泰加塞罗德对吲哚美辛致大鼠胃损伤的保护作用

K. Venkova, D. Earnest, B. Meerveld
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引用次数: 6

摘要

非甾体抗炎药(NSAIDs)引起的胃收缩有助于粘膜溃疡。本研究的目的是研究维持正常胃运动是否对非甾体抗炎药有保护作用。采用吲哚美辛致大鼠胃粘膜损伤及肌肉肥厚模型,比较5-HT4受体激动剂tegaserod (1 mg/kg b.d)预处理与质子泵抑制剂奥美拉唑(20 mg/kg b.d)预处理对胃粘膜损伤及肌肉肥厚的保护作用。吲哚美辛引起的粘膜溃疡与离体胃窦肌条在KCl, carbachol, 5-HT或电场刺激下的过度收缩有关。用替加塞罗德单独或联合奥美拉唑进行预处理可防止粘膜溃疡和肌肉过度收缩。相反,奥美拉唑保护了粘膜,但没有阻止肌肉过度收缩的发展。结果表明,外周5-HT4受体的激活可促进胃窦的正常收缩,提示对非甾体抗炎药的气体保护机制不同。
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Protective Effect of Tegaserod Against Indomethacin-Induced Gastric Injury in the Rat
Gastric contractions induced by non-steroidal anti-inflammatory drugs (NSAIDs) contribute to mucosal ulceration. The goal of the present study was to investigate whether maintaining normal gastric motility provides protection against NSAIDs. A rat model of indomethacin-induced gastric mucosal injury and muscle hypercontratility was used to evaluate the protective effect of pretreatment with the 5-HT4 receptor agonist tegaserod (1 mg/kg b.i.d.) in comparison to the effect of the proton pump inhibitor omeprazole (20 mg/kg b.i.d). Indomethacin induced mucosal ulceration associated with hypercontractility of isolated antral muscle strips in response to KCl, carbachol, 5-HT or electrical field stimulation. Pretreatment with tegaserod alone or in combination with omeprazole prevented both mucosal ulceration and muscle hypercontractility. In contrast, omeprazole protected the mucosa without preventing the development of muscle hypercontractility. The results show that activation of peripheral 5-HT4 receptors promotes normal contractility of the antrum suggesting a different mechanism of gasrtoprotection against NSAIDs.
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