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高甲硫氨酸诱发高同型半胱氨酸血症对抗凝血酶-Ⅲ,蛋白C和血管性血友病因子的影响 被引量:2

Effects of methionine-induced hyperhomocysteinemia on protein C,antithrombin-Ⅲ and von willebrand factor
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摘要 目的 :观察高甲硫氨酸喂饲动物诱发高同型半胱氨酸血症对凝血和抗凝作用的影响。方法 :新西兰白兔随机分为甲硫氨酸组和对照组各 9只 ,16周末检测凝血和抗凝及有关生化指标 ,同时行主动脉血管性血友病因子免疫组化检查。结果 :甲硫氨酸组的血清甲硫氨酸和同型半胱氨酸均显著高于对照组 ,分别为(4 9 97± 5 34 ) μmol/L比 (14 78± 1 97) μmol/L和 (13 30± 2 19) μmol/L比 (5 36± 1 19) μmol/L (P <0 0 1) ;血浆抗凝血酶 -Ⅲ浓度 (AT -Ⅲ :Ag)和活性 (AT -Ⅲ :A)、蛋白C(PC)浓度均显著低于对照组 (P <0 0 1) ;血管性血友病因子 (vWF)显著高于对照组 (P <0 0 1)。血管内皮细胞vWF表达显著低于对照组 (P <0 0 1)。结论 :高甲硫氨酸诱发高同型半胱氨酸血症具有促进凝血和抑制抗凝的作用。 AIM: To observe the effects of methionine-induced hyperhomocysteinemia on protein C(PC), antithrombin-Ⅲ (AT-Ⅲ) and von willebrand factor (vWF). METHODS:Eighteen New Zealand rabbits were randomized as methionine group (group M,n=9) and control(group C,n=9), which were fed with methionine-rich diet(600 mg/d) and regular diet respectively for sixteen weeks.By the end of sixteen weeks,the serum biochemistry and PC,AT-Ⅲ and vWF in plasma were determined and vWF expression of endothelial cells of aorta were examined.RESULTS:In group M, the levels of methionine(29.97±5.34 μmol/L) and homocysteine(13.30±2.19 μmol/L) in serum were signifficantly higher than those(14.48±1.97 μmol/L and 5.36±1.19 μmol/L, respectively,P<0.01) of group C.The levels of AT-Ⅲ and PC of group M were signifficantly lower than those of group C (P<0.01). The level of vWF in plasma of group M was higher than that of group C (P<0.01). Immunohistochemistry showed that vWF expression in endothelial cells of aorta was decreased. CONCLUSION:Methionine-induced hyperhomocysteinemia had promotive effects on coagulation and inhibiting effects on antioagulation.
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出处 《中国病理生理杂志》 CAS CSCD 北大核心 2000年第11期1225-1227,I001,共3页 Chinese Journal of Pathophysiology
关键词 高甲硫氨酸 高同型半胱氨酸血症 蛋白C VWF Homocysteine Von Willebrand factor Protein C Antithrombin-Ⅲ
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  • 1张旭明,邓仲端,瞿智龄,倪娟.氧化型低密度和极低密度脂蛋白诱导人血单核细胞表达巨噬细胞炎性蛋白-1α[J].中国动脉硬化杂志,2001,9(3):198-201. 被引量:8
  • 2Senaratne MP,Griffiths J ,et al. Elevation of plasma homocysteine levels associated with acute myocadial infarction. CLin Ivest Med,2000,239(4) :220 - 6.
  • 3Kekt P, Alfthan G, et al. Homocysteine and major coronay events:a prospective population study among women. J inter Med,2001,249(5) :41 - 5.
  • 4Chai AU, Abrams J ,et al. Homoystein: a new cadiac risk factor? Clin Cardiol,2001,249(5) :461 - 5.
  • 5Cleophas, TJ, Hornstra N, et al. Homocysteine, a risk factor for coronay artery disease or not? A Meta- analysis. AM J Cardiol, 2000,86(9) : 1005 - 9.
  • 6Obaidi MK, Stubbs PJ, et al. Acute and convalcscnt changcs in plasma homocystcinc concentration in acute coronary syndromes.Heart,2001,85(4):380-4.
  • 7Stang IK,Cascorbi I, et al. Hyperhomocysteimia and adverse events in coronary catheter interventions. Int J Cardiol,2000,76(2-3):211-7.
  • 8Fryer RH, Wilson BD, et al. Homocysteine: a risk factor for premature vascular disease and thrombosis induces tissue factor activity in endotheliar cells. Arteriosler Thromb, 1993,13 :1327- 1333.
  • 9Tyagi SC. Homocysteine redox recetor and regulation of extracelluar matrix components in vascuar cells. Am J Physiol,1998,274: C396 - 405.
  • 10Mayer EL, Jacobsen DM, Robinson K. Homocystein and coronary atherosclerosis. JACC, 1996,27(3) :517 - 527.

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