Myers S I, Inman L R, Kalley-Taylor B, Riva A, Bartula L
Department of Surgery, University of Texas Southwestern Medical Center, Dallas 75235-9031.
Prostaglandins. 1994 Jul;48(1):53-66. doi: 10.1016/0090-6980(94)90096-5.
The stimulus for increased gallbladder eicosanoid synthesis during cholecystitis is unknown. This study examines the hypothesis that increased intragallbladder pressure stimulates endogenous gallbladder eicosanoid release. Rabbit gallbladders were perfused in vitro at 1 ml/minute with oxygenated Krebs-Henseleit buffer and subjected to 0, 12 or 24 mm Hg of intraluminal gallbladder pressure. Release of 6-keto-PGF1 alpha infinity PGE2 and thromboxane B2 were measured in all groups after 15 and 30 and 60 minutes of perfusion by enzyme immunoassay and gallbladders were examined histologically. Increasing intraluminal gallbladder pressure concomitantly increased gallbladder 6-keto-PGF1 alpha release 2 fold or more at all time of perfusion and altered gallbladder mucosal architecture by increasing basolateral edema in the submucosal space. Infusion of indomethacin (10 micrograms/ml in the perfusion media) decreased 6-keto-PGF1 alpha release from the in vitro perfused gallbladders subjected to 24 mm Hg by 70%. Increased gallbladder eicosanoid release during early cholecystitis may in part be related to the physical force of increased gallbladder intraluminal pressure on the gallbladder mucosa.
胆囊炎期间胆囊类花生酸合成增加的刺激因素尚不清楚。本研究检验了以下假设：胆囊内压升高会刺激内源性胆囊类花生酸释放。兔胆囊在体外以1毫升/分钟的速度用含氧的克雷布斯 - 亨塞尔特缓冲液灌注，并承受0、12或24毫米汞柱的胆囊腔内压力。灌注15、30和60分钟后，通过酶免疫测定法测量所有组中6 - 酮 - PGF1α、PGE2和血栓素B2的释放，并对胆囊进行组织学检查。增加胆囊腔内压力在灌注的所有时间点均使胆囊6 - 酮 - PGF1α释放增加2倍或更多，并通过增加黏膜下层基底外侧水肿改变了胆囊黏膜结构。在灌注介质中输注吲哚美辛（10微克/毫升）使承受24毫米汞柱压力的体外灌注胆囊的6 - 酮 - PGF1α释放减少70%。早期胆囊炎期间胆囊类花生酸释放增加可能部分与胆囊腔内压力升高对胆囊黏膜的物理作用力有关。
