Kuroda T, Sodeyama H, Hanazaki K, Horigome N, Kajikawa S, Yamagishi K, Horiuchi A, Iwatsuki K, Chiba S, Homma T
Department of Surgery, Shinshu University School of Medicine, Matsumoto, Japan.
Pancreas. 1989;4(6):702-7. doi: 10.1097/00006676-198912000-00008.
The involvement of endogenous prostaglandins (PGs) in pancreatic endocrine and exocrine secretion was investigated, using the isolated and perfused dog pancreas. Spontaneous production of both PGE2 and 6-keto-PGF1 alpha was recorded in venous effluent. Prostaglandin production increased following stimulation with both 10 x 10(-11) and 20 x 10(-11) mol of CCK-8, but was not affected by a 5 x 10(-11) mol infusion. Insulin, glucagon, and amylase release was stimulated by 10 x 10(-11) mol of CCK-8. Indomethacin pretreatment with 10 mg/kg totally abolished endogenous PG production, but failed to suppress an insulin and glucagon response. On the other hand, an amylase response was accelerated by indomethacin pretreatment. Although low dose CCK-8 failed to stimulate endogenous prostaglandin production, a brisk exocrine secretion was not suppressed by indomethacin pretreatment. From the above results, we conclude that endogenous PGs do not appear to play an important role in pancreatic endocrine and exocrine secretion, but might have a cytoprotective effect on the pancreatic acinar cells damaged by CCK-8.
利用离体灌注的犬胰腺，研究内源性前列腺素（PGs）在胰腺内分泌和外分泌中的作用。在静脉流出液中记录到PGE2和6-酮-PGF1α的自发产生。用10×10⁻¹¹和20×10⁻¹¹摩尔的CCK-8刺激后，前列腺素的产生增加，但5×10⁻¹¹摩尔的输注未对其产生影响。10×10⁻¹¹摩尔的CCK-8刺激胰岛素、胰高血糖素和淀粉酶的释放。10mg/kg的吲哚美辛预处理完全消除了内源性PG的产生，但未能抑制胰岛素和胰高血糖素的反应。另一方面，吲哚美辛预处理加速了淀粉酶的反应。虽然低剂量的CCK-8未能刺激内源性前列腺素的产生，但吲哚美辛预处理并未抑制旺盛的外分泌。根据上述结果，我们得出结论，内源性PGs似乎在胰腺内分泌和外分泌中不发挥重要作用，但可能对CCK-8损伤的胰腺腺泡细胞具有细胞保护作用。
