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Establishment of irritable bowel syndrome rat model by combination of intestinal infection with Trichinella spiralis and acute stress


, : Establishment of irritable bowel syndrome rat model by combination of intestinal infection with Trichinella spiralis and acute stress. Zhonghua Yi Xue Za Zhi 89(42): 2992-2996

To establish the irritable bowel syndrome (IBS) rat model by the combination of acute stress and transient intestinal infection with Trichinella spiralis (T.S.). The rat model of acute cold restraint stress post-infection (PI + ACRS) was established as following: the intestinal infection with 1500 T.S. in 1 ml saline to adult male BN rats was performed at Day 0 by gastric lavage. Then a 2-hour stimulus of ACRS was administered at Day 100. Age matched transiently infected without stress rats (PI) and normal rats served as controls (CON) (n = 6, for each). After anesthesia, all the rats underwent colonic manometry in vivo at Day 100. The colonic pressures at 3 different states (baseline for 20 min; 1 ml balloon distension stimulation for 5 min and 2 ml balloon distension stimulation for 20 min) were traced with a 5-minute interval between each two. The following parameters were recorded: (1) Duration (Dur.): total time of contractions during each state. (2) Maximum (Max.): highest amplitude of constructional waves (mm Hg). (3) Area: area under contraction waves. (4) Number (Num.): frequencies of contraction wave during each state. The visceromoter response to colorectal distension (CRD) was analyzed at Day 100 post-infection. And the distension volume of AWR 3 was detected for 5 times with a 20-min interval in each rat. The histological damage of intestine induced by T.S. infection is transient. Although such acute infectious features as epithelial edema, hyperemia and marked eosinophil infiltration appeared at Day 10 PI, the histological changes almost recovered at Day 100 PI in both the PI group and the PI + ACRS group. Both the stimuli of transient infection and the ACRS post-infection induced intestinal dysmotility and visceral hypersensitivity. The ACRS post infection further worsened the transiently induced infection. The parameters of Num, Max and Area in the PI + ACRS group were all significantly higher than those of the PI group [Max: (41 +/- 17) mm Hg vs (22 +/- 6) mm Hg, P = 0.000; Area: (7693 +/- 2822) mm Hg.s vs (5092 +/- 1687) mm Hgxs, P = 0.000; Num: 9.5 +/- 2.6 vs 6.6 +/- 3.1, P = 0.000]; so was the distension volume of AWR3 [(2.25 +/- 0.29) ml vs (2.52 +/- 0.32) ml, P = 0.004]. As compared with the range of normal values from controls, the abnormality rates of motility parameters and visceral threshold in PI + ACRS group also had an larger increment than those of the PI group (PI + ACRS: 50.0% - 87.5% and 100% respectively, PI: 25.0% - 37.5% and 90.0% respectively). The pathophysiological changes in the PI + ACRS rats are consistent with those of IBS. Aggravated by psychological factors, these rats reproduce the symptoms of intestinal dysmotility and visceral hypersensitivity. A proper animal model has been established for the investigation of IBS.

US$29.90

PMID: 20137711


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