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目的 观察缺氧性肺动脉高压动物的血红素氧合成酶 1(HO 1)及一氧化氮合酶 (i NOS及cNOS)的含量变化。方法 用免疫组织化学和组织原位杂交技术观察对照组及缺氧后2、 3、 5周组的HO 1、iNOS、iNOSmRNA、cNOS及其cNOSmRNA在肺内的定位分布和含量 ,并用图像分析方法检测其在肺内三种不同管径的动脉中的平均积分光密度值。结果 ( 1)肺内动脉HO 1含量在H组较N组增高 ,且以H3、H5组增高明显。 ( 2 )三种不同管径的动脉中 ,HO 1增高量以Ⅱ级、Ⅲ级动脉较明显。 ( 3)iNOS及其mRNA在N组无表达 ,在H组则随缺氧时间的延长其相对含量显著性升高。 ( 4)iNOS及mRNA在三种不同管径的动脉中增高量差别不显著。 ( 5 )cNOS及其mRNA的表达及相对含量在N组与H组中无显著差别。结论 缺氧所诱导的HO 1及iNOS表达的血管级不同 ,但均随缺氧时间延长而逐渐增强 ,提示其对HPH起一定抑制作用。
Objective To observe the change of heme oxygenase 1 (HO 1) and nitric oxide synthase (i NOS and cNOS) in hypoxic pulmonary hypertensive animals. Methods The distribution and content of HO 1, iNOS, iNOS mRNA, cNOS and cNOS mRNA in lungs of control group and 2, 3, 5 weeks after hypoxia were observed by immunohistochemistry and in situ hybridization. The mean integrated optical density of the three different diameters of the arteries in the lungs was measured. Results (1) The contents of HO 1 in intrapulmonary arteries increased in group H compared with those in group N, and increased significantly in groups H3 and H5. (2) Among the three kinds of arteries with different diameters, the increase of HO 1 was more obvious in grade Ⅱ and Ⅲ grade arteries. (3) iNOS and its mRNA were not expressed in N group, while in H group, the relative content of iNOS and mRNA increased significantly with the prolongation of hypoxia. (4) There was no significant difference in the increase of iNOS and mRNA among the three arteries with different diameters. (5) The expression and relative content of cNOS and its mRNA in N group and H group had no significant difference. Conclusions The expression of HO 1 and iNOS induced by hypoxia are different in blood vessel level, but all of them are gradually increased with the prolongation of hypoxia, suggesting that it may play an inhibitory role on HPH.