Befrits R, Uvnäs-Moberg K, Johansson C
Department of Medicine, Karolinska Hospital, Stockholm, Sweden.
Digestion. 1990;45(1):9-18. doi: 10.1159/000200219.
The role of endogenous prostaglandins as modulators of antral hormone release and gastric acid secretion was studied in the intact human stomach. The subjects (n = 9) received indomethacin prior to gastric perfusion at pH greater than 7 or less than 2 and subsequent vagal stimulation. Indomethacin was also tested against parenteral somatostatin (n = 10) and pentagastrin (n = 8). The release of somatostatin into the circulation was biphasic after vagal stimulation, and the plasma levels were inversely proportional to those of plasma gastrin. Acidification of the gastric antrum from pH greater than 7 to less than 2 increased twofold the basal plasma levels of somatostatin (p less than 0.05) and suppressed basal and vagally stimulated gastrin release (p less than 0.05) and gastric acid secretion (p less than 0.05). Indomethacin prior to acidification had little effect in the basal state. Following stimulation the release of somatostatin increased, as indicated by a twofold elevation of somatostatinlike immunoreactivity in the gastric lumen (p less than 0.05), but there was less inhibition of plasma gastrin (p less than 0.05) and gastric acid secretion (p less than 0.05) as compared to acidification alone. During alkaline gastric perfusion, indomethacin increased circulating somatostatin (p less than 0.05) levels without affecting plasma gastrin or gastric acid. Indomethacin given against intravenously infused somatostatin (0.1 microgram.kg-1.h-1) partially reversed the inhibited gastrin response to vagal stimulation without affecting somatostatin-suppressed gastric acid secretion. The effects of indomethacin against pentagastrin were marginal.
Gastric acidification in man stimulates plasma release of somatostatin in parallel to suppressing gastrin release and gastric acid secretion. Endogenous prostanoids participate to regulate antral hormone interactions and may have dual actions on antral somatostatin, as negative modulators of release and as mediators of somatostatin effects on the gastrin cell. It is suggested that an unrestricted release of antral somatostatin is reflected in the gastric lumen rather than in the circulation.
在内窥镜下的人胃中研究了内源性前列腺素作为胃窦激素释放和胃酸分泌调节剂的作用。受试者（n = 9）在胃灌注前接受消炎痛，胃灌注的pH值大于7或小于2，随后进行迷走神经刺激。消炎痛还与胃肠外注射生长抑素（n = 10）和五肽胃泌素（n = 8）进行了对比测试。迷走神经刺激后，生长抑素释放到循环中呈双相性，血浆水平与血浆胃泌素水平呈反比。胃窦pH值从大于7酸化到小于2，使生长抑素的基础血浆水平增加了两倍（p < 0.05），并抑制了基础和迷走神经刺激引起的胃泌素释放（p < 0.05）以及胃酸分泌（p < 0.05）。酸化前给予消炎痛在基础状态下几乎没有影响。刺激后，生长抑素的释放增加，胃腔内生长抑素样免疫反应性升高两倍表明了这一点（p < 0.05），但与单独酸化相比，血浆胃泌素（p < 0.05）和胃酸分泌（p < 0.05）的抑制作用较小。在碱性胃灌注期间，消炎痛增加了循环中生长抑素（p < 0.05）水平，而不影响血浆胃泌素或胃酸。针对静脉注射生长抑素（0.1微克·千克-1·小时-1）给予消炎痛，部分逆转了迷走神经刺激引起的胃泌素反应受抑制的情况，但不影响生长抑素抑制的胃酸分泌。消炎痛对五肽胃泌素的作用很小。
人体胃酸化刺激生长抑素的血浆释放，同时抑制胃泌素释放和胃酸分泌。内源性前列腺素参与调节胃窦激素相互作用，可能对胃窦生长抑素有双重作用，作为释放的负调节剂和生长抑素对胃泌素细胞作用的介质。提示胃窦生长抑素不受限制的释放反映在胃腔内而非循环中。
