Collares E F
Departamento de Pediatria and Núcleo de Medicina e Cirurgia Experimental, Faculdade de Ciências Médicas, Universidade Estadual de Campinas, SP, Brasil.
Braz J Med Biol Res. 1997 Feb;30(2):207-11. doi: 10.1590/s0100-879x1997000200008.
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 micrograms/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 micrograms/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 micrograms/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.
1)研究细菌脂多糖(LPS)对大鼠胃排空(GE)的影响;2)研究迷走神经是否可能参与LPS的胃作用。将来自大肠杆菌(055:B5菌株)的内毒素以最大剂量50微克/千克动物体重皮下、腹腔内或静脉内给予雄性Wistar大鼠(体重220 - 280克)。对照动物接受等量的无菌盐溶液。在给予LPS后的特定时间段,通过在经口胃内注入试验餐(2毫升/100克动物体重,由0.9%氯化钠加标记物酚红(6毫克/分升)组成)10分钟后测量胃潴留来评估胃排空。一组动物在试验前15天进行双侧膈下迷走神经切断术或假手术。静脉内给予50微克/千克动物体重剂量的内毒素后5小时,观察到试验餐的胃排空明显延迟。LPS诱导的胃排空延迟在内毒素给药后30分钟最早检测到,并持续至8小时。使用5至50微克/千克动物体重的不同剂量LPS表明,胃排空的改变呈剂量依赖性。此外,接受LPS的迷走神经切断动物的胃排空与假手术对照组相比无显著差异。然而,由于迷走神经切断术本身会引起该胃参数的变化,这些实验无法明确证明迷走神经参与LPS诱导的胃排空延迟。本研究为确定LPS对胃排空影响的潜在机制提供了一个合适的模型。