Cholecystokinin induced protection against gastric injury is independent of endogenous somatostatin. Mercer, David W., Klaus Klemm, James M. Cross, Gregory S. Smith, Mary Cashman, and Thomas A. Miller. Department of Surgery, University of Texas - Houston, Medical School, Houston, Texas 77030
APStracts 3:0078G, 1996.
Cholecystokinin (CCK) prevents macroscopic injury to the stomach from luminal irritants by an unknown mechanism. The present study was undertaken in conscious rats to ascertain what role gastric mucosal blood flow, sensory neurons, and endogenous somatostatin play in CCK -induced gastric protection. Subcutaneous administration of CCK (10 -100 [mu]g/kg) significantly reduced macroscopic injury to the acid secreting portion of the stomach caused by 1 ml of orally administered acidified ethanol (150 mM HCl/50% ethanol) and augmented gastric mucosal blood flow (fluorescent microspheres) in a dose dependent fashion. However, while the protective response to CCK (100 [mu]g/kg) was still present at 2 hours, the blood flow response had returned to baseline by 45 minutes. Ablation of capsaicin sensitive afferent neurons with capsaicin (125 mg/kg SC) did not negate CCK -induced protection. Pretreatment with exogenous somatostatin (1 pmol - 1 nmol/kg SC) failed to prevent the damaging effects of acidified ethanol to gastric mucosa. Immunoneutralization of endogenous somatostatin with somatostatin monoclonal antibody (2 mg IP) did not reverse the protective actions of CCK. Thus, the data suggest that while CCK may prepare the gastric mucosa to withstand a damaging insult by augmenting gastric mucosal blood flow, its protective mechanism is independent of intact sensory neurons and endogenous somatostatin. 

Received 2 May 1995; accepted in final form 19 March 1996.
APS Manuscript Number G182-5.
Article publication pending Am. J. Physiol. (Gastrointest. Liver
Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 16 April 96