[Effect of ligation of mesenteric lymph duct on inflammation response of liver in hemorrhagic shock in rats].
OBJECTIVE
To observe the effect of ligation of mesenteric lymph duct on changes in free radicals and pro-inflammatory mediators in the liver of rats with serious hemorrhagic shock at different periods, and explore the effect of blockage of intestinal lymphatic pathway on inflammation response of liver.


METHODS
Seventy-eight male Wistar rats were randomly divided into the sham group (n=6), shock group (n=42), and ligation group (n=30). The model of serious hemorrhagic shock was reproduced in shock group and ligation group. Mesenteric lymph was blocked by ligating mesenteric lymph duct in ligation group after resuscitation. Six rats were sacrificed at 0, 1, 3, 6, 12, and 24 hours, and the livers were harvested and homogenized for the determination of malondialdehyde (MDA), nitric oxide (NO), nitric oxide synthase (NOS), superoxide dismutase (SOD), tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6) and myeloperoxidase (MPO) activity. The expression of inducible nitric oxide synthase (iNOS) mRNA in liver was detected by reverse transcription-polymerase chain reaction (RT-PCR).


RESULTS
The contents of TNF-alpha, IL-6, NO, NOS, MDA, MPO and iNOS mRNA in liver homogenate of shock group were increased after transfusion and resuscitation, and their levels were higher at 6 and 12 hours. The values were significantly higher than those of the sham group, while the activity of SOD was significantly lower than that of sham group (P<0.05 or P<0.01). The contents of TNF-alpha, IL-6, NO, NOS, MDA, MPO and iNOS mRNA in liver homogenate were lower significantly after transfusion and 3, 6, 12 and 24 hours after resuscitation than those of shock group at each time points, and the SOD activity was higher (P<0.05 or P<0.01).


CONCLUSIONS
The results demonstrate that the ligation of mesenteric lymph duct could reduce the polymorphonuclear leucocyte (PMN) detain, and its mechanism might relate to reduction of neutrophil aggregation, thus decreases the release of TNF-alpha and IL-6, reduces the NO and expression of iNOS mRNA, reduces the release of free radicals and consumption of SOD, as a result, it reduces the inflammation response of liver in serious hemorrhagic shock rats.
Zhao
Zi-gang
ZG
Department of Pathophysiology, Hebei North University, Zhangjiakou 075029, Hebei, China.
Niu
Chun-yu
CY
Zhang
Jing
J
Chen
Rui-hua
RH
Zhang
Yu-ping
YP
Jiang
Hua
H
Li
Ji-cheng
JC
D000818:Animals; D004195:Disease Models, Animal; D015850:Interleukin-6 / Q000378:metabolism; D008026:Ligation; D008099:Liver / Q000378:metabolism / Q000473:pathology; D042601:Lymphatic Vessels / Q000601:surgery*; D008297:Male; D008643:Mesentery / Q000601:surgery*; D009569:Nitric Oxide / Q000378:metabolism; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017208:Rats, Wistar; D012771:Shock, Hemorrhagic / Q000378:metabolism* / Q000473:pathology / Q000601:surgery; D013482:Superoxide Dismutase / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D009569:Nitric Oxide; D052247:Nitric Oxide Synthase Type II; C496318:Nos2 protein, rat; D013482:Superoxide Dismutase