Hellström P M, al-Saffar A, Ljung T, Theodorsson E
Department of Medicine, Karolinska Hospital, Stockholm, Sweden.
Dig Dis Sci. 1997 Aug;42(8):1640-51. doi: 10.1023/a:1018897028463.
The lipopolysaccharide (endotoxin) of gram-negative bacteria has systemic effects in animals and man. Our aim was to investigate the effects of E. coli lipopolysaccharide on motility and transit through the small intestine in rats and to analyze plasma and tissue concentrations of intestinal neuropeptides. When lipopolysaccharide (20-160 micrograms/kg) was administered intravenously, the migrating myoelectric complex was replaced by spike bursts accompanied by rapid transit. Tissue concentrations of substance P and neurokinin A decreased, while plasma levels of calcitonin gene-related peptide increased N omega-Nitro-L-arginine, N omega-L-arginine methyl ester, dexamethasone, or indomethacin prevented these changes in myoelectric activity and tissue contents of neuropeptides. All of these compounds, except indomethacin, prevented the increased rate of transit. Thus, lipopolysaccharide changes motility through the nitric oxide and arachidonic pathways, resulting in rapid transit through the gut.
革兰氏阴性菌的脂多糖（内毒素）对动物和人类具有全身作用。我们的目的是研究大肠杆菌脂多糖对大鼠小肠运动和通过情况的影响，并分析肠道神经肽的血浆和组织浓度。静脉注射脂多糖（20 - 160微克/千克）时，移行性复合肌电被伴有快速通过的尖峰爆发所取代。P物质和神经激肽A的组织浓度降低，而降钙素基因相关肽的血浆水平升高。Nω-硝基-L-精氨酸、Nω-L-精氨酸甲酯、地塞米松或吲哚美辛可防止肌电活动和神经肽组织含量的这些变化。除吲哚美辛外，所有这些化合物均可防止通过速率增加。因此，脂多糖通过一氧化氮和花生四烯酸途径改变运动，导致肠道快速通过。
