ACTH and cortisol responses to hypoxia in dogs

Publisher Website
Google Scholar
Abstract
To determine the role of endogenous ACTH and hyperventilation in the adrenocortical response to hypoxia, pentobarbital-anesthetized dogs equipped with left adrenal venous cannulas for measurement of cortisol secretion rate (CSR) and arterial cannulas for measurement of plasma ACTH were exposed to 20 min of normoxia (group I), spontaneous ventilation, normocapnic hypoxic hypoxia (group II), controlled ventilation, normocapnic hypoxic hypoxia (group III), controlled ventilation, normocapnic CO hypoxia (group IV) or hypoxic hypoxia with elevated HbCO (group V). Group I showed no change in ACTH and CSR. Groups II and III greatly increased CSR; only group III increased ACTH significantly. Group IV greatly increased ACTH; CSR increased but less than group III. Group V showed a significant increase in ACTH but no significant CSR response. ACTH (5 U was also) infused in several animals from groups I, III and IV. Exogenous ACTH caused increases in CSR that were larger in group I than groups III and IV. Apparently, ACTH in arterial blood is not the sole controller of CSR during hypoxic stress.