人的胆汁分泌。生长抑素、血管活性肠肽和分泌素的作用。

B Nyberg
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引用次数: 0

摘要

在41例胆总管结石手术患者中,通过t管和foley导管与可闭塞的球囊实现了临时胆瘘。为了进一步了解多肽对胆汁分泌的控制作用,我们在术后6-8天分别观察了生长抑素、血管活性肠肽和分泌素三种多肽输注前后的胆汁流量。结果如图17所示:1。在注入生长抑素期间,胆汁分泌减少30%,胆汁脂质输出减少约10%。[14C]-赤藓糖醇清除率降低25%,表明对胆汁酸依赖性小管胆汁分泌有影响(论文1)。血管活性肠肽(VIP)使胆汁分泌增加65%。胆脂浓度降低,但输出量不受影响。碳酸氢盐浓度升高,钠、钾浓度不受影响。VIP输注对[14C]-赤藓糖醇清除率无影响。因此,VIP刺激了小管水平的胆汁分泌(论文二)。VIP使胆汁分泌增加60%,而分泌素又使胆汁分泌增加70%。这两种多肽都不影响胆汁酸的输出。VIP和分泌素都增加了碳酸氢盐的输出,而只有VIP增加了浓度。VIP输注对[14C]-赤四糖醇的清除率没有影响,但分泌素后清除率增加,[14C]-甘露醇的清除率也增加。因此,VIP在小管水平刺激胆汁分泌,而分泌素似乎在小管水平和胆汁酸非依赖性小管水平同时刺激胆汁分泌(Paper III)。而VIP刺激胆汁分泌,生长抑素使其减少约40%。即使在VIP输注期间给予生长抑素,VIP诱导的胆汁分泌也没有减少。VIP增加碳酸氢盐浓度和输出,而生长抑素有相反的效果。注射VIP后氯离子浓度升高,注射生长抑素后氯离子浓度降低。胆汁酸的输出量不受VIP输注的影响,生长抑素降低了胆汁酸的输出量,而总脂质浓度在生长抑素输注期间升高,添加VIP后降低。因此,生长抑素作用于胆汁酸依赖的小管胆汁分泌,在一定程度上也作用于小管分泌。两种多肽对胆汁分泌的影响是相互独立的(论文IV)。禁食时,胆管手术后6-8天,胆汁分泌平均为290微升/分钟。通过[14C]-赤藓糖醇清除率测量,小管胆汁分泌约占总胆汁流量的80%。胆汁酸的最大从头合成为8.7 mmol/24 h,这意味着由于肠肝循环中断而产生了8-9倍的刺激(论文V)。该方法对胆管手术后暂时性胆管瘘无严重副作用。因此,推荐该方法用于人体胆汁分泌的进一步研究(论文V)。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Bile secretion in man. The effects of somatostatin, vasoactive intestinal peptide and secretin.

In 41 patients, operated upon for common bile duct stones, a temporary bile fistula was achieved by means of a T-tube and a Foley-catheter with an occludable balloon. To learn more about peptide control of bile secretion, 6-8 days after surgery, bile flow was studied before as well as during infusion of the three peptides somatostatin, vasoactive intestinal peptide and secretin. The findings, also presented in Figure 17, were: 1. During somatostatin infusion, bile secretion decreased by 30%, and bile lipid output was reduced by some 10%. The clearance of [14C]-erythritol decreased by 25%, indicating an effect on the bile acid-dependent canalicular bile secretion (Paper I). 2. Vasoactive intestinal peptide (VIP) increased bile secretion by 65%. The concentration of bile lipids decreased, whereas the output was uneffected. The bicarbonate concentration increased, and the concentrations of sodium and potassium were uneffected. [14C]-erythritol clearance was not influenced by VIP infusion. Thus, VIP stimulated bile secretion at the ductular level (Paper II). 3. VIP increased bile secretion by 60%, whereupon secretin increased it by another 70%. Neither of the two peptides effected bile acid output. Both VIP and secretin increased bicarbonate output, whereas only VIP increased the concentration. The clearance of [14C]-erythritol was uneffected by VIP infusion, but increased following secretin, as did the clearance of [14C]-mannitol. Thus, VIP stimulated bile secretion at the ductular level, whereas secretin seemed to stimulate bile secretion both at the ductular level and at the bile acid non-dependent canalicular level (Paper III). 4. Whereas VIP stimulated bile secretion, somatostatin decreased it by some 40%. Even when somatostatin was administered during VIP infusion, no reduction of the VIP-induced choleresis was seen. VIP increased both bicarbonate concentration and output, whereas somatostatin had the opposite effect. The concentration of chloride increased following VIP infusion, but decreased following somatostatin. The output of bile acids was not influenced by VIP infusion and decreased by somatostatin, whereas total lipid concentration increased during somatostatin infusion with a decrease when VIP was added. Thus, somatostatin acts on the bile acid-dependent canalicular bile secretion and also, to some extent, on the ductular secretion. The effects of the two peptides on bile secretion are independent of each other (Paper IV). 5. While fasting, 6-8 days after bile duct surgery, bile secretion averaged 290 microliters/min. Canalicular bile secretion, as measured by the clearance of [14C]-erythritol, constituted some 80% of total bile flow. Maximum de novo synthesis of bile acids was 8.7 mmol/24 h, implying a 8-9 fold stimulation due to interrupted enterohepatic circulation (Paper V). 6. No serious side effects from this method with temporary bile fistulas following bile duct surgery were found. Therefore, the method is recommended for further research on human bile secretion (Paper V).

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