Effect of gastric mucosa cell turnover on the adaptive cytoprotection in chronic alcohol drinking rat / 中国应用生理学杂志

<p><b>AIM</b>To investigate the correlation between the gastric adaptive cytoprotection and the low concentration alcohol intake in a chronic drinking rat model and the effect of chronic ethanol exposures on the cell turnover of the gastric mucosa and its possible role in adaptive cytoprotection.</p><p><b>METHODS</b>Sprague-Dawley rats received the drinking water containing 6% (v/v) ethanol as their only water intake for 28 days. In the different stages of the 28 days (1st, 3rd, 7th, 14th and 28th days), the stomachs of the rats were cannulated and perfused with pure ethanol, and the severity of mucosal lesions was measured in 2 hours at the end of perfusion respectively. The cell proliferation and apoptosis in gastric mucosa of rats in different groups were analyzed by flow cytometer, immunohistochemistry and computer image analysis.</p><p><b>RESULTS</b>Pure ethanol caused ulcer and haemorrhagic damage in the corpus and antral mucosa of the control rats. These lesions were prevented by pretreatment of the animals with ethanol exposure in the 3 rd to 14 th days. The damage index was decreased by 80%, as compared with those in control rats. There was no significant difference in the rats exposed to the ethanol in the 1st and 28th days. Compared with control, the cell apoptosis in gastric mucosa of the rats was enhanced during they exposure to the ethanol in the 3rd to 28th days. Otherwise the cell proliferation was increased in the 3rd to 28th days, and decreased in the 28th days, respectively.</p><p><b>CONCLUSION</b>Chronic adequate alcohol intake may enhance the cell turnover of gastric mucosa and lead to an adaptive cytoprotection. Long-term stimulus with the low concentration ethanol may cause the atrophy of gastric mucosa and reduce the gastric mucosal cytoprotective effect.</p>

Capsaicin-sensitive afferent fibers and endogenous NO mediate the gastric acid secretion and gastric mucosal blood flow in intragastric distention in rats / 中国应用生理学杂志

<p><b>AIM AND METHODS</b>By hydrogen gas clearance technique to measure gastric mucosal blood flow (GMBF) and a high dose of capsaicin to ablate the capsaicin-sensitive afferent fibers, the roles of capsaicin-sensitive afferent fibers and endogenous NO in the gastric acid secretion and hyperemic response to intragastric distention were studied in rats.</p><p><b>RESULTS</b>(1) There was an increase in acid secretion associated with the increase in GMBF to intragastric distention. (2) Pretreatment with a high dose of capsaicin to ablate afferent fibers completely abolished the GMBF and partially inhibited the acid secretion during the intragastric distention. (3) The increase in GMBF to intragastric distention was completely blocked by pretreatment with L-NAME, whereas the acid secretion was significantly attenuated.</p><p><b>CONCLUSION</b>Capsaicin-sensitive afferent fibers and endogenous NO are involved in the increases of gastric acid secretion and GMBF.</p>

The effects of neuropeptides on the regulations of gastric mucosal blood flow in central nervous system and periphery in rats / 中国应用生理学杂志

<p><b>AIM</b>To investigate the effects of calcitonin gene-related peptide (CGRP), gastrin 17 (G17), bombesin (Bom), met-enkephalin (Met-enk), neuropeptide Y (NPY) and somatostatin (SS) on GMBF and the role of endogenous NO in increased GMBF induced by neuropeptides in rats.</p><p><b>METHODS</b>By hydrogen gas clearance technique to measure gastric mucosal blood flow (GMBF) and arterial infusion close to stomach or intracerebroventricular (icv) to microinject neuropeptides.</p><p><b>RESULTS</b>(1) Arterial infusions of CGRP and G17 (5, 50 and 100 pmol x min(-1)) increased GMBF significantly in dose-dependent manners. CGRP had more effective effect on increasing GMBF than that of G17. Intravenous pretreatment of L-nitro-L-arginine methyl ester (L-NAME) to inhibit the synthesis of endogenous NO could abolish completely or partially the increases in GMBF response to CGRP or G17 respectively. (2) Arterial infusions of Bom and Met-enk (50 and 100 pmol x min(-1)) increased GMBF significantly. The increases in GMBF induced by Bom or Met-enk were abolished completely or partially by pretreatment of L-NAME respectively. (3) Arterial infusion of NPY (5, 50 and 100 pmol x min(-1)) led to reduction of GMBF significantly in a dose-dependent manner. SS (50 and 100 pmol x min(-1)) also reduced GMBF significantly. (4) icv microinjection of CGRP (10 microg) and G17 (10 Microg) increased GMBF significantly. The increases in GMBF induced by icv microinjection of CGRP or G17 were blocked completely or partially respectively by pretreatments with L-NAME. (5) icv microinjection of NPY (10 microg) decreased GMBF significantly.</p><p><b>CONCLUSION</b>Neuropeptides play important roles in the regulation of GMBF in rats and NO is involved in the increase of GMBF induced by some neuropeptides.</p>