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组胺对猪和人Oddi括约肌活动的调控作用

Histamine in the control of porcine and human sphincter of Oddi activity.

作者信息

Sand J, Arvola P, Pörsti I, Jäntti V, Oja O S, Baer G, Nordback I

机构信息

Department of Surgery, Tampere University Hospital, Tampere, Finland.

出版信息

Neurogastroenterol Motil. 2000 Dec;12(6):573-9. doi: 10.1046/j.1365-2982.2000.00234.x.

Abstract

Histamine decreases sphincter of Oddi (SO) contractility in vivo in opossum, but increases contractility in vitro in guinea-pig. In resistor-like SO, such as in pig and man, the histamine effect is poorly known. We investigated the effect of histamine on pig SO in vivo and in vitro and on human SO in vitro. Perfusion manometry catheter and two silver electrodes for simultaneous pressure and electromyography registration were inserted into the SO transduodenally by laparotomy in six anaesthetized pigs weighing for 25-28 kg. Histamine (5-10 microgram kg-1) was infused intra-arterially (i.a.) into the pancreaticoduodenal artery with and without diphenhydramine (75 microgram kg-1) i.a. premedication. Acetylcholine (4 microgram kg-1) i.a., a potent SO stimulator, was used as positive control. After these experiments, the SO was removed and, together with seven human SO from Whipple specimens, were cut into 1.0-1.5 mm thick transverse sections (rings). The rings were placed between two hooks in oxygenated organ bath solution at 37 degrees C. The SO contraction force was measured with isometric force-displacement transducers and registered on a polygraph. SO rings were incubated with histamine (10-100 micromol L-1) and acetylcholine (100 micromol L-1) with or without diphenhydramine (10 micromol L-1), cimetidine (10 micromol L-1), or atropine (1 micromol L-1). Acetylcholine induced huge electrical bursts, and basal SO pressure increased by 20 +/- 10 mmHg. Histamine (10 microgram kg-1) induced strong SO contraction and the SO remained oedematous for over 10 min. Histamine (5 microgram kg-1) resulted in electromyographic burst activity with phasic SO contractions and increase in basal SO pressure by 34 +/- 19 mmHg for over 15 min. Diphenhydramine did not alter acetylcholine-induced SO motility, but significantly decreased histamine-induced contractions and almost abolished electrical activity. In vitro, acetylcholine induced SO contractions in pig (335 +/- 111 mg) and in man (323 +/- 54 mg). Histamine did not change SO tone in man, but in pig it induced dose-dependent contractions in the same way as acetylcholine. These contractions could be inhibited by diphenhydramine, but not by cimetidine or atropine. We conclude that histamine has a stimulatory effect, mediated by H1-receptor, on the pig SO motility. The SO response to histamine is different in adult humans from that observed in young pigs.

摘要

组胺可降低负鼠体内奥狄括约肌(SO)的收缩性,但在豚鼠体外实验中可增强其收缩性。在猪和人类等具有电阻样特性的SO中,组胺的作用尚不清楚。我们研究了组胺对猪体内和体外SO以及人类体外SO的影响。通过剖腹术经十二指肠将灌注测压导管和用于同时记录压力和肌电图的两个银电极插入六只体重为25 - 28千克的麻醉猪的SO中。在有或没有预先动脉内注射苯海拉明(75微克/千克)的情况下,将组胺(5 - 10微克/千克)动脉内注入胰十二指肠动脉。动脉内注射乙酰胆碱(4微克/千克),一种强效的SO刺激剂,用作阳性对照。这些实验完成后,取出SO,并将其与来自惠普尔标本的七个人类SO一起切成1.0 - 1.5毫米厚的横切片(环)。将这些环置于37℃充氧的器官浴溶液中的两个挂钩之间。用等长力位移换能器测量SO的收缩力,并在记录仪上记录。将SO环与组胺(10 - 100微摩尔/升)和乙酰胆碱(100微摩尔/升)一起孵育,同时加入或不加入苯海拉明(10微摩尔/升)、西咪替丁(10微摩尔/升)或阿托品(1微摩尔/升)。乙酰胆碱诱发巨大的电爆发,基础SO压力增加20±10毫米汞柱。组胺(10微克/千克)诱发强烈的SO收缩,且SO水肿超过10分钟。组胺(5微克/千克)导致肌电图爆发活动,伴有SO的阶段性收缩,基础SO压力在超过15分钟内增加34±19毫米汞柱。苯海拉明不改变乙酰胆碱诱发的SO运动,但显著降低组胺诱发的收缩并几乎消除电活动。在体外,乙酰胆碱在猪(335±111毫克)和人类(323±54毫克)中诱发SO收缩。组胺在人类中不改变SO张力,但在猪中它以与乙酰胆碱相同的方式诱发剂量依赖性收缩。这些收缩可被苯海拉明抑制,但不能被西咪替丁或阿托品抑制。我们得出结论,组胺通过H1受体对猪的SO运动具有刺激作用。成人人类SO对组胺的反应与幼猪中观察到的不同。

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