Evidence for modulation of motilin secretion by pancreatico-biliary juice in health and in chronic pancreatitis.
Evidence for modulation of motilin secretion by pancreatico-biliary juice in health and in chronic pancreatitis.
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在健康和慢性胰腺炎中胰胆汁调节胃动素分泌的证据。
DOI：
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发表时间：
1983
影响因子：
5.8
通讯作者：
A. Vinik
中科院分区：
文献类型：
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作者：
C. Owyang;A. Funakoshi;A. Vinik
胃肠激素胃动素可启动消化间期移行性复合运动。消化间期血浆胃动素样免疫反应性（MLI）水平与胰胆分泌存在同步的周期性变化，二者可能存在因果关系。本研究的目的是研究胰胆分泌物进入肠道作为血浆MLI浓度调节剂的作用。在6名健康受试者中，平均基础血浆MLI水平为130 +/- 16 pg/ml。八肽胆囊收缩素（CCK-8）的输注刺激MLI分泌，具有2028 +/- 340 pg/min X ml的积分（30 min）响应。胰胆液十二指肠内灌注产生了类似的血浆MLI增加，30分钟的综合反应为2190 +/- 270 pg/min X ml。无论是酶活性，渗透压，或pH值占的响应。在6例胰腺外分泌功能不全患者中，尽管他们的平均基础血浆MLI浓度为205 +/- 44 pg/ml，显著高于健康受试者，但输注CCK-8后血浆MLI没有显著增加。这些患者的胰腺外分泌严重受损，脂肪酶峰值（3.8 +/- 0.6 kU/h）和胰蛋白酶峰值（2.4 +/- 0.5 kU/h）输出明显减少即可证明这一点。相比之下，输注从健康受试者获得的胰胆液引起血浆MLI升高，60 min积分反应为3912 +/- 1031 pg/min X ml，与健康受试者的3947 +/- 472 pg/min X ml相似。我们的结论是，有一个不确定的因素，胰胆液刺激MLI的释放。胰腺外分泌的不足可能是慢性胰腺炎中MLI对CCK-8刺激的反应受损的原因。由于已知MLI可启动消化间期移行性运动复合体的形成，继发于胰腺外分泌缺陷的胃动素释放减少可能导致慢性胰腺炎患者胃肠运动活动紊乱。
The gut hormone motilin can initiate the interdigestive migrating motor complex. There are synchronous cyclic changes in plasma motilin-like immunoreactivity (MLI) levels and pancreatico-biliary secretion during the interdigestive period which may be causally related. The purpose of this study was to investigate the role of pancreatico-biliary secretion into the gut as a modulator of plasma MLI concentrations. In six healthy subjects, the mean basal plasma MLI level was 130 +/- 16 pg/ml. Infusion of cholecystokinin octapeptide (CCK-8) stimulated MLI secretion, with an integrated (30 min) response of 2028 +/- 340 pg/min X ml. Intraduodenal perfusion of pancreatico-biliary juice produced a similar increase in plasma MLI, with a 30 min integrated response of 2190 +/- 270 pg/min X ml. Neither enzyme activity, osmolarity, or pH accounted for the response. In six patients with exocrine pancreatic insufficiency, although their mean basal plasma MLI concentration of 205 +/- 44 pg/ml was significantly higher than that observed in healthy subjects, there was no significant plasma MLI increase after CCK-8 infusion. Pancreatic exocrine secretion was severely compromised in these patients, as evidenced by the markedly reduced peak lipase (3.8 +/- 0.6 kU/h) and trypsin (2.4 +/- 0.5 kU/h) outputs. In contrast, infusion of pancreatico-biliary juice obtained from healthy subjects caused a rise in plasma MLI, with a 60 min integrated response of 3912 +/- 1031 pg/min X ml, which was similar to that of 3947 +/- 472 pg/min X ml in healthy subjects. We conclude that there is an undefined factor in pancreatico-biliary juice that stimulates MLI release. A deficiency of pancreatic exocrine secretion may be responsible for the impaired MLI response to CCK-8 stimulation in chronic pancreatitis. Since MLI is known to initiate the formation of the interdigestive migrating motor complexes, diminished motilin release secondary to pancreatic exocrine deficiency may result in disordered gastrointestinal motor activity in patients with chronic pancreatitis.