The role of endogenous corticotropin‐releasing factor (CRF) in mediating surgery‐induced delay in gastric emptying of a noncaloric solution was studied in rats using intracisternal injection of a CRF antagonist, α‐helical CRF9‐41. Intracisternal injections and surgery (abdominal or trephination) were performed under ether anesthesia. After rats recovered from anesthesia, a methylcellulose phenol red solution was administered oropharyngeally and gastric emptying was measured 20 minutes later. Laparotomy, followed by exteriorization of the cecum for 60 seconds (abdominal surgery), trephination, intracisternal injection, of CRF (130 pmol), and ether exposure alone for 120 to 140 or 70 to 80 seconds, inhibited gastric emptying by 83%, 81%, 60%, 56%, and 32%, respectively, as compared with an untreated control group. Intracisternal injection of α‐helical CRF9‐41 significantly enhanced gastric emptying by 27% and prevented by 79% to 87% the inhibition of gastric emptying induced by intracisternal injection of CRF and ether exposure (70–80 s) alone or combined with abdominal surgery. Intracisternal injection of the CRF antagonist (13–26 nmol) dose dependently prevented ether‐induced (120–140 s) and trephination‐induced inhibition of gastric emptying. These results suggest that central CRF may be involved in mediating the acute postoperative delay in gastric emptying.

Intracisternal injection of ovine corticotropin-releasing factor (CRF) into the pylorus-ligated rat or the rat with gastric fistula resulted in a dose-dependent inhibition of gastric secretion stimulated with pentagastrin or thyrotropin-releasing hormone. When injected into the lateral hypothalamus--but not when injected into the cerebral cortex—CRF suppressed pentagastrin-stimulated acid secretion. The inhibitory effect of CRF was blocked by vagotomy and adrenalectomy but not by hypophysectomy or naloxone treatment. These results indicate that CRF acts within the brain to inhibit gastric acid secretion through vagal and adrenal mechanisms and not through hypophysiotropic effects.