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目的 :探讨全反式维甲酸 (all-transretinoicacid ,atRNA)对主肺动脉段胶原含量和肺动脉高压肺血管重建的干预作用。方法 :所有动物分成三组 :对照组、模型组和atRNA组。利用野百合碱 (monocrotalineMCT)诱导大鼠肺动脉高压模型 ,同时给予atRA治疗。经导管介入测定平均肺动脉压力 ,比色法测定肺动脉段羟脯氨酸含量。结果 :对照组大鼠平均肺动脉压于不同时间差异无显著性 ,而模型组平均肺动脉压于第 2 1天 ,并继续升高至本次实验的第 2 8天。肺动脉段羟脯氨酸含量第 14天异常降低 ,以后随肺压力的升高而升高。atRNA降低第 2 1天和 2 8天肺动脉段羟脯氨酸含量 ,明显降低肺动脉压 ,差异均有显著性。结论 :atRA能抑制细胞外基质中胶原积聚 ,降低平均肺动脉压 ,阻止肺高压进展
Objective: To investigate the effect of all-transretinoic acid (atRNA) on collagen content in pulmonary artery and pulmonary vascular remodeling in pulmonary hypertension. Methods: All animals were divided into three groups: control group, model group and atRNA group. The monocrotaline (MCT) -induced pulmonary hypertension in rats was induced by atRA. The mean pulmonary artery pressure was measured by catheterization and the hydroxyproline content in the pulmonary artery segment was measured by colorimetry. Results: The average pulmonary arterial pressure in the control group was not significantly different at different time points, while the mean pulmonary artery pressure in the model group was on the 21st day and continued to increase to the 28th day of this experiment. Pulmonary arterial hydroxyproline content decreased abnormally on the 14th day, and then increased with the increase of pulmonary pressure. AtRNA decreased the content of hydroxyproline in the pulmonary artery on day 21 and day 28, and significantly decreased the pulmonary arterial pressure. The difference was significant. Conclusions: atRA inhibits collagen accumulation in the extracellular matrix, decreases mean pulmonary arterial pressure, and prevents progression of pulmonary hypertension