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Effect of bacterial lipopolysaccharide on gastric emptying of liquids in rats

机译:细菌脂多糖对大鼠胃液排空的影响

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The objectives of the present investigation were 1) to study the effect of bacterial lipopolysaccharide (LPS) on rat gastric emptying (GE) and 2) to investigate a possible involvement of the vagus nerve in the gastric action of LPS. Endotoxin from E. coli (strain 055:B5) was administered sc, ip or iv to male Wistar rats (220-280 g body weight) at a maximum dose of 50 μg/kg animal weight. Control animals received an equivalent volume of sterile saline solution. At a given time period after LPS administration, GE was evaluated by measuring gastric retention 10 min after the orogastric infusion of a test meal (2 ml/100 g animal weight), which consisted of 0.9% NaCl plus the marker phenol red (6 mg/dl). One group of animals was subjected to bilateral subdiaphragmatic vagotomy or sham operation 15 days before the test. A significant delay in GE of the test meal was observed 5 h after iv administration of the endotoxin at the dose of 50 μg/kg animal weight. The LPS-induced delay of GE was detected as early as 30 min and up to 8 h after endotoxin administration. The use of different doses of LPS ranging from 5 to 50 μg/kg animal weight showed that the alteration of GE was dose dependent. In addition, vagotomized animals receiving LPS displayed a GE that was not significantly different from that of the sham control group. However, a participation of the vagus nerve in LPS-induced delay in GE could not be clearly demonstrated by these experiments since vagotomy itself induced changes in this gastric parameter. The present study provides a suitable model for identifying the mechanisms underlying the effects of LPS on gastric emptying
机译:本研究的目的是1)研究细菌脂多糖(LPS)对大鼠胃排空(GE)的影响,以及2)研究迷走神经可能参与LPS的胃功能。以50μg/ kg动物体重的最大剂量对雄性Wistar大鼠(体重220-280 g)经皮下,腹膜内或静脉内施用大肠杆菌的内毒素(菌株055:B5)。对照动物接受等体积的无菌盐溶液。在LPS给药后的给定时间段内,通过在经口输注0.9%NaCl和标志物酚红(6 mg NaCl)的试验餐(2 ml / 100 g动物体重)后10分钟的胃retention留率来评估GE / dl)。在测试前15天,对一组动物进行双侧sub肌下迷走神经切断术或假手术。在以50μg/ kg动物体重的剂量静脉内施用内毒素后5小时,观察到测试膳食的GE显着延迟。 LPS诱导的GE延迟可在内毒素给药后30分钟至8小时内检测到。使用5至50μg/ kg动物体重的不同剂量LPS​​表明,GE的改变是剂量依赖性的。另外,接受LPS迷走神经切断的动物表现出的GE与假对照组相比无显着差异。然而,由于迷走神经切开术本身引起了该胃参数的改变,这些实验不能清楚地证明迷走神经参与了LPS诱导的GE延迟。本研究提供了一种合适的模型,用于确定LPS对胃排空的影响的潜在机制

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