exceeding 0.1 units/min.