Inhibition by pentobarbital of ether-induced ACTH secretion in the rat.

Abstract

Ether anesthesia is a powerful stimulus for ACTH release, apparently acting directly on the hypothalamic median eminence. Pentobarbital anesthesia does not cause ACTH release and does not block increased ACTH secretion produced by traumatic stress. The following studies were performed to see if pentobarbital would prevent ether activation of ACTH release, measured indirectly by plasma corticosterone levels. A 2-min ether inhalation induced a 5-fold rise in plasma corticosterone in 15 min. This response was prevented by 3.5–5 mg/100 g pentobarbital ip 30 min prior to ether. To delineate the site of action of pentobarbital, chronic (11–20 day) basal hypothalamic-pituitary island preparations were made in which all neural connections of the basal hypothalamus with the remaining brain were severed. The chronic island rats had high resting plasma corticosterone levels which increased after ether. If pentobarbital was given, plasma corticosterone decreased to approximately the basal level of intact rats. Subseq...