Olazábal A
Gastroenterology. 1983 May;84(5 Pt 1):928-34.
Alterations in the permeability and histology of the pancreatic ductal mucosa have been demonstrated in the cat after an intraductal infusion of deoxycholic acid. In order to define the role of prostaglandins in the pathogenesis of the mucosal lesion, an isotonic electrolyte solution was perfused through a segment of the pancreatic duct of anesthetized rats for 1 h, before and after a 10-min perfusion with 10 mM deoxycholic acid. Prostaglandin E2 or I2 was infused (intraarterially, intravenously, or intraductally) for 30 min beginning 20 min before deoxycholic acid infusion. Indomethacin (5 mg/kg intravenously) was given 30 min before deoxycholic acid. Deoxycholic acid increased ductal permeability and produced severe epithelial necrosis. Neither prostaglandin nor indomethacin affected the alterations induced by deoxycholic acid. In the experimental model tested, neither inhibition of prostaglandin synthesis nor administration of exogenous prostaglandins altered the effects of deoxycholic acid.
在猫身上,经导管内注入脱氧胆酸后,已证实胰管黏膜的通透性和组织学发生了改变。为了确定前列腺素在黏膜病变发病机制中的作用,在给麻醉大鼠的一段胰管灌注10 mM脱氧胆酸10分钟之前和之后,用等渗电解质溶液灌注该段胰管1小时。在注入脱氧胆酸前20分钟开始,经动脉、静脉或导管内注入前列腺素E2或I2 30分钟。在注入脱氧胆酸前30分钟静脉注射吲哚美辛(5毫克/千克)。脱氧胆酸增加了导管通透性并导致严重的上皮坏死。前列腺素和吲哚美辛均未影响脱氧胆酸诱导的改变。在所测试的实验模型中,抑制前列腺素合成或给予外源性前列腺素均未改变脱氧胆酸的作用。