Influence of mesenteric lymph reperfusion on neurotransmitter expression in brain tissue of a superi

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BACKGROUND: Previous studies have shown that mesenteric lymph reperfusion (MLR) exacerbates brain injury in a rat model of superior mesenteric artery occlusion (SMAO) shock. However, little is known about the influence of MLR on neurotransmitter expression in brain tissue. OBJECTIVE: To observe the effect of MLR on brain tissue injury by measuring monoamine and cholinergic neurotransmitter levels.DESIGN, TIME AND SETTING: A randomized, controlled, animal experiment was performed at the Institute of Microcirculation, Hebei North University, China; Research Room of Microcirculation and Laboratory of Biochemistry, Department of Pathophysiology, Basic Medical College, Hebei North University between December 2007 and March 2009.MATERIALS: Choline acetyltransferase (ChAT) and acetylcholine esterase (AChE) kits were provided by Nanjing Jiancheng Bioengineering Institute, China; dopamine (DA) and noradrenalin (NE) standards were provided by the National Institute for the Control of Pharmaceutical and Biological Products; HP1100 chromatograph of liquid was provided by Agilent, USA. METHODS: A total of 24 male, Wistar rats were randomly assigned to 4 groups: sham-surgery, MLR, SMAO, and MLR + SMAO groups, with 6 rats in each group. In the MLR or SMAO groups, the mesenteric lymph duct or superior mesenteric artery was blocked for 1 hour. In the MLR + SMAO group, the mesenteric lymph duct and superior mesenteric artery were occluded for 1 hour, followed by 2-hour reperfusion. ChAT and AChE levels were measured using the synthesized and hydrolyzed acetylcholine method, respectively. Liquid chromatography was employed to quantitatively analyze DA and NE levels, using relative retention time and the external standard method. MAIN OUTCOME MEASURES: ChAT, AChE, DA, and NE levels. RESULTS: AChE levels were significantly increased, but ChAT levels were significantly decreased in the MLR and MLR + SMAO groups following 2-hour reperfusion (P < 0.01). However, AChE activity in the MLR + SMAO group was greater than in the MLR group (P < 0.05). DA and NE levels were significantly decreased in the SMAO and MLR + SMAO groups (P < 0.01), while DA levels in the MLR + SMAO group were less than in the SMAO group (P < 0.05). CONCLUSION: MLR exacerbated brain injury in a rat model of SMAO shock, which correlated with the intestinal lymphatic pathway. MLR decreased DA levels, but increased AChE activity, in a rat model of SMAO shock.
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