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Abstract
Vasopressin is emerging as a rational therapy for the hemodynamic support of septic
shock and vasodilatory shock due to systemic inflammatory response syndrome. The goal
of this review is to understand the physiology of vasopressin relevant to septic shock
in order to maximize its safety and efficacy in clinical trials and in subsequent
therapeutic use. Vasopressin is both a vasopressor and an antidiuretic hormone. It
also has hemostatic, GI, and thermoregulatory effects, and is an adrenocorticotropic
hormone secretagogue. Vasopressin is released from the axonal terminals of magnocellular
neurons in the hypothalamus. Vasopressin mediates vasoconstriction via V1-receptor
activation on vascular smooth muscle and mediates its antidiuretic effect via V2-receptor
activation in the renal collecting duct system. In addition, vasopressin, at low plasma
concentrations, mediates vasodilation in coronary, cerebral, and pulmonary arterial
circulations. Septic shock causes first a transient early increase in blood vasopressin
concentrations that decrease later in septic shock to very low levels compared to
other causes of hypotension. Vasopressin infusion of 0.01 to 0.04 U/min in patients
with septic shock increases plasma vasopressin levels to those observed in patients
with hypotension from other causes, such as cardiogenic shock. Increased vasopressin
levels are associated with a lesser need for other vasopressors. Urinary output may
increase, and pulmonary vascular resistance may decrease. Infusions of > 0.04 U/min
may lead to adverse, likely vasoconstriction-mediated events. Because clinical studies
have been relatively small, focused on physiologic end points, and because of potential
adverse effects of vasopressin, clinical use of vasopressin should await a randomized
controlled trial of its effects on clinical outcomes such as organ failure and mortality.