Gastric mucosal blood flow (GMBF) was measured in the ex vivo stom achs of anesthetized rats simultaneously with mean arterial blood pressure (MBP), luminal pH and transmucosal potential difference (PD) in an attempt to characterize these responses induced by capsaicin. The stomach was mounted on a Lucite cham ber, perfused with saline at the flow rate of 1 ml/min, and GMBF was measured by Laser flowmetry. Under these conditions, the pH, PD and GMBF were 3.5 to 4.0,-30 to-35 mV and 8-12 ml/min/100 g, respectively. Mucosal application of cap saicin (0.03-1 mg/ml for 10 min) increased GMBF in a concentration-dependent manner, without any change in PD, pH and MBP. The increased GMBF response caused by capsaicin was abolished by chemical deafferentation following systemic cap saicin injections (total dose: 100 mg/kg), significantly attenuated by pretreatment with indomethacin (5 mg/kg, sc) or ruthenium red (300, ug/kg, iv), but was not affected by spantide (100, ug/kg, iv), atropine (300 pg/kg, ip) or disodium cromoglycate (30 mg/kg, ip). In addition, when the mucosa was exposed to capsaicin repeatedly, this response showed a marked tachyphylaxis at a high concentration (6 mg/ml). These re sults suggest that intragastric capsaicin increased GMBF selectively through capsaicin sensitive sensory neurons, and this action may involve endogenous prostaglandins.

Capsaicin, a pungent principle of hot red pepper, is a selective stimulant of primary afferent neurons (1-3). Recent studies showed that intragastric capsaicin protects the rat gastric mucosa against various ulcerogenic stimuli (1, 4), while chemical deafferentation by systemic capsaicin injections produces aggravation of lesions in experimental ulcer models (1, 5, 6). However, the mechanism underlying capsaicin-induced gastric protection remains unknown.