[The expression of tyrosine-kinase receptor flk-1 and hypoxic pulmonary vascular remodeling in the lung of rats exposed to hypoxia].

D Cheng, X Xiao, W Chen
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Abstract

Objective: To assess the role of tyrosine-kinase receptor flk-1 in the development of hypoxic pulmonary vascular remodeling.

Methods: We divided 20 male Wistar rats into two groups(control vs hypoxia) and exposed them to normoxic condition and isobaric hypoxia for 3 weeks respectively. The pulmonary artery pressure was measured by right cardiac catheterization. The expression of flk-1 in lung tissues was measured by immunohistochemical staining. Histologic sections of the lungs were examined by a computerized image analyser.

Results: In hypoxic rats, the pulmonary artery pressure was significantly raised to a higher level, P < 0.01; the cell number of vascular wall was significantly increased. The results also demonstrated that chronic hypoxia brought about the significant increment in thickness of wall with narrowing of lumen of pulmonary arterioles, and the increment in the percent of vascular wall thickness/vascular external diameter (WT%) and the percent of vascular wall area/total vascular area (WA%), P < 0.01. The positive staining of flk-1 in the wall of pulmonary arteriole of rats treated with hypoxia was significantly stronger than that of normal rats, P < 0.01. Positive correlations were seen between the increment of expression of flk-1 with WT% and WA% (r = 0.714, 0.738, P < 0.01).

Conclusion: Chronic hypoxia can induce an increasing expression of flk-1, and the flk-1 may play an important role in the pathogenesis of hypoxic pulmonary vascular remodeling.

[缺氧大鼠肺组织中酪氨酸激酶受体flk-1的表达及缺氧肺血管重构]。
目的:探讨酪氨酸激酶受体flk-1在缺氧肺血管重构中的作用。方法:将20只雄性Wistar大鼠分为对照组和低氧组,分别置于常氧和等压低氧环境下3周。右心导管测肺动脉压。免疫组化染色检测肺组织中flk-1的表达。用计算机图像分析仪检查肺的组织学切片。结果:缺氧大鼠肺动脉压明显升高,P < 0.01;血管壁细胞数量显著增加。慢性缺氧使肺小动脉管壁厚度显著增加,管腔变窄,血管壁厚度/血管外径百分比(WT%)和血管壁面积/总血管面积百分比(WA%)均显著增加,P < 0.01。缺氧大鼠肺小动脉壁flk-1阳性染色明显强于正常大鼠,P < 0.01。flk-1的表达量增量与WT%、WA%呈显著正相关(r = 0.714、0.738,P < 0.01)。结论:慢性缺氧可诱导flk-1表达升高,flk-1可能在缺氧肺血管重构的发病机制中起重要作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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