Schubert M L, Edwards N F, Makhlouf G M
Department of Medicine, Medical College of Virginia, Richmond.
Gastroenterology. 1988 Feb;94(2):317-22. doi: 10.1016/0016-5085(88)90418-0.
The present study was designed to determine whether somatostatin secretion induced by histamine or pentagastrin in the isolated luminally perfused mouse stomach was a direct effect of the secretagogues on gastric somatostatin cells or an indirect effect mediated by the increase in luminal acidity. Perfusion of the lumen with exogenous acid (80-480 nmol/min) caused an increase in somatostatin secretion in proportion to the increase in luminal acidity. The increase in somatostatin secretion was resistant to tetrodotoxin and attained maximal levels (61.6% +/- 8.7% above basal level) similar to those elicited by maximal doses of secretagogues. Conversely, neutralization of basal acid secretion with bicarbonate (20-160 nmol/min) caused a decrease in somatostatin secretion in proportion to the decrease in luminal acidity. Similarly, neutralization of the secretagogue-induced increments in acid secretion with bicarbonate or inhibition of the increments with cimetidine abolished the corresponding increments in somatostatin secretion. It is proposed that acid-induced release of somatostatin in proximity to parietal cells serves as a negative feedback mechanism restraining acid secretion.
本研究旨在确定在离体的经腔内灌注的小鼠胃中，组胺或五肽胃泌素诱导的生长抑素分泌是促分泌剂对胃生长抑素细胞的直接作用，还是由腔内酸度增加介导的间接作用。用外源酸（80 - 480 nmol/分钟）灌注腔，导致生长抑素分泌随着腔内酸度的增加而成比例增加。生长抑素分泌的增加对河豚毒素有抗性，并且达到了与最大剂量促分泌剂引起的水平相似的最大水平（比基础水平高61.6%±8.7%）。相反，用碳酸氢盐（20 - 160 nmol/分钟）中和基础酸分泌，导致生长抑素分泌随着腔内酸度的降低而成比例减少。同样，用碳酸氢盐中和促分泌剂诱导的酸分泌增加或用西咪替丁抑制该增加，消除了生长抑素分泌的相应增加。有人提出，壁细胞附近酸诱导的生长抑素释放作为一种负反馈机制抑制酸分泌。
