Inhibitory effect of atropine on cholecystokinin-induced gallbladder contraction in man.

Inhibitory effect of atropine on cholecystokinin-induced gallbladder contraction in man.
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阿托品对胆囊收缩素诱导的人胆囊收缩的抑制作用。

DOI:
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发表时间:
1984
期刊:
影响因子:
3.2
通讯作者:
G. Labó
G. Labó
中科院分区:
医学3区
文献类型:
--
作者:
L. Gullo;L. Bolondi;P. Priori;P. Casanova;G. Labó

文献摘要

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我们通过实时超声检查研究了阿托品对 7 名健康志愿者胆囊收缩素 (CCK) 诱导的胆囊收缩的影响。两个系列的测试是在不同的日子以随机顺序进行的。在一系列测试中,单独注射 CCK 4 个连续 15 分钟周期,剂量依次增加为 0.0021、0.0042、0.0084 和 0.0168 Ivy 狗单位 (IDU) X kg-1 X min-1。在其他系列的测试中,在激素输注中添加了低剂量阿托品(5微克X kg-1 X h-1)的输注。显着收缩胆囊的CCK最小剂量为0.0042 IDU X kg-1 X min-1。 CCK 输注的最高剂量为 0.0168 IDU X kg-1 X min-1,几乎产生了器官的完全收缩。在所有受试者中,输注阿托品完全阻断了胆囊对 0.0042 和 0.0084 IDU X kg-1 X min-1 的反应,并部分抑制(52%)对最高剂量的反应。在 2 名接受较高剂量阿托品(15 微克 X kg-1 X h-1)的受试者中,即使输注了最大剂量的 CCK,胆囊收缩也完全消失。与普遍认为的相反,结果表明人胆囊对 CCK 的反应很大程度上取决于胆碱能神经支配。
We have studied the effect of atropine on cholecystokinin (CCK)-induced gallbladder contraction in 7 healthy volunteers by means of real-time ultrasonography. Two series of tests were carried out in random order and on separate days. In one series of tests, CCK alone was infused for 4 successive 15-min periods at sequentially increasing doses of 0.0021, 0.0042, 0.0084, and 0.0168 Ivy dog units (IDU) X kg-1 X min-1. In the other series of tests, an infusion of a low dose of atropine, 5 micrograms X kg-1 X h-1, was added to the hormone infusion. The smallest dose of CCK which significantly contracted the gallbladder was 0.0042 IDU X kg-1 X min-1. The highest dose of CCK infused, 0.0168 IDU X kg-1 X min-1, produced almost total contraction of the organ. In all subjects, the infusion of atropine completely blocked the gallbladder response to 0.0042 and 0.0084 IDU X kg-1 X min-1, and partially inhibited (by 52%) the response to the highest dose. In 2 subjects in whom a higher dose of atropine, 15 micrograms X kg-1 X h-1, was tested, gallbladder contraction was totally abolished, even when the largest dose of CCK was infused. Contrary to what is generally believed, the results indicate that the response of human gallbladder to CCK is largely dependent on cholinergic innervation.