Vasopressin-mediated adrenocorticotropin release increases plasma cortisolconcentrations during cardiopulmonary resuscitation

Objective: Vasopressin is a possible stimulus for both adrenocorticotropin (ACTH) and endothelin-1 release. The aim of this study was to compare plasm a concentrations of ACTH, cortisol, and endothelin-1 after epinephrine or v asopressin administration in an experimental animal model of cardiopulmonar y resuscitation (CPR). Design: Prospective, randomized, controlled animal study. Setting: A university research laboratory. Subjects: Fourteen 12- to 14-wk-old domestic pigs. Interventions: After 4 mins of cardiac arrest and 3 mins of external chest compression, the pigs were randomly assigned to receive either 0.045 mg/kg epinephrine (n = 7) or 0.4 units/kg vasopressin (n = 7). At 5 mins after dr ug administration, defibrillation was attempted. Measurements and Main Results:Coronary perfusion pressure, ACTH, cortisol, and endothelin-1 were measured before cardiocirculatory arrest, during CPR before drug administration, and at 90 sees and 5 mins after drug administra tion. Coronary perfusion pressure was comparable between groups. All seven animals in the vasopressin group survived, but only one pig in the epinephr ine group survived (p = .005). ACTH and cortisol concentrations remained un changed in epinephrine-treated animals, but increased significantly after v asopressin administration and were significantly higher than in epinephrine -treated animals 5 mins after drug administration. Endothelin-1 concentrati ons remained unchanged during the study period and were comparable between both groups. Conclusions: Vasopressin is a potent stimulus for ACTH secretion, but does not trigger endothelin-1 release from vascular cells during cardiac arrest and CPR. The increased plasma cortisol concentrations caused by the enhance d ACTH release after vasopressin may be one factor contributing to the impr oved outcome repeatedly observed with vasopressin in animal models of CPR.