REGULATION OF GASTRIC-EMPTYING IN HUMANS BY CHOLECYSTOKININ
REGULATION OF GASTRIC-EMPTYING IN HUMANS BY CHOLECYSTOKININ
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DOI：
10.1172/jci112401
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发表时间：
1986-03-01
影响因子：
15.9
通讯作者：
WILLIAMS, JA
中科院分区：
文献类型：
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作者：
LIDDLE, RA;MORITA, ET;WILLIAMS, JA
在本研究中，我们使用了一种生物测定系统来测定血浆中的CCK，以评估CCK是否在调节人体胃排空方面具有生理学作用。测定了5名正常男性志愿者的血浆CCK水平和进食混合流质餐后的胃排空。空腹CCK水平平均为0.8。+-。下午0.1分，增加到6.5分。+-。下午1点，在饮用混合餐点后10分钟内。CCK水平持续升高达90分钟。餐后胃排空缓慢；90min结束时，68%的原始容量仍留在胃中。然后，在同一个体中同时注入生理盐水或两种剂量的CCK(每小时12pmol/kg和24pmol/kg)之一的情况下，测量胃排空水的速率。注入生理盐水后，血浆CCK水平不高于基础水平，胃内容物迅速排空。在90min结束时，胃中只剩下原来容量的7%。较低剂量的CCK导致血浆水平为3.4 pm，这既恢复了餐后平均血浆水平，又导致胃排空显着延迟。较高剂量的CCK达到晚上8点的血浆水平，并导致胃排空延迟，与混合餐的情况相似。由于餐后出现的外源性CCK浓度延迟胃排空，我们得出结论，CCK是胃排空的生理调节因子。
In the present study we used a bioassay system for measuring plasma cholecystokinin (CCK) to evaluate whether CCK has a physiologic role in regulating gastric emptying in humans. Plasma CCK levels and gastric emptying after ingestion of a mixed liquid meal were determined in five normal male volunteers. Fasting CCK levels averaged 0.8 .+-. 0.1 pM and increased to 6.5 .+-. 1.0 pM within 10 min of drinking the mixed meal. CCK levels remained elevated for up to 90 min. Gastric emptying after a meal was slow; at the end of the 90 min 68% of the original volume remained in the stomach. The rate of gastric emptying of water was then measured in the same individuals with a simultaneous infusion of either saline, or one of two doses of CCK (12 pmol/kg per h and 24 pmol/kg per h). With the saline infusion, plasma CCK levels did not increase above basal and gastric contents emptied rapidly. At the end of 90 min only 7% of the original volume remained in the stomach. The lower dose of CCK resulted in a plasma level of 3.4 pM which both reproduced the average postprandial plasma level and caused a significant delay in gastric emptying. The higher dose of CCK achieved plasma levels of 8 pM and resulted in a delay in gastric emptying that was similar to that seen with the mixed meal. Since exogenous CCK at concentrations which occur postprandially delays gastric emptying, we conclude that CCK is a physiologic regulator of gastric emptying.