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胆囊收缩素对分离血管灌注大鼠结肠运动的作用机制。

Mechanism of action of cholecystokinin on colonic motility in isolated, vascularly perfused rat colon.

机构信息

Department of Internal Medicine, Cheongju St. Mary's Hospital, Cheongju, Chungcheongbuk-do, Korea.

出版信息

J Neurogastroenterol Motil. 2011 Jan;17(1):73-81. doi: 10.5056/jnm.2011.17.1.73. Epub 2011 Jan 26.

DOI:10.5056/jnm.2011.17.1.73
PMID:21369495
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3042223/
Abstract

BACKGROUND/AIMS: It is generally believed that cholecystokinin (CCK) stimulates colonic motility, although there are controversial reports. It has also been suggested that postprandial peptide YY (PYY) release is CCK-dependent. Using a totally isolated, vascularly perfused rat colon, we investigated: (1) the roles of CCK and PYY on colonic motility, (2) to determine if CCK modulates PYY release from the colon to influence the motility and (3) to clarify whether the action of CCK and PYY on colonic motility is mediated via the influence of cholinergic input.

METHODS

An isolated whole rat colon was used. Luminal pressure was monitored via microtip catheter pressure transducers from proximal and distal colon. After a control period, CCK-8 or PYY was administerd intraarterially with or without an anti-PYY serum, loxiglumide or atropine at 12, 60 and 240 pM. Each dose was given for a period of 15-minute and the contractile response was expressed as % changes over basal. PYY concentration in the portal effluent was determined by radioimmunoassay.

RESULTS

Exogenous CCK-8 increased colonic motility which paralleled the increase in PYY release in the portal effluent. Exogenous PYY also significantly increased colonic motility although it was less potent than CCK. The stimulating effect of CCK-8 was significantly inhibited by an anti-PYY serum, and was completely abolished by loxiglumide, and almost completely abolished by atropine.

CONCLUSIONS

CCK increases colonic motility via CCK(1) receptor and it is mediated partly by PYY. Cholinergic input is required for the increased motility by either PYY or CCK.

摘要

背景/目的:人们普遍认为胆囊收缩素(CCK)会刺激结肠蠕动,尽管也有一些有争议的报告。也有人认为餐后肽 YY(PYY)的释放是 CCK 依赖性的。本研究使用完全分离的血管灌注大鼠结肠,研究了:(1)CCK 和 PYY 对结肠运动的作用,(2)确定 CCK 是否调节 PYY 从结肠释放以影响运动,以及(3)阐明 CCK 和 PYY 对结肠运动的作用是否通过影响胆碱能输入来介导。

方法

使用分离的整个大鼠结肠。通过微tip 导管压力换能器从近端和远端结肠监测腔内腔压力。在对照期后,以 12、60 和 240 pM 的剂量经动脉内给予 CCK-8 或 PYY,同时或不给予抗 PYY 血清、loxiglumide 或阿托品。每个剂量给药 15 分钟,收缩反应表示为相对于基础的百分比变化。通过放射免疫测定法测定门静脉流出物中的 PYY 浓度。

结果

外源性 CCK-8 增加了结肠蠕动,与门静脉流出物中 PYY 释放的增加平行。外源性 PYY 也显著增加了结肠蠕动,尽管其效力低于 CCK。CCK-8 的刺激作用被抗 PYY 血清显著抑制,loxiglumide 完全抑制,阿托品几乎完全抑制。

结论

CCK 通过 CCK(1)受体增加结肠蠕动,部分通过 PYY 介导。无论是 PYY 还是 CCK,增加的运动都需要胆碱能输入。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/27c80f5ba727/jnm-17-73-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/8aac2669580b/jnm-17-73-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/412a3f68e626/jnm-17-73-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/56b06021d606/jnm-17-73-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/6314e80aace6/jnm-17-73-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/902bfe0b5df2/jnm-17-73-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/9a8c456ae120/jnm-17-73-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/d9de96ed9761/jnm-17-73-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/5f2cd4e98a15/jnm-17-73-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/29509066c85c/jnm-17-73-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/27c80f5ba727/jnm-17-73-g010.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/8aac2669580b/jnm-17-73-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/412a3f68e626/jnm-17-73-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/56b06021d606/jnm-17-73-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/6314e80aace6/jnm-17-73-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/902bfe0b5df2/jnm-17-73-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/9a8c456ae120/jnm-17-73-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/d9de96ed9761/jnm-17-73-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/5f2cd4e98a15/jnm-17-73-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/29509066c85c/jnm-17-73-g009.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9b1a/3042223/27c80f5ba727/jnm-17-73-g010.jpg

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本文引用的文献

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Br J Pharmacol. 2004 Apr;141(8):1275-84. doi: 10.1038/sj.bjp.0705769.
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Release of peptide YY by fat in the proximal but not distal gut depends on an atropine-sensitive cholinergic pathway.近端而非远端肠道中的脂肪对肽YY的释放取决于一条对阿托品敏感的胆碱能途径。
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