Mechanism of cholecystokinin-induced contraction of the opossum gallbladder.
Mechanism of cholecystokinin-induced contraction of the opossum gallbladder.
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胆囊收缩素引起负鼠胆囊收缩的机制。
DOI：
10.1016/0016-5085(90)90348-5
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发表时间：
1990
期刊：
影响因子：
29.4
通讯作者：
Takahashi,I
中科院分区：
文献类型：
--
作者：
Hanyu,N;Dodds,WJ;Layman,RD;Hogan,WJ;Chey,WY;Takahashi,I
本研究评估了清醒负鼠胆囊收缩素诱导胆囊收缩的机制。 19 种慢性动物制剂中的每一种都具有用于监测胆囊体积变化的留置胆囊插管和用于施用缩胆囊素八肽和药物的颈静脉导管。十二指肠内导管允许十二指肠内输注 Isocal（Mead Johnson Laboratories，Evansville，Ind.）。胃、十二指肠和空肠中的双极电极能够监测十二指肠迁移肌电复合体循环。在第 3 期十二指肠迁移性肌电复合体活动停止后 20 分钟，开始输注一小时缩胆囊素八肽 (10 ng/kg/min)、十二指肠内 Isocal (0.4 ml/min) 或喂养。在八肽胆囊收缩素输注、Isocal 输注或喂养开始前 10 分钟和后 20 分钟，静脉推注潜在药理拮抗剂。每个测试挑战在 30 分钟时诱导约 60% 的胆囊排空，在 60 分钟时诱导约 70% 的胆囊排空。胆囊收缩素八肽诱导的胆囊排空被六甲铵转化为充盈，并且几乎被阿托品消除。通过喂养或十二指肠输注 Isocal 诱导的胆囊排空也获得了类似的结果。酚妥拉明在 30 分钟时引起胆囊收缩素八肽诱导的胆囊收缩适度减少，而餐后或 Isocal 诱导的胆囊收缩不受影响。胆囊收缩素八肽诱导的胆囊收缩不受哌仑西平、4-二苯乙酰氧基-N-甲基哌啶甲碘、哌唑嗪、吡拉明、西咪替丁、美西麦角、纳洛酮或普萘洛尔的影响。在麻醉动物的急性研究中，Dloa 静脉推注胆囊收缩素八肽（800 ng/kg）诱导的胆囊收缩不会被六甲铵、阿托品或河豚毒素拮抗。结论是（a）胆囊收缩素诱导的负鼠胆囊生理收缩是通过神经机制发生的，而不是胆囊收缩素对胆囊平滑肌的直接作用，（b）使用药理推注剂量的胆囊收缩素八肽和河豚毒素的研究表明，胆囊收缩素受体存在于胆囊平滑肌上，但似乎在胆囊平滑肌中没有任何生理作用。胆囊排空。
The present study evaluated the mechanism of cholecystokinin-induced gallbladder contraction in awake opossums. Each of 19 chronic animal preparations had an indwelling gallbladder cannula for monitoring changes in gallbladder volume and a jugular catheter for administration of cholecystokinin octapeptide and drugs. An intraduodenal catheter allowed intraduodenal infusion of Isocal (Mead Johnson Laboratories, Evansville, Ind.). Bipolar electrodes in the stomach, duodenum, and jejunum enabled monitoring of the duodenal migratory myoelectric complex cycle. One-hour infusions of cholecystokinin octapeptide (10 ng/kg/min), intraduodenal Isocal (0.4 ml/min), or feeding were started 20 min after cessation of phase 3 duodenal migratory myoelectric complex activity. Bolus intravenous doses of potential pharmacological antagonists were given 10 min before and 20 min after the onset of cholecystokinin octapeptide infusion, Isocal infusion, or feeding. Each test challenge induced about 60% gallbladder emptying at 30 min and 70% at 60 min. Cholecystokinin octapeptide-induced gallbladder emptying was converted to filling by hexamethonium and nearly abolished by atropine. Similar results were obtained for gallbladder emptying induced by feeding or duodenal infusion of Isocal. Phentolamine caused a modest decrease of cholecystokinin octapeptide-induced gallbladder contraction at 30 min, whereas postprandial or Isocal-induced gallbladder contraction was unaffected. Cholecystokinin octapeptide-induced gallbladder contraction was not affected by pirenzepine, 4-diphenylacetoxy-N-methylpiperidine methiodide, prazosin, pyrilamine, cimetidine, methysergide, naloxone, or propranolol. In acute studies of anesthetized animals, gallbladder contraction induced by a Dloa intravenous bolus of cholecystokinin octapeptide (800 ng/kg) was not antagonized by hexamethonium, atropine, or tetrodotoxin. It is concluded (a) that cholecystokinin-induced physiologic contraction of the opossum gallbladder occurs through neural mechanisms rather than by a direct action of cholecystokinin on gallbladder smooth muscle, and (b) that studies using pharmacologic bolus doses of cholecystokinin octapeptide and tetrodotoxin indicate that cholecystokinin receptors exist on the gallbladder smooth muscle which do not seem to have any physiological role in gallbladder emptying.
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