期刊文献+

内皮细胞损伤对于经皮冠状动脉介入术后血流的意义 被引量:5

Significance of endothelial cell injury for coronary blood flow in patients after percutaneous coronary intervention
下载PDF
导出
摘要 目的:研究经溶栓或经皮冠脉介入术(PCI)治疗后冠脉恢复正常血流患者和冠脉无复流患者内皮细胞的损伤情况,并探讨其临床意义。方法:选择90例PCI患者,根据术后血流分级(TIMI分级)分为两组,冠状动脉血流≤TIMI2级40例,为无复流组,TIMI3级50例,为对照组。检测两组患者冠脉血中内源性一氧化氮(NO)、内皮素(ET)、血小板表面活化标志蛋白(CD63)水平,以此判断内皮细胞受损情况。结果:PCI术后无复流组较对照组冠脉中NO明显减少[(41.52±6.1):(61.94±10.7)μmol/L],而ET[(117.42±11.1):(59.08±9.8)mg/L]、CD63[(7.43±8.2)%:(2.05±2.8)%]显著增加(P均<0.05)。提示在PCI后患者出现无复流现象者较血流恢复正常者冠状动脉内皮损伤更严重。结论:内皮细胞损伤是冠状动脉PCI术后无复流的重要原因。 Objective: To research the significance of endothelial cell injury for coronary blood flow in patients after percutaneous coronary intervention. Methods: A total of .90 patients after PCI were divided into coronary blood flow TIMI 2 group (40 cases) as no-reflow group, coronary blood flow〉TIM1 3 group, as the control group (50 cases) according TIMI blood flow grade. The nitric oxide (NO), endothelin (ET). platelet activation marker proteins (CD63) were detected in each group. Results: The level of NO was lower and ET, CD63 significantly increased in noreflow group, compared with those of control group [ (41.52±6.1) μmol/L vs. (61.94±10.7) μmol/L (117.42± 11.1) mg/Lvs. (59.08±9.8) mg/L, (7.43±8.2)% vs. (2.05±2.8)% respectively, P〈0. 05 all. Conclusion: The injury of endothelial cell after coronary artery PCI is the important reasons of no-reflow.
出处 《心血管康复医学杂志》 CAS 2010年第3期262-264,共3页 Chinese Journal of Cardiovascular Rehabilitation Medicine
基金 佳木斯大学2008年立项项目(S2008-012)
关键词 血管成形术 经腔 经皮冠状动脉 内皮细胞 一氧化氮 Angioplasty, transluminal, percutaneous coronary Endothelial cell Nitric oxide
  • 相关文献

参考文献7

二级参考文献31

共引文献2702

同被引文献64

  • 1Esper R, Nordaby R, Vilarino J, et al. Endothelial dysfunction: a comprehensive appraisal [J]. Cardiovasc Diabetol, 2006, 5: 4--21.
  • 2Panza JA, Quyyumi AA, Brush JE, et al. Abnormal endothelium dependent vascular relaxation in patients with essential hypertension [J]. N Engl J Med, 1990, 323: 22--27.
  • 3Nakagawa T, Kang DH, Feig D, et al. Unearthing uric acid: an ancient factor with recently found significance in renal and cardiovascular disease [J]. Kidney Int, 2006, 69:1722--1725.
  • 4Mazzali M, Hughes J, Kim YG, et al. Elevated uric acid increases blood pressure in the rat by a novel crystal-independent mechanism [J]. Hypertension, 2001, 38: 1101--1106.
  • 5Johnson RJ, Segal MS, Srinivas T, et al. Essential hypertension, progressive renal disease, and uric acid: a pathogenetic link [J]. J Am Soc Nephrol, 2005, 16: 1909--1919.
  • 6Feig DI, Johnson RJ. Hyperuricemia in childhood primary hypertension [J]. Hypertension, 2003, 42: 247--252.
  • 7Laura G, Snchez L, Virgilia S, et al. Role of oxidative stress in the renal abnormalities induced by experimental hyperuricemia [J]. Am J Physiol Renal Physiol, 2008, 295: 1134--1141.
  • 8Khosla UM, Zharikov S, Finch JL, et al. Hyperuricemia induces endothelial dysfunction [J]. Kidney Int, 2005, 67:1739 --1742.
  • 9Zoccali C, Maio R, Mallamaci F, et al. Uric acid and endothelial dysfunction in essential hypertension [J].J Am Soc Nephrol, 2006, 17: 1466--1471.
  • 10Marilda M, John K, Lin H, et al. Hyperuricemia induces a primary renal arteriolopathy in rats by a blood pressure--independent mechanism [J]. Am J Physiol Renal Physiol, 2002,282: 991--997.

引证文献5

二级引证文献31

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部