Abstract
A possible defensive mechanism in the basal region of the gastric mucosa was hypothesized in the present study. In vivo microscopy was performed to observe the basal region after thermal injury to the back skin of rats. A donor of nitric oxide, 3‐morpholinosydnonimine hydrochloride (SIN‐1), or a serine protease inhibitor, camostat mesilate, was administered. Anti‐vascular endothelial growth factor (VEGF) neutralizing antibody was administered 5 hours after thermal injury (anti‐VEGF group). Post‐capillary venules could be observed in the basal region of the gastric mucosa (PV‐BGM). The PV‐BGM was dilated 5 hours after thermal injury, and it was reduced by the administration of SIN‐1 or pre‐treatment with camostat mesilate. In the control group, the erosions did not reach the basal region of the gastric mucosa. Most of the erosions healed within 72 hours. Delayed healing was observed in the anti‐VEGF group. In this group, exudation and congestion in the basal region were observed at 24 hours, and ulcer formation was observed at 72 hours after thermal injury. It is thus hypothesized that blood flow of the PV‐BGM increases when superficial mucosal circulation is disturbed. The PV‐BGM can contribute to defensive mechanisms in the basal region of gastric mucosa. The abnormal healing process may disturb the defensive mechanism at the base of the gastric mucosa, thereby resulting in ulcer formation.