Effects of endotoxin on neurally-mediated gastric acid secretion in the rat.

The effects of a peripheral administration of E. coli endotoxin on neurally-mediated gastric acid secretion and the role of endogenous opioids or PAF receptors in endotoxin effects have been evaluated in the continuously perfused stomach of the anaesthetized rat. Gastric acid secretion stimulated by distension (20 cm H2O) was reduced dose-dependently by single intravenous bolus injection of endotoxin (0.1-10 microg kg(-1)). Doses of 5 microg kg(-1) induced a peak reduction of distension-stimulated acid output and significantly reduced the secretory response induced by an intravenous bolus of 2-deoxy-D-glucose (150 mg kg(-1)). This dose of endotoxin did not significantly modify mean systemic arterial blood pressure throughout the experimental period. Pretreatment with the opioid receptor antagonist naloxone (1 mg kg(-1) , i.v.) or the platelet-activating factor (PAF) receptor antagonist WEB 2086 (2 mg kg(-1), i.v.) did not reverse the inhibitory effects of endotoxin (5 microg kg(-1) , i.v.) on acid secretion stimulated by both distension and 2-deoxy-D-glucose. These findings suggest that endotoxin-induced acute inhibition of neurally-mediated acid responses, stimulated by gastric distension or administration of 2-deoxy-D-glucose, do not involve the activation of endogenous opioids or PAF receptors.