ROLE OF MUCOSAL MICROCIRCULATION IN GASTRIC-LESIONS INDUCED BY LATERAL HYPOTHALAMIC-LESIONS IN RATS

To evaluate the pathophysiology underlying gastric mucosal lesions ind uced by lateral hypothalamic (LH) lesions, we investigated the changes in acid secretion, gastric mucosal blood flow, gastric mucus and muco sal integrity in the corpus during the 4 h period and 48 h after the p roduction of bilateral electrolytic LH lesions in male Sprague-Dawley rats. Gastric mucosal lesions were macroscopically produced 24 h (63%) and 48 h (83%) after LH lesions, although there were no visible lesio ns at 7 h. Gastric acid secretion was significantly increased 48 h aft er LH lesions, compared with that in the control group. Gastric mucosa l blood flow and transmucosal potential difference (PD) in the LH lesi on group immediately decreased after LH lesions and did not recover du ring 4 h and at 48 h. On the contrary, in the control group, gastric m ucosal blood flow decreased after the brain surgery but soon recovered , and there was no significant change in PD. LH lesions resulted in th e reduction of intramucosal mucus to 50% 3 h after LH lesions. Moreove r, we exposed the stomach to 10 mmol/L taurocholic acid (TCA) 3 h afte r LH lesions to examine the disruption in gastric mucosal defensive fu nction in rats with LH lesions. The recovery of the reduced PD by TCA was slow and gastric mucosal lesions were easily formed in the LH lesi on group. These results suggest that gastric mucosal ischaemia after l esioning of LH immediately results in the disruption of mucosal defens ive function before the formation of visible gastric lesions, and pred isposes to the formation of gastric mucosal lesions by a delayed incre ase in acid secretion.