Abstract
OBJECTIVE: The object of this study was to investigate the mechanisms of postoperative gastric ileus in an experimental model of abdominal surgery in anesthetized rats. SUMMARY BACKGROUND DATA: Sensory neurons partly mediate postoperative gastric ileus. Among other neuropeptides, sensory neurons contain calcitonin gene-related peptide (CGRP) and release CGRP in response to noxious stimulation. Because CGRP inhibits gastric motility, it was hypothesized that abdominal surgery stimulates sensory neurons, which then releases CGRP, thereby inhibiting gastric motility. METHODS: Postoperative ileus was induced by abdominal surgery. Gastric corpus motility was measured by an intragastric catheter. CGRP action was blocked by CGRP immunoneutralization or by a CGRP receptor antagonist. Spinal sensory neurons were ablated by application of a sensory neurotoxin (capsaicin) to the celiac and superior mesenteric ganglia. RESULTS: Abdominal surgery decreased gastric corpus motility in the first 5 minutes after abdominal surgery by 59 +/- 5% and by 24 +/- 4% during the 1st postoperative hour. Capsaicin pretreatment of the celiac and superior mesenteric ganglia, CGRP immunoneutralization, or CGRP receptor antagonism reversed the postoperative decrease in gastric corpus motility during the 1st postoperative hour by 50%, 100%, and 59%, respectively. CONCLUSIONS: These data indicate that spinal sensory neurons and CGRP partly mediate postoperative gastric ileus. CGRP may be released from spinal sensory neuron terminals in the celiac and superior mesenteric ganglia as part of an extraspinal intestinogastric inhibitory reflex activated by abdominal surgery.