CAPSAICIN-SENSITIVE SENSORY NERVES IN RECOVERY OF GASTRIC-MUCOSAL INTEGRITY AFTER DAMAGE BY SODIUM TAUROCHOLATE IN RATS

Citation
K. Takeuchi et al., CAPSAICIN-SENSITIVE SENSORY NERVES IN RECOVERY OF GASTRIC-MUCOSAL INTEGRITY AFTER DAMAGE BY SODIUM TAUROCHOLATE IN RATS, Japanese Journal of Pharmacology, 63(4), 1993, pp. 479-485
Citations number
22
Categorie Soggetti
Pharmacology & Pharmacy
ISSN journal
00215198
Volume
63
Issue
4
Year of publication
1993
Pages
479 - 485
Database
ISI
SICI code
0021-5198(1993)63:4<479:CSNIRO>2.0.ZU;2-2
Abstract
We compared the recovery process of gastric mucosal integrity after da mage by 20 mM sodium taurocholate (TC) in control, sensory deafferente d and indomethacin-treated rats. Under anesthetized conditions, the st omach was mounted on a chamber and perfused with saline or 50 mM HCl. Application of TC (30 min) to the saline-perfused stomach produced a m arked reduction in the potential difference (PD) (surface epithelial d amage), followed by increases of gastric mucosal blood how (GMBF) and luminal pH (alkalinization), but there was a rapid recovery of PD with out development of gross lesions. Chemical ablation of capsaicin-sensi tive sensory nerves had no influence on the PD reduction and luminal a lkalinization, but significantly inhibited the rise in GMBF and the PD recovery. Indomethacin pretreatment (5 mg/kg, s.c.) significantly inh ibited these changes seen after exposure to TC, except for PD reductio n. In contrast, TC caused a sizable amount of H+ back-diffusion and a more pronounced and persistent rise in GMBF in the stomach perfused wi th 50 mM HCl, yet only minimal damage was observed in the control anim als. Under these conditions, both sensory deafferentation and indometh acin inhibited such GMBF responses, leading to hemorrhagic damage with out affecting the degree of H+ back-diffusion. These results suggest t hat capsaicin-sensitive sensory nerves contribute to the recovery of g astric mucosal integrity after damage, probably by maintaining GMBF re sponses associated with H+ back-diffusion and preventing the later ext ension to gross damage in the presence of acid.