Lu Y F, Mizutani M, Neya T, Nakayama S
Dept. of Physiology, Okayama University Medical School, Japan.
Scand J Gastroenterol. 1995 May;30(5):445-50. doi: 10.3109/00365529509093305.
Indomethacin induces intestinal lesions. The change in contractility of segments with lesions was studied.
Motility was recorded in segments with lesions isolated from the rat small intestine 24 h after a subcutaneous injection of indomethacin (20 mg/kg).
Concentration-contraction curves for acetylcholine shifted leftward independently of the degree of severity of lesions, but the curves for carbachol and 5-hydroxytryptamine did not. Contractions produced by intramural nerve stimulation were enhanced in segments with no visible damage but decreased with progression of lesions. Neostigmine augmented them in normal rats but not in indomethacin-treated rats. The peristaltic activity was enhanced in segments with no visible lesions.
The results suggest that treatment of the rat with indomethacin enhances contractility of the small intestine owing to diminution of acetylcholinesterase activity independently of the degree of lesions and reduces it owing to decreased responsiveness of enteric neurons with the progression of lesions.
吲哚美辛可诱发肠道病变。本研究对有病变肠段的收缩性变化进行了研究。
皮下注射吲哚美辛(20mg/kg)24小时后,从大鼠小肠分离出有病变的肠段,记录其运动情况。
乙酰胆碱的浓度-收缩曲线向左移位,与病变严重程度无关,但卡巴胆碱和5-羟色胺的曲线未发生移位。在无可见损伤的肠段中,壁内神经刺激引起的收缩增强,但随着病变进展而减弱。新斯的明可增强正常大鼠的收缩,但对吲哚美辛处理的大鼠无效。在无可见病变的肠段中,蠕动活动增强。
结果表明,吲哚美辛处理大鼠可增强小肠收缩性,这是由于乙酰胆碱酯酶活性降低,与病变程度无关;而随着病变进展,肠神经元反应性降低,又会导致小肠收缩性减弱。