Abstract
Background—Epidermal growth factor (EGF) and capsaicin protect against experimental gastric mucosal injury. Capsaicin exerts its gastroprotective effect by stimulating afferent neurones leading to release of calcitonin gene related peptide (CGRP) which causes gastric hyperaemia. EGF also causes gastric hyperaemia but whether it acts via capsaicin sensitive neurones is unknown. Aims—To assess the influence of: (1) capsaicin desensitisation on EGF effects on gastric mucosal injury and gastric mucosal blood flow; and (2) close arterial infusion of hCGRP8-37, a CGRP antagonist, on EGF effects on gastric mucosal blood flow. Methods—The absolute ethanol induced gastric mucosal injury model in the rat was used. Gastric mucosal damage was assessed by planimetry and light microscopy. Gastric mucosal blood flow was measured by laser Doppler flowmetry in a gastric chamber preparation. Results—Capsaicin desensitisation abolished the gastroprotective and gastric hyperaemic effects of EGF. Close arterial infusion of hCGRP8-37 antagonised the hyperaemic effect of both capsaicin and EGF. Conclusion—Results show that EGF may exert its gastroprotective and gastric hyperaemic effects via capsaicin sensitive afferent neurones.
Keywords: capsaicin; epidermal growth factor; gastric mucosal injury; gastric mucosal blood flow; calcitonin gene related peptide antagonist; rat
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Figure 1 .

Effect of EGF, capsaicin, and their combination on gastric mucosal blood flow. (A) Animals with intact innervation; (B) capsaicin desensitised animals; (C) data shown as areas under the curve. Results are expressed as mean (SEM), n=8 per group.
Figure 2 .

Effect of close arterial infusion of hCGRP8-37 on the gastric hyperaemic response to EGF and capsaicin. (A) Vehicle; (B) concomitant infusion of hCGRP8-37 (500 pmol/kg/min); (C) data shown as areas under the curve.
Selected References
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