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Mesenteric lymph reperfusion may exacerbate brain injury in a rat model of superior mesenteric artery occlusion shock

查看全文 作　　者：Zigang Zhao Chunyu Niu Aimin Shang Jiaming Tian Rui Han Chunhui Zhang Yuping Zhang Jing [1]Zhang 高影响力作者 机构地区：[1]Institution of Microcirculation, Department of Pathophysiology, Basic Medical College, Hebei North University, Zhangjiakou 075029, HebeiProvince, China高影响力机构 出　　处：《Neural Regeneration Research》索引2010年第5卷第9期,共7页高影响力期刊 基　　金：the National Natural Science Foundation of China,No. 30370561,30770845;the Natural Science Foundation of Hebei Province,No. C2004000649,C2008000503;the Science & Technology Pillar Program of Hebei Province,No. 09276101D-31;Science and Technology Program of Zhangjiakou,No. 0711046D-3 摘　　要：BACKGROUND:The intestinal lymphatic pathway and intestinal ischemia/reperfusion are mainly involved in mesenteric lymph duct ligation or drainage;moreover,intervention by reducing the lymph liquid reflux might relieve lung and other organ dysfunction induced by intestinal ischemia/reperfusion;however,research addressing mesenteric lymph reperfusion (MLR) and brain injury has not yet to be reported.OBJECTIVE:To observe the effect of MLR on brain tissue in a rat model of superior mesenteric artery occlusion (SMAO) shock,and to explore the molecular mechanism of MLR.DESIGN,TIME AND SETTING:A randomized,controlled,animal experiment at a neuro-pathophysiology level was performed at the Institute of Microcirculation,Hebei North University;Department of Pathophysiology,Basic Medical College;Department of Pathology,the First Hospital of Hebei North University between December 2007 and March 2009.MATERIALS:Adenosine triphosphate (ATP) standard was provided by the National Institute for the Control of Pharmaceutical and Biological Products;lactic acid (LA),superoxide dismutase (SOD),malonaldehyde (MDA),nitrogen monoxidum (NO),nitric oxide synthase (NOS),myeloperoxidase (MPO) and ATPase assay kits were provided by Nanjing Jiancheng Bioengineering Institute,China.METHODS:A total of 24 male Wistar rats were randomly divided into four groups.In the sham-surgery group (n=6),both the mesenteric lymph duct and the superior mesenteric artery were not blocked;in the MLR group (n=6),the mesenteric lymph duct was occluded for 1 hour followed by 2-hour reperfusion;in the SMAO group (n=6),the superior mesenteric artery was occluded for 1 hour followed by 2-hour reperfusion;in the MLR + SMAO group (n=6),both the mesenteric lymph duct and superior mesenteric artery were occluded for 1 hour followed by 2-hour reperfusion.MAIN OUTCOME MEASURES:Mean arterial blood pressure prior to and following ischemia/reperfusion;brain tissue morphology levels of LA,MDA,SOD,NO,NOS,MPO,ATPase and ATP following reperfusion.RESULTS:MLR did not cause changes in mean arterial blood pressure,brain tissue morphology,LA,MDA,NO,ATP,SOD,NOS,MPO and ATPase.However,SMAO caused a rapid decrease and gradual increase of mean arterial blood pressure.Neuronal necrosis,degeneration and swelling were observed in brain tissue.Contents of MDA,NO,LA and ATP as well as activities of NOS and MPO were significantly increased (P < 0.05),but activities of SOD and Na+-K+-ATPase were significantly decreased (P < 0.05).MLR aggravated neuronal damage in a rat model of SMAO shock.Following MLR,mean arterial blood pressure was significantly decreased (P < 0.05),contents of MDA and NO as well as activities of NOS and MPO were significantly increased (P < 0.05),but activities of Ca2+-ATPase,Mg2+-ATPase and Ca2+-Mg2+-ATPase as well as ATP content were significantly decreased (P < 0.05).CONCLUSION:MLR aggravates brain injury in a rat model of SMAO shock,which correlates with oxygen-derived free radical injury,NO synthesis and release,sequestration of neutrophilic granulocytes,decreasing activity of cell membrane pumps and energy metabolism dysfunction.Pathogenesis of the intestinal lymphatic pathway should be thoroughly investigated to prevent ischemia/reperfusion injury. 关 键 词：mesenteric lymph reperfusion shock superior mesenteric artery occlusion brain injury neural regeneration
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