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脂多糖性休克大鼠血浆和主要器官中硫化氢含量的变化和意义
引用本文:崔晓辉,黄新莉,羡晓辉,凌亦凌. 脂多糖性休克大鼠血浆和主要器官中硫化氢含量的变化和意义[J]. 中国病理生理杂志, 2007, 23(4): 780-784. DOI: 1000-4718
作者姓名:崔晓辉  黄新莉  羡晓辉  凌亦凌
作者单位:河北医科大学病理生理教研室,河北 石家庄 050017
基金项目:河北省科技厅科技计划;河北省教育厅科研项目;河北医科大学校科研和教改项目
摘    要:目的:探讨内毒素休克(endotoxic shock,ES)大鼠血浆及肝、肾、心、肺、主动脉等主要器官组织中内源性硫化氢(hydrogen sulfide,H2S)的含量变化及意义。方法:用静脉注射脂多糖(lipopolysaccharide,LPS)法制备LPS攻击大鼠模型,将雄性Wistar大鼠随机分为正常对照组、LPS组、LPS+硫氢化钠(NaHS,H2S供体)组、LPS+炔丙基甘氨酸(PPG,H2S代谢酶抑制剂)组。观察给药后240 min内大鼠平均动脉压(mean arterial pressure,MAP)的变化及测定血浆和以上主要器官中H2S含量,并分析其相关性;光镜观察主要器官的形态学变化。结果:与正常对照组相比,LPS组大鼠血压迅速下降,血浆H2S含量于LPS注射后显著增高,肝、肾、心、肺和主动脉组织中H2S含量亦明显增高(均P<0.05),并出现组织结构损伤;给予PPG能显著抑制血浆以及各组织中H2S含量的增高,并可显著减轻LPS所致的血压下降(均P<0.05)和组织损伤;而给予H2S供体NaHS后,与LPS组相比,大鼠血浆以及各组织中H2S含量显著增高,血压明显下降(均P<0.05),组织损伤加重。LPS攻击大鼠血浆及组织中H2S含量与血压呈高度负相关(均P<0.05)。结论:H2S是一种新的内源性介质,可能参与了ES的一系列病理生理过程。

关 键 词:硫化氢  脂多糖类  休克  
文章编号:1000-4718(2007)04-0780-05
收稿时间:2006-11-13
修稿时间:2006-11-132007-01-10

Changes of hydrogen sulfide content in plasma and tissues of rats with LPS-induced shock
CUI Xiao-hui,HUANG Xin-li,XIAN Xiao-hui,LING Yi-ling. Changes of hydrogen sulfide content in plasma and tissues of rats with LPS-induced shock[J]. Chinese Journal of Pathophysiology, 2007, 23(4): 780-784. DOI: 1000-4718
Authors:CUI Xiao-hui  HUANG Xin-li  XIAN Xiao-hui  LING Yi-ling
Affiliation:Department of Pathophysiology, Hebei Medical University, Shijiazhuang 050017,China. E-mail: lingyiling@tom.com
Abstract:AIM: To investigate the changes and significance of hydrogen sulfide(H2S) in both plasma and various tissues,including liver,kidney,heart,lung and arteriae aorta,in rats with LPS-induced shock.METHODS: A rat model of shock induced by injection of lipopolysaccharide(LPS) was developed.Male Wistar rats were divided into four groups: control group,LPS group,LPS NaHS(H2S donor) group and LPS propargylglycine(PPG,metabolic enzyme inhibitor of H2S) group.The mean arterial pressure(MAP) of rats within 240 min was observed,and H2S contents were determined.The structures of various tissues were observed.RESULTS: Administration of LPS to male Wistar rats caused a sustained fall in MAP,various tissue injuries and a significant increase in H2S contents in plasma as well as liver,kidney,heart,lung and arteriae aorta within 240 min(all P<0.05).Treatment with metabolic enzyme inhibitor of H2S,propargylglycine,was shown to reduce H2S content elevation in plasma as well as liver,kidney,heart,lung,and arteriae aorta,and ameliorate the hypotension and tissue injuries caused by LPS(all P<0.05).However,treatment with H2S donor-NaHS was shown to increase H2S content elevation in plasma as well as liver,kidney,heart,lung and arteriae aorta,and aggravate the hypotension and tissue injuries caused by LPS(all P<0.05).Endogenous H2S contents in both plasma and various tissues were negatively correlated with MAP(all P<0.05).CONCLUSION: H2S may be a new endogenous mediator and play a role in the pathogenesis of endotoxic shock.
Keywords:Hydrogen sulfide   Lipopolysaccharides    Shock
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