Primary sensory nerves mediate in part the protective mesenteric hyperemia after intraduodenal acidification in rats.

Abstract

The mechanism of intraduodenal HCl-induced mesenteric hyperemia is unknown. In anesthetized rats, the hypothesis that the primary sensory nerves mediate the intraduodenal HCl-induced protective mesenteric hyperemia was tested. The hyperemic response in the superior mesenteric artery (SMA) and superficial villus damage after intraduodenal bolus administration of saline, 0.03N, or 0.1N HCl were measured. These changes induced by 0.1N HCl after mucosal anesthesia (1% lidocaine) or afferent nerve ablation (125 mg/kg subcutaneous capsaicin) were evaluated. The duodenal villus damage induced by intraduodenal perfusion of 0.1N HCl after mucosal afferent nerve stimulation by intraduodenal capsaicin or afferent nerve ablation by subcutaneous capsaicin was examined. Intraduodenal bolus administration of HCl produced a dose-related increase in SMA blood flow and villus tip damage. The mesenteric hyperemia induced by 0.1N HCl was significantly reduced, but the villus tip damage was not altered by prior intraduodenal lidocaine or subcutaneous capsaicin. The deep duodenal villus damage produced by intraduodenal perfusion of 0.1N HCl was decreased by intraduodenal but increased by subcutaneous capsaicin. The capsaicin-sensitive afferent nerves mediate in part the HCl-induced mesenteric hyperemia. They protect against the deep but not the superficial duodenal villus damage induced by HCl.