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神经介素 - N抑制大鼠小肠移行性肌电复合波并诱导不规则锋电位发放;与神经降压素的比较。

Neuromedin-N inhibits migrating myoelectric complex and induces irregular spiking in the small intestine of rats; comparison with neurotensin.

作者信息

Schultz I, Wallin B, Mogard M H, Hellström P M

机构信息

Department of Surgery, Karolinska Hospital, Stockholm, Sweden.

出版信息

Regul Pept. 1991 Sep 3;35(3):197-205. doi: 10.1016/0167-0115(91)90083-s.

DOI:10.1016/0167-0115(91)90083-s
PMID:1758975
Abstract

The effects of neuromedin-N on migrating myoelectric complexes in the small intestine of rats were studied. As neuromedin-N and neurotensin are structurally related peptides a comparison with neurotensin was made. Myoelectric activity was recorded by means of three bipolar electrodes implanted into the wall of the small intestine at 5, 15 and 25 cm distal to the pylorus. The peptides were administered as intravenous infusions to fasted conscious rats. Neuromedin-N at doses of 100-800 pmol kg-1 min-1 caused a dose-dependent disruption of the migrating myoelectric complexes and induced irregular spiking activity (n = 7, P less than 0.05). Neurotensin induced a similar response, but at doses of 1.0-8.0 pmol kg-1 min-1 (n = 5, P less than 0.05). Thus, on a molar basis, neuromedin-N appeared to be about 100-times less potent than neurotensin. Hexamethonium (20 mg kg-1 i.v.) inhibited the migrating motor complexes and induced quiescence, but did not block the effect of neuromedin-N at a dose of 800 pmol kg-1 min-1. Atropine (1 mg kg-1 i.v.) and mepyramine (2 mg kg-1 i.v.) did not affect the migrating motor complexes, nor did they block the effect of neuromedin-N. Simultaneous infusion of neuromedin-N and neurotensin in a 1:1 molar ratio at doses of 2 pmol kg-1 min-1 showed inhibition of the response to neurotensin in eight out of ten experiments. In conclusion, neuromedin-N changes the myoelectric activity in the small intestine from a fasting to a fed pattern.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

研究了神经介素 - N对大鼠小肠移行性肌电复合波的影响。由于神经介素 - N和神经降压素在结构上是相关肽,因此对两者进行了比较。通过将三个双极电极植入幽门远端5、15和25厘米处的小肠壁来记录肌电活动。将这些肽静脉输注给禁食的清醒大鼠。剂量为100 - 800 pmol kg-1 min-1的神经介素 - N导致移行性肌电复合波出现剂量依赖性破坏,并诱导不规则的尖峰活动(n = 7,P < 0.05)。神经降压素在剂量为1.0 - 8.0 pmol kg-1 min-1时也诱导了类似反应(n = 5,P < 0.05)。因此,按摩尔计算,神经介素 - N的效力似乎比神经降压素低约100倍。六甲铵(20 mg kg-1静脉注射)抑制移行性运动复合波并诱导静止,但在剂量为800 pmol kg-1 min-1时不阻断神经介素 - N的作用。阿托品(1 mg kg-1静脉注射)和甲氧苄胺(2 mg kg-1静脉注射)不影响移行性运动复合波,也不阻断神经介素 - N的作用。以2 pmol kg-1 min-1的剂量同时按1:1摩尔比输注神经介素 - N和神经降压素时,在十分之八的实验中显示对神经降压素的反应受到抑制。总之,神经介素 - N将小肠中的肌电活动从空腹模式改变为进食模式。(摘要截断于250字)

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