Rebollar E, Arruebo M P, Plaza M A, Murillo M D
Pharmacology and Physiology Department (Physiology), Veterinary Faculty, Zaragoza University, Spain.
Neurogastroenterol Motil. 2002 Dec;14(6):633-42. doi: 10.1046/j.1365-2982.2002.00364.x.
The purpose of this study was to investigate the effect of lipopolysaccharide (LPS) on spontaneous contractions and acetylcholine (ACh) induced contractions of rabbit intestinal segments in vitro, with two different protocols: intestinal segments isolated from LPS-treated rabbits and intestinal segments incubated with LPS. The frequency of spontaneous movements decreased significantly in LPS-treated rabbits at 2 microg kg-1 in the duodenum and 20 microg kg-1 in the duodenum, jejunum and ileum. LPS (0.2 microg kg-1) reduced significantly the ACh contractions (10-6 mol L-1) in the duodenum (61%), jejunum (48%) and ileum (21%). Indomethacin (1, 5 and 10 mg kg-1) administered 15 min before LPS (0.2 microg kg-1) antagonized the LPS effects on the ACh-induced contractions. Prostaglandin (PG)E2 (8 microg kg-1) inhibited significantly the frequency of spontaneous contractions in the ileum and reduced the ACh-induced contractions in the three segments, mimicking the LPS effects. The amplitude and frequency of contractions in rabbit intestinal segments previously incubated with LPS (0.03, 0.3, 3 and 30 microg mL-1) were not modified with respect to the control. The ACh-induced contractions (10-4 mol L-1) were significantly reduced after 90 min of incubation with LPS. The inhibition of LPS (0.3 microg mL-1) was 43% in the duodenum, 35% in the jejunum and 17% in the ileum. Indomethacin added before LPS blocked the effect of LPS on the ACh-induced contractions in the duodenum, jejunum and ileum. These results show that LPS decreases intestinal contractility in rabbits and suggest that PGs are implicated in these actions.
本研究的目的是采用两种不同方案,研究脂多糖(LPS)对兔离体肠段自发收缩及乙酰胆碱(ACh)诱导收缩的影响:从经LPS处理的兔分离出的肠段和与LPS孵育的肠段。LPS处理的兔在十二指肠2 μg kg-1以及十二指肠、空肠和回肠20 μg kg-1时,自发运动频率显著降低。LPS(0.2 μg kg-1)显著降低十二指肠(61%)、空肠(48%)和回肠(21%)中ACh(10-6 mol L-1)诱导的收缩。在LPS(0.2 μg kg-1)给药前15分钟给予吲哚美辛(1、5和10 mg kg-1)可拮抗LPS对ACh诱导收缩的作用。前列腺素(PG)E2(8 μg kg-1)显著抑制回肠自发收缩频率,并降低三段中ACh诱导的收缩,模拟了LPS的作用。先前与LPS(0.03、0.3、3和30 μg mL-1)孵育的兔肠段收缩的幅度和频率与对照组相比未发生改变。与LPS孵育90分钟后,ACh(10-4 mol L-1)诱导的收缩显著降低。LPS(0.3 μg mL-1)在十二指肠的抑制率为43%,在空肠为35%,在回肠为17%。在LPS之前添加吲哚美辛可阻断LPS对十二指肠、空肠和回肠中ACh诱导收缩的作用。这些结果表明,LPS降低兔肠道收缩性,并提示PG参与了这些作用。