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 relie...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.展开更多
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 inf...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 Agllent, 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 repeffusion. 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 repeffusion （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.展开更多
目的:探讨黄芪注射液对肠系膜上动脉闭塞性(superior mesenteric artery occlusion,SMAO)休克脂质过氧化损伤的防治作用及其机制.方法:经腹分离兔肠系膜上动脉并夹闭2h后松夹,复制SMAO休克动物模型,并于松夹前、后各15min分别将黄芪注射...目的:探讨黄芪注射液对肠系膜上动脉闭塞性(superior mesenteric artery occlusion,SMAO)休克脂质过氧化损伤的防治作用及其机制.方法:经腹分离兔肠系膜上动脉并夹闭2h后松夹,复制SMAO休克动物模型,并于松夹前、后各15min分别将黄芪注射液1mL/kg以2倍的NS配制自耳缘iv,观察动物血压、血浆及红细胞膜丙二醛(MDA)、红细胞膜微黏度、红细胞超氧化物歧化酶(SOD)、血浆黄嘌呤氧化酶(XOD)、乳酸脱氢酶(LDH)及酸性磷酸酶(ACP)含量的变化;并进行小肠组织病理学检查.结果:与对照组比较,SMAO组血压和红细胞SOD降低(均P<0.01),红细胞膜微粘度、红细胞膜MDA以及血浆MDA,XOD,LDH和ACP的水平明显升高(均P<0.01),光镜下小肠病理损害明显.黄芪注射液治疗后上述各指标均较SMAO组明显改善(80.1±3.6 vs 39.4±5.2,4.63±0.57 vs 3.44±0.61,3.35±0.34 vs 4.09±0.38,0.23±0.02 vs 0.41±0.02,3.61±0.41 vs 4.32±0.92,71.4±13.1 vs 92.5±13.9,50.2±18.2 vs 105.5±37.0,37.0±11.8 vs 71.7±22.0,均P<0.01).结论:SMAO休克伴有氧自由基代谢紊乱,体内脂质过氧化过程加强.黄芪注射液通过抗脂质过氧化稳定细胞膜,改善红细胞膜微黏度,减轻组织损伤,延缓SMAO休克的发展.展开更多
基金the National Natural Science Foundation of China,No. 30370561,30770845the Natural Science Foundation of Hebei Province,No. C2004000649,C2008000503+1 种基金the Science & Technology Pillar Program of Hebei Province,No. 09276101D-31Science and Technology Program of Zhangjiakou,No. 0711046D-3
文摘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.
基金the National Natural Science Foundation of China, No. 30370561, 30770845the Natural Science Foundation of Hebei Province, No. C2004000649, C2008000503+1 种基金the Science & Technology Pillar Program of Hebei Province, No. 09276101D-31Science and Technology Program of Zhangjiakou, No. 0711046D-3
文摘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 Agllent, 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 repeffusion. 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 repeffusion （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.
文摘目的:探讨黄芪注射液对肠系膜上动脉闭塞性(superior mesenteric artery occlusion,SMAO)休克脂质过氧化损伤的防治作用及其机制.方法:经腹分离兔肠系膜上动脉并夹闭2h后松夹,复制SMAO休克动物模型,并于松夹前、后各15min分别将黄芪注射液1mL/kg以2倍的NS配制自耳缘iv,观察动物血压、血浆及红细胞膜丙二醛(MDA)、红细胞膜微黏度、红细胞超氧化物歧化酶(SOD)、血浆黄嘌呤氧化酶(XOD)、乳酸脱氢酶(LDH)及酸性磷酸酶(ACP)含量的变化;并进行小肠组织病理学检查.结果:与对照组比较,SMAO组血压和红细胞SOD降低(均P<0.01),红细胞膜微粘度、红细胞膜MDA以及血浆MDA,XOD,LDH和ACP的水平明显升高(均P<0.01),光镜下小肠病理损害明显.黄芪注射液治疗后上述各指标均较SMAO组明显改善(80.1±3.6 vs 39.4±5.2,4.63±0.57 vs 3.44±0.61,3.35±0.34 vs 4.09±0.38,0.23±0.02 vs 0.41±0.02,3.61±0.41 vs 4.32±0.92,71.4±13.1 vs 92.5±13.9,50.2±18.2 vs 105.5±37.0,37.0±11.8 vs 71.7±22.0,均P<0.01).结论:SMAO休克伴有氧自由基代谢紊乱,体内脂质过氧化过程加强.黄芪注射液通过抗脂质过氧化稳定细胞膜,改善红细胞膜微黏度,减轻组织损伤,延缓SMAO休克的发展.
