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Effects Of Endotoxin Translocation On Mesenteric Lymph Reperfusion Aggravating Multiple Organs Injure In SMAO Shock Rats

Posted on:2012-07-13Degree:MasterType:Thesis
Country:ChinaCandidate:L N YangFull Text:PDF
GTID:2154330335984566Subject:Pathology and pathophysiology
Abstract/Summary:PDF Full Text Request
The superior mesenteric artery occlusion (SMAO) shock is severe pathological process and events due to various reasons caused by superior mesenteric artery occlusion, what leads to intestinal ischemia and after restoration reperfusion of blood appeared The intestinal ischemia- reperfusion not only can cause intestinal local tissue damage, but also which may the intestinal barrier dysfunction, intestinal permeability, result in bacteria and bacterial endotoxin production and absorption increased, and translocate to the entire body, thus causing massive inflammatory mediators and cytokines released and the systemic inflammatory response syndrome (SIRS) and the structural damage and dysfunction of distant organs, such as the myocardium, liver, lungs, kidneys, induce multiple organs dysfunction syndrome (MODS), worse still multiple organs failure (MOF) can lead to sever patients'death. So SMAO shock plays an important role in the process of organs dysfunction, because it can give rise to the enterogenous bacteria and bacterial endotoxin translocation.In recent years, lymph circulation as an important component of the circulatory system, its role in critical care medicine has drawn many scholars'close attention. Research shows that simple ligature mesenteric lymph duct (MLD) as the intestinal mesenteric lymphatic reperfusion (MLR) does not cause the body damage. But MLR can aggravate distant organ dysfunction and injuredness, reduce mean arterial pressure (MAP) and 24h survival in the SMAO shock rats. Its mechanism is related to aggravating the radical injury and the inflammation out of control in multiple organs. The key role of enterogenous bacterial endotoxin translocation (BET) in the distant organ function in SMAO shock makes us wonder wether the influence of MLR on intensifying organ damage in SMAO shock, is related to enterogenous BET and is the mechanism associated with lipopolysaccharide-binding protein (LBP) / lipopolysaccharide receptor (CD14) endotoxin sensitizing system? Is it worth studying?Therefore, this research, based on replication of the SMAO shock rats model and establishing method of the MLR, is to observe the changes in plasma and organs homogenates ET levels and LBP, CD14, tumor necrosis factor-α(TNF-α) contents in hepatic, renal, myocardial and pulmonary organs homogenates of the mechanism of MLR aggravates multiple organs injury in SMAO shock rats, and to investigate their potential role in the MLR aggravates multiple organs injury in SMAO shock.Twenty four SPF male Wistar rats were randomly divided into four groups (n=6): in Sham group, only anesthetization and operation were performed; in MLR group, occlusion of MLD for 60 min followed by 120 min of reperfusion; in SMAO group, occlusion of superior mesenteric artery (SMA) for 60 min followed by 120 min reperfusion; in SMAO+ MLR group, occlusion of SMA and MLD for 60 min followed by 120 min of reperfusion. After blood reperfusion of 120 min respectively, take blood in abdominal aortic and to remain the liver, kidney, myocardium, lung organs in fixed position and to make homogenates at once. The homogenates of liver, kidney, myocardium and lung were prepared for determining the levels and activities of endotonxin with TAL dynamic turbidity method, and determining the CD14, LBP, TNF-αwith the enzyme-linked immunosorbent assay (ELISA) method.Research results showed that the ET levels of the plasma in SMAO and SMAO+MLR group were significant higher than those in Sham and MLR group (P<0.01, P<0.05), and these indexes in SMAO+MLR were increased significantly than those in SMAO group(P<0.05), after the superior mesenteric artery ischemia 60 min reperfusion 120 min, and ET contents of plasma in MLR group compared with Sham groups, there are no significant difference(P>0.05). The ET contents in hepatic, renal, myocardial and pulmonary organs homogenates in SMAO and SMAO+MLR group were higher than those in Sham and MLR group (P<0.01, P < 0.05), and these indexes in SMAO+MLR were increased significantly than those in SMAO group too (P<0.01, P<0.05). The ET contents of liver, kidney, myocardium and lung organs homogenates in MLR group has no significant difference when compared with Sham groups (P>0.05). In SMAO group the CD14, LBP and TNF-αlevels in liver, kidney, myocardium and pulmonary organs homogenates are significantly higher than MLR group and Sham group (P<0.01, P<0.05), and SMAO + MLR group are higher than SMAO group (P<0.01, P<0.05); The CD14, LBP and TNF-αcontents in MLR group are no statistically significant when compared with Sham groups (P>0.05); The contents of ET, CD14,LBP and the levels of TNF-αin hepatic, renal, myocardial and pulmonary organs homogenates presents parallelly changed.The results of the study indicate that the MLR enhances the multiple organs injury in SMAO shock may be associated with enterogenous ET through intestinal lymphatic pathway to translocate, activate the key molecule of multiple organs in cascaded inflammatory response and activate LBP/CD14 as endotoxin sensitizing system and promote inflammatory response in SMAO shock rats. So these results of the study demonstrate that the bacterial endotoxin translocation (BET), LBP /CD14 sensitizing system and intestinal lymphatic pathway plays an important role in the pathogenesis of the MLR exacerbating the multiple organs injury in SMAO shock. So we can make LBP/CD14 of endotoxin sensitizing system and intestinal lymphatic pathway for targets, and perhaps provide a new strategy for the prevention and control of multiple organs dysfunction in SMAO shock.
Keywords/Search Tags:mesenteric lymph reperfusion (MLR), superior mesenteric artery occlusion (SMAO) shock, multiple organ dysfunction syndrome (MODS), bacterial endotoxin translocation (BET), lipopolysaccharide binding protein (LBP), lipopolysaccharide receptor (CD14)
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