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脑梗死与血管活性物质及同型半胱氨酸的相互关系 被引量:1

The correlation between cerebral infarction and vasoactivators and homocysteinemia
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摘要 目的 探讨脑梗死患者颈动脉病变 ,血管活性物质 [一氧化氮 (NO)、内皮素 (ET 1) ]及同型半胱氨酸 (Hcy)的相互关系。方法 选择 14 9例高血压患者 ,按有无缺血性脑卒中分为 2组 ,A组 :高血压并发缺血性脑卒中组 (74例 )。B组 :单纯高血压病组 (75例 ) ,对上述患者测定血清中NO、ET 1、Hcy值 ,颈动脉超声。结果 缺血性脑卒中组Hcy、ET 1生成增加 ,NO生成减少 ,差异有显著性 (P <0 .0 5 )。颈动脉斑块的发生A组较B组明显增多 ,差异有显著性 (P <0 .0 5 )。结论 高Hcy加重了高血压对血管壁的损伤 ,使血管内皮细胞中NO生成减少 ,ET 1生成增加 ,斑块的形成增加 ,从而促进了血管内血栓的形成 。 Objective To assess the relationship between carotid lesions and some vasoactivators as well as homocysteinemia in patients with hypertension.Methods 149 Hypertensive patients were divided into two groups:group A,74 patients with both hypertension and cerebral infarction;group B,75 hypertensive patients without infarction.The homocysteine(Hcy),nitrogen monoxide(NO) and endothelin(ET 1) levels of all these patients were assessed.The ultrasonography of carotid artery was also performed at the same time.Results In group A,Hcy and ET 1 levels were higher and NO level was lower than those in group B with significant difference (P< 0.05 ).The incidence of carotid artery plaque in group A was much higher than that in group B(P<0.05).Conclusion The impairment of the arterial wall induced by hypertension was aggravated by hyperhomocysteinemia,thus enhancing the development of arterial thrombosis and the risk of cerebral infarction.
出处 《中华老年心脑血管病杂志》 CAS 2002年第5期325-326,共2页 Chinese Journal of Geriatric Heart,Brain and Vessel Diseases
关键词 脑梗死 血管活性物质 同型半胱氨酸 缺血性脑卒中 cerebral infarction hypertension cysteamine nitric oxide
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  • 1[1]Britten MB, Zeiher AM, Schachinger V. Clinical importance of coronary endothelial vasodilator dysfunction and therapeutic options[J]. J Intern Med, 1999,245; 315-327.
  • 2[2]Hankey GJ, Eikeboom JW. Homocysteine and vascular disease[ J]. Lancet, 1999,354:407-413.
  • 3[3]Stein JH, Mcbride PE, Hyperhomocysteinemia and atherosclerotic vascular disease[J]. Arch Intern Med, 1998,158:1301-1306.
  • 4[4]Tawakol A, Omland T, Gerhard M, et al. Hyperhomocysteinemia is associated with impaired endothelium-dependent vasodilation in humans [J]. Circulation, 1997,955: 1119-1121.

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