摘要
AIM: To investigate the intragastric mechanisms forregulation of gastric neuroendocrine functions during gastricdistention in isolated vascularly perfused rat stomach.METHODS: Isolated vascularly perfused rat stomach wasprepared, then the gastric lumen was distended with either5,10 or 15 ml pH7 isotonic saline during a period of 20 min.During the distention, the axonal blocker tetrodotoxin (TTX),the cholinergic antagonist atropine, or the putativesomatostatin-antagonist cyclo [7-aminoheptanoyl-Phe-D-Trp-Lys-Thr(Bzl)] were applied by vascular perfusion. Thereleases of gastrin and somatostatin were then examinedby radioimmunoassay.RESULTS: The graded gastricdistention caused a significantvolume-dependent decrease in gastrin secretion [-183±75 (5ml), -385±86 (10 ml) and -440±85 (15 ml) pg/20 min] and asignificant increase of somatostatin secretion [260±102 (5 ml),608±148 (10 ml) and 943±316 (15 ml) pg/20 min]. In responseto 10 ml distention, the infusion of either axonal blocker TTX(10-6 M) or cholinergic blocker atropine (10-7 M) had a similaraffect. They both attenuated the decrease of gastrin releaseby approximately 50 %, and attenuated the increase ofsomatostatin release by approximately 40 %. The infusion ofsomatostatin-antagonist cyclo [7-aminoheptanoyl-Phe-D-Trp-Lys-Thr (Bzl)] (10-6M) attenuated the decrease of gastrin releaseby about 60 %. Furthermore, combined infusion of thesomatostatin-antagonist and atropine completely abolisheddistention-induced inhibition of gastrin release.CONCLUSION: The present data suggest that distention ofisolated rat stomach stimulates somatostatin release viacholinergic and non-cholinergic TTX-insensitive pathways. Bothsomatostatin and intrinsic cholinergic pathways are responsiblefor distention-induced inhibition of gastrin release.
AIM:To investigate the intragastric mechanisms for regulation of gastric neuroendocrine functions during gastric distention in isolated vascularly perfused rat stomach. METHODS:Isolated vascularly perfused rat stomach was prepared,then the gastric lumen was distended with either 5,10 or 15 ml pH7 isotonic saline during a period of 20 min. During the distention,the axonal blocker tetrodotoxin(TTX), the cholinergic antagonist atropine,or the putative somatostatin-antagonist cyclo[7-aminoheptanoyl-Phe-D-Trp- Lys-Thr(Bzl)]were applied by vascular perfusion.The releases of gastrin and somatostatin were then examined by radioimmunoassay. RESULTS:The graded gastric distention caused a significant volume-dependent decrease in gastrin secretion[-183±75(5 ml),-385±86(10 ml)and -440±85(15 ml)pg/20 min]and a significant increase of somatostatin secretion[260±102(5 ml), 608±148(10 ml)and 943±316(15 ml)pg/20 min].In response to 10 ml distention,the infusion of either axonal blocker TTX (10^(-6)M)or cholinergic blocker atropine(10^(-7)M)had a similar affect.They both attenuated the decrease of gastrin release by approximately 50%,and attenuated the increase of somatostatin release by approximately 40%.The infusion of somatostatin-antagonist cyclo[7-aminoheptanoyl-Phe-D-Trp- Lys-Thr(Bzl)](10^(-6)M)attenuated the decrease of gastrin release by about 60%.Furthermore,combined infusion of the somatostatin-antagonist and atropine completely abolished distention-induced inhibition of gastrin release. CONCLUSION:The present data suggest that distention of isolated rat stomach stimulates somatostatin release via cholinergic and non-cholinergic TTX-insensitive pathways.Both somatostatin and intrinsic cholinergic pathways are responsible for distention-induced inhibition of gastrin release.
