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梗阻性急性胰腺炎时循环中胆囊收缩素增加。I. 伴有和不伴有胰管梗阻的胆管梗阻

Increased circulating cholecystokinin in obstruction-induced acute pancreatitis. I. Bile duct obstruction with and without pancreatic duct obstruction.

作者信息

Murayama K M, Samuel I, Toriumi Y, Solomon T E, Turkelson C M, Joehl R J

机构信息

Surgical Service, Veterans Affairs Lakeside Medical Center, Chicago, Illinois.

出版信息

J Surg Res. 1993 Feb;54(2):126-31. doi: 10.1006/jsre.1993.1019.

Abstract

Bile exclusion from the gut exacerbates pancreatic duct obstruction-induced acute pancreatitis. We hypothesized that obstruction-induced acute pancreatitis involves an increase in circulating cholecystokinin (CCK), as bile and pancreatic juice exclusion from the gut stimulates duodenal CCK release. We studied 54 rats after the following operations: (1) sham operation (n = 18), (2) hepatic bile duct obstruction alone (n = 18), (3) hepatic bile duct and common bile-pancreatic duct obstruction (n = 18). Rats recovered and were killed in subgroups of six rats each at 3, 6, and 18 hr after operation; blood was collected for measurement of plasma CCK and amylase concentrations. Each pancreas was excised, weighed, and processed for histological examination; an acute pancreatitis score was determined. Combined bile and pancreatic duct obstruction induced acute pancreatitis and was associated with a marked increase of circulating CCK concentration. Bile duct obstruction alone did not induce acute pancreatitis but was associated with an increase of circulating CCK of lower magnitude. The time course of circulating CCK increase showed an early peak. These findings support our hypothesis and suggest that CCK plays a role in the pathogenesis of obstruction-induced acute pancreatitis.

摘要

肠道胆汁排除会加剧胰管阻塞诱导的急性胰腺炎。我们推测,阻塞诱导的急性胰腺炎涉及循环中胆囊收缩素(CCK)的增加,因为肠道胆汁和胰液排除会刺激十二指肠CCK释放。我们对54只大鼠进行了以下手术后进行研究:(1)假手术(n = 18),(2)单纯肝胆管阻塞(n = 18),(3)肝胆管和胆总管 - 胰管阻塞(n = 18)。大鼠恢复后,在术后3、6和18小时以每组6只大鼠的亚组形式处死;采集血液以测量血浆CCK和淀粉酶浓度。切除每个胰腺,称重并进行组织学检查;确定急性胰腺炎评分。胆管和胰管联合阻塞诱导了急性胰腺炎,并与循环CCK浓度的显著增加相关。单纯胆管阻塞未诱导急性胰腺炎,但与循环CCK的较小幅度增加相关。循环CCK增加的时间进程显示出早期峰值。这些发现支持了我们的假设,并表明CCK在阻塞诱导的急性胰腺炎发病机制中起作用。

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