Reversal by vasopressin of intractable hypotension in the late phase of hemorrhagic shock. Circulation 100

Background—Hypovolemic shock of marked severity and duration may progress to cardiovascular collapse unresponsive to volume replacement and drug intervention. On the basis of clinical observations, we investigated the action of vasopressin in an animal model of this condition. Methods and Results—In 7 dogs, prolonged hemorrhagic shock (mean arterial pressure [MAP] of '40 mm Hg) was induced by exsanguination into a reservoir. After '30 minutes, progressive reinfusion was needed to maintain MAP at '40 mm Hg, and by '1 hour, despite complete restoration of blood volume, the administration of norepinephrine '3 mg z kg21 z min21 was required to maintain this pressure. At this moment, administration of vasopressin 1 to 4 mU z kg21 z min21 increased MAP from 3966 to 12869 mm Hg (P,0.001), primarily because of peripheral vasoconstriction. In 3 dogs subjected to similar prolonged hemorrhagic shock, angiotensin II 180 ng z kg21 z min21 had only a marginal effect on MAP (45612 to 49615 mm Hg). Plasma vasopressin was markedly elevated during acute hemorrhage but fell from 319666 to 2969 pg/mL before administration of vasopressin (P,0.01). Conclusions—Vasopressin is a uniquely effective pressor in the irreversible phase of hemorrhagic shock unresponsive to volume replacement and catecholamine vasopressors. Vasopressin deficiency may contribute to the pathogenesis of this condition. (Circulation. 1999;100:226-229.) Key Words: vasopressin n shock n hemorrhag