Vasopressin-mediated adrenocorticotropin release increases plasma cortisol concentrations 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 plasma concentrations of ACTH, cortisol, and endothelin-1 after epinephrine or vasopressin administration in an experimental animal model of cardiopulmonary resuscitation (CPR).


METHODS
Prospective, randomized, controlled animal study.


METHODS
A university research laboratory.


METHODS
Fourteen 12- to 14-wk-old domestic pigs.


METHODS
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 drug administration, defibrillation was attempted.


RESULTS
Coronary perfusion pressure, ACTH, cortisol, and endothelin-1 were measured before cardiocirculatory arrest, during CPR before drug administration, and at 90 secs and 5 mins after drug administration. Coronary perfusion pressure was comparable between groups. All seven animals in the vasopressin group survived, but only one pig in the epinephrine group survived (p = .005). ACTH and cortisol concentrations remained unchanged in epinephrine-treated animals, but increased significantly after vasopressin administration and were significantly higher than in epinephrine-treated animals 5 mins after drug administration. Endothelin-1 concentrations 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 enhanced ACTH release after vasopressin may be one factor contributing to the improved outcome repeatedly observed with vasopressin in animal models of CPR.
Kornberger
E
E
Department of Anesthesiology and Critical Care Medicine, University of Innsbruck, Austria. p.mair@uibk.ac.at
Prengel
A W
AW
Krismer
A
A
Schwarz
B
B
Wenzel
V
V
Lindner
K H
KH
Mair
P
P
D000324:Adrenocorticotropic Hormone / Q000097:blood*; D000818:Animals; D016887:Cardiopulmonary Resuscitation / Q000379:methods*; D004195:Disease Models, Animal; D004353:Drug Evaluation, Preclinical; D004554:Electric Countershock; D019332:Endothelin-1 / Q000097:blood*; D004837:Epinephrine / Q000494:pharmacology / Q000627:therapeutic use*; D006323:Heart Arrest / Q000378:metabolism* / Q000503:physiopathology / Q000628:therapy*; D006439:Hemodynamics / Q000187:drug effects; D006854:Hydrocortisone / Q000097:blood*; D011897:Random Allocation; D016019:Survival Analysis; D013552:Swine; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000494:pharmacology / Q000627:therapeutic use*; D014667:Vasopressins / Q000494:pharmacology / Q000627:therapeutic use*
D019332:Endothelin-1; D014662:Vasoconstrictor Agents; D014667:Vasopressins; D000324:Adrenocorticotropic Hormone; D006854:Hydrocortisone; D004837:Epinephrine