Gastric inflammation triggers hypersensitivity to acid in awake rats

Changes in visceral sensation contribute to the development of dyspepsia. Nonhuman models have previously focused on responses to mechanical stimulation. We studied the response to acid stimulation in the normal and inflamed stomach in rats.

A balloon and gastrostomy catheter were implanted into the stomach. Electromyographic responses to gastric balloon distention or acid administration through the gastrostomy were recorded from the acromiotrapezius muscle. To characterize chemonociceptive pathways, 0.75 mL HCl (0.05-0.3 N) or saline were given intragastrically in controls and animals after vagotomy, splanchnic nerve resection, or chemical denervation with capsaicin. The effect of inflammation was examined after induction of mild diffuse gastritis using iodoacetamide or creating gastric ulcers by injecting 60% acetic acid for 45 seconds into a clamped area of the stomach.

Visceromotor electromyographic responses increased within 2 minutes after HCl administration (0.15 and 0.3 mol/L) but not saline or lower acid concentrations. Vagotomy and pretreatment with capsaicin but not splanchnic nerve resection abolished this response. Prior acid administration did not acutely sensitize animals to subsequent gastric distention. Gastritis and gastric ulcers enhanced the visceromotor responses to intragastric acid.

In awake rats, visceromotor responses to intragastric acid are quantifiable, reliable, and reproducible. Aversive responses to acute noxious chemical stimuli primarily require vagal but not spinal sensory pathways. Injury-induced sensitization to intragastric acid administration is consistent with a potential role of chemical stimulation in triggering dyspeptic symptoms.