(Circulation. 1999;100:226-229.)
© 1999 American Heart Association, Inc.
Brief Rapid Communications |
Reversal by Vasopressin of Intractable Hypotension in the Late Phase of Hemorrhagic Shock
From the Departments of Medicine, Surgery, and Anesthesiology, Columbia University College of Physicians and Surgeons, 630 W 168th St, New York, NY 10032.
Correspondence to Donald W. Landry, MD, PhD, Director, Division of Clinical Pharmacology and Experimental Therapeutics, Columbia University, P&S Building, 10th Floor, Room 445, 630 W 168th St, New York, NY 10032.
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 µg · kg-1
· min-1 was required to maintain this pressure. At this
moment, administration of vasopressin 1 to 4 mU ·
kg-1 · min-1 increased MAP from 39±6
to 128±9 mm Hg (P<0.001), primarily because of
peripheral vasoconstriction. In 3 dogs subjected to similar
prolonged hemorrhagic shock, angiotensin II 180 ng ·
kg-1 · min-1 had only a marginal
effect on MAP (45±12 to 49±15 mm Hg). Plasma vasopressin was
markedly elevated during acute hemorrhage but fell from 319±66
to 29±9 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.
Key Words: vasopressin • shock • hemorrhage
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