Li Yong-Yu
Department of Pathophysiology, Medical College of Tongji University, Shanghai 200331, China.
World J Gastroenterol. 2003 Jan;9(1):129-33. doi: 10.3748/wjg.v9.i1.129.
To investigate the intragastric mechanisms for regulation of gastric neuroendocrine functions during gastric distention in isolated vascularly perfused rat stomach.
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.
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.
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.
研究在离体血管灌注大鼠胃中，胃扩张期间调节胃神经内分泌功能的胃内机制。
制备离体血管灌注大鼠胃，然后在20分钟内用5、10或15毫升pH7等渗盐水扩张胃腔。在扩张期间，通过血管灌注应用轴突阻滞剂河豚毒素（TTX）、胆碱能拮抗剂阿托品或假定的生长抑素拮抗剂环（7-氨基庚酰基-苯丙氨酸-D-色氨酸-赖氨酸-苏氨酸（苄基））。然后通过放射免疫分析法检测胃泌素和生长抑素的释放。
分级胃扩张导致胃泌素分泌显著呈体积依赖性下降（-183±75（5毫升）、-385±86（10毫升）和-440±85（15毫升）皮克/20分钟），生长抑素分泌显著增加（260±102（5毫升）、608±148（10毫升）和943±316（15毫升）皮克/20分钟）。响应10毫升扩张，输注轴突阻滞剂TTX（10⁻⁶摩尔/升）或胆碱能阻滞剂阿托品（10⁻⁷摩尔/升）有类似作用。它们都使胃泌素释放的减少减弱约50%，使生长抑素释放的增加减弱约40%。输注生长抑素拮抗剂环（7-氨基庚酰基-苯丙氨酸-D-色氨酸-赖氨酸-苏氨酸（苄基））（10⁻⁶摩尔/升）使胃泌素释放的减少减弱约60%。此外，生长抑素拮抗剂和阿托品联合输注完全消除了扩张诱导的胃泌素释放抑制。
目前的数据表明，离体大鼠胃的扩张通过胆碱能和非胆碱能TTX不敏感途径刺激生长抑素释放。生长抑素和内在胆碱能途径均参与扩张诱导的胃泌素释放抑制。
