Myers S I, Bartula L, Kalley-Taylor B
Department of Surgery, University of Texas Southwestern Medical School, Dallas.
Prostaglandins Leukot Essent Fatty Acids. 1992 Sep;47(1):35-9. doi: 10.1016/0952-3278(92)90183-j.
The relationship of bradykinin and cholecystokinin (CCK) to inflamed gallbladder prostanoid synthesis and release was examined in rabbits treated with common bile duct ligation (BDL) for 24 or 72 h. Gallbladders removed from control and BDL groups were incubated in oxygenated Krebs buffer at 37 degrees C (pH 7.4) for 60 min. The slices were then placed every 20 min in vials containing increasing doses of bradykinin (30-3000 ng) or CCK (30-1000 ng). Incubation fluid was analyzed by RIA for 6-keto-prostaglandin (PG)F1 alpha (PGI2 metabolite), PGE2 and thromboxane (TX) B2. Bradykinin stimulated control gallbladder 6-keto-PGF1 alpha and PGE2 release was modest. Gallbladders from 24- and 72-h BDL groups released 3- to 10-fold higher levels of 6-keto-PGF1 alpha and PGE2 (not TXB2) following bradykinin stimulation when compared to controls, which was abolished with indomethacin pretreatment. CCK did not stimulate gallbladder prostanoid release in the control or BDL groups. These data show that bradykinin and not CCK stimulated PGI2 and PGE2 release from inflamed rabbit gallbladder. Increased BDL gallbladder PGI2 release may be prolonged or augmented by bradykinin as gallbladder distention and progressive acute inflammation stimulate local bradykinin formation.
在接受胆总管结扎（BDL）24或72小时的兔子中，研究了缓激肽和胆囊收缩素（CCK）与炎症胆囊前列腺素合成和释放的关系。从对照组和BDL组取出的胆囊在含氧量充足的Krebs缓冲液中于37摄氏度（pH 7.4）孵育60分钟。然后每隔20分钟将切片放入含有递增剂量缓激肽（30 - 3000纳克）或CCK（30 - 1000纳克）的小瓶中。通过放射免疫分析法（RIA）分析孵育液中的6 - 酮 - 前列腺素（PG）F1α（前列环素I2代谢物）、前列腺素E2和血栓素（TX）B2。缓激肽刺激对照组胆囊释放6 - 酮 - PGF1α和前列腺素E2的量适中。与对照组相比，来自24小时和72小时BDL组的胆囊在缓激肽刺激后释放的6 - 酮 - PGF1α和前列腺素E2（而非血栓素B2）水平高出3至10倍，吲哚美辛预处理可消除这种差异。CCK在对照组或BDL组中均未刺激胆囊前列腺素的释放。这些数据表明，刺激炎症兔胆囊释放前列环素I2和前列腺素E2的是缓激肽而非CCK。随着胆囊扩张和进行性急性炎症刺激局部缓激肽形成，缓激肽可能会延长或增强BDL胆囊前列环素I2的释放。
