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作 者:尹宗涛[1] 朱洪玉[1] 汪曾炜[1] 王辉山[1] 李新民[1] 方敏华[1]
出 处:《中华胸心血管外科杂志》2009年第5期343-345,共3页Chinese Journal of Thoracic and Cardiovascular Surgery
基 金:本课题受全军十一五卫生科研基金青年学者项目资助(06Q015)
摘 要:目的研究长期肺循环无搏动血流对微血管床结构和功能的影响。方法建立犬右肺单侧无搏动血流灌注的动物模型,6个月后对比研究两侧肺组织毛细血管床微小动脉结构以及血管内皮细胞一氧化氮合酶(endothelial nitric oxide synthase,eNos)的变化。结果无搏动血流灌注的右肺微小动脉eNOS表达显著低于左肺(t=2.24,P〈0.05),细胞凋亡fas表达显著高于左肺(t=2.16,P〈O.05),两者显著负相关(r=-0.82,t=0.151,P〈0.05)。图像分析显示,微小动脉管壁面积与血管总面积比值右肺显著低于左肺(t=2.14,P〈0.05)。结论长期无搏动性血流灌注会引起肺血管内皮细胞对eNOS合成减少,导致微动脉血管壁平滑肌细胞凋亡增加,动脉静脉化。Objective To demonstrate changes in pulmonary capillary structure and endothelial function induced by chronic nonpulsatile flow in Fantan circulation. Methods Canine models with nonpulsatile flow in the right lung was estabhshed, and sacririced 6 months later, compare the structure, eNOS, and apoptosis in pulmonary arterioles. Results Compared to the left, in the right nonpulsatile flow perfusing lung, the expression of eNOS was weaker ( t = 2.24; P 〈 0.05), the fas was stronger ( t = 2.16; P〈0.05), r = -0.82(t =0.151; P〈0.05). The wall thickness of the pulmonary arterioles was thinner(t =2.14; P〈0.05). Conclusion Long-term nonpulsatile flow can decrease the expression of eNOS, increase the arteriole apoptosis, leading to vascular structure remedeling.
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