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十二指肠前机制可完全代偿胰腺酶缺乏,从而在餐后刺激胆囊。

Preduodenal mechanisms compensate completely for absent pancreatic enzymes to stimulate gallbladder after meals.

作者信息

Meyer J H, Hlinka M, Jehn D, Gu Y G

机构信息

Department of Medicine, VA Medical Center, Sepulveda, California, USA.

出版信息

Dig Dis Sci. 1995 Apr;40(4):739-44. doi: 10.1007/BF02064971.

Abstract

We studied gallbladder emptying with gamma scintigraphy in nine dogs prepared with chronic pancreatic fistulas, so that pancreatic enzymes could be either completely excluded from the duodenum or supplied in normal amounts. During duodenal perfusion of the fasted dogs with fat emulsions, gallbladder emptying was significantly less rapid when the emulsion contained inactive vs active enzymes, confirming the potency of lipolytic products in the intestine as stimuli of gallbladder emptying. However, after feeding either a 115-g or a 460-g meal, each 18% fat, the gallbladders emptied identically whether or not pancreatic enzymes were excluded from the duodenum. We concluded that while products of pancreatic lipolysis in the small intestine are potent stimuli of gallbladder contraction, preduodenal mechanisms can compensate completely for the absence of pancreatic hydrolysis in stimulating gallbladder emptying after a meal.

摘要

我们用γ闪烁扫描术研究了9只患有慢性胰瘘的狗的胆囊排空情况,以便使胰酶要么完全不进入十二指肠,要么以正常量供应。在给空腹的狗十二指肠灌注脂肪乳剂时,当乳剂中含有无活性酶而非活性酶时,胆囊排空明显较慢,这证实了肠内脂解产物作为胆囊排空刺激物的效力。然而,在喂食含18%脂肪的115克或460克餐食后,无论十二指肠是否排除胰酶,胆囊的排空情况相同。我们得出结论,虽然小肠中胰脂肪分解产物是胆囊收缩的有效刺激物,但餐前机制可以完全补偿餐后刺激胆囊排空时胰水解作用缺失的影响。

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