The cardiopulmonary and metabolic effects of hypoxia during acute adrenocortical suppression by etomidate in the dog.

Cortisol is secreted as part of the stress response and has been shown to be potentially beneficial to protect against acute stress. Etomidate specifically suppresses endogenous cortisol production. The author studied cardiopulmonary and metabolic effects of hypoxia in dogs during acute adrenocortical suppression by etomidate. Six chronically tracheotomized dogs were induced with either etomidate or thiamylal. Spontaneous ventilation with constant enflurane concentration was maintained. Two hours after induction of anesthesia, isocarbic hypoxia was induced for 20 minutes. Cardiopulmonary and metabolic variables were recorded at specific intervals. The exact sequence was repeated after 1 hour. Cortisol was measured before, during the experiment, and 24 hours later. The experimental protocol was repeated 6 weeks later on the same dog using the other induction agent (thiamylal group versus etomidate group). Two-factor analysis of variance with contrasts tests was used for statistical analysis. The thiamylal group had a significant decrease in minute ventilation, respiratory rate, partial pressure of oxygen in arterial blood, with increases in partial pressure of carbon dioxide in arterial blood, heart rate and cortisol as compared to the etomidate group. Cardiopulmonary and metabolic responses to hypoxia were comparable in both groups. Therefore, acute suppression of cortisol secretion by etomidate did not adversely alter the responses to hypoxia under enflurane anesthesia in dogs.