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研究脉动脉压力对肺小动脉壁原弹性蛋白表达与分布的影响以帮助阐明先天性心脏病(先心病)肺动脉高压(肺高压)肺血管重建的发病机制。将15例患儿分为对照组(组1)、先心病高肺血流组(组2)及先心病肺高压组(组3)。用免疫组化技术研究弹性蛋白在肺小动脉壁的含量与分布以了解弹性蛋白的合成情况;用原位杂交技术在转录水平研究肺小动脉壁原弹性蛋白mRNA的表达分布。结果:各组患儿间年龄比较无差异。组2、组3间肺动脉压力有显著差异(P<0.01),Qp/Qs无差异(P>0.05)。原位杂交:组1、组2均未见阳性信号表达,组3有不同程度表达,其阳性率与肺动脉压力呈正相关(r=0.89,P<0.01),而与肺血流量无关(r=-0.59,P=0.08>0.05)。表达部位主要集中于肺小动脉的外膜及其周围。免疫组化:组1、组2各例阳性显色主要集中于血管壁中层内外弹力层区域,组3外膜及其周围还可见不同强度及区域大小的阳性信号区。结论:左向右分流型先心病肺高压时出现原弹性蛋白mRNA再表达且蛋白积聚位置异常,肺血管壁高张力(高压力)是弹性蛋白合成增加的主要促成因素。这对阐明先心病肺高压肺血管重建的发病机制有重要作用。
To study the effect of pulse pressure on the expression and distribution of proANALP in the small pulmonary arteries to help elucidate the pathogenesis of pulmonary vascular remodeling in patients with congenital heart disease (CHD). Fifteen children were divided into control group (group 1), congenital heart disease with high pulmonary blood flow group (group 2) and congenital heart disease with pulmonary hypertension group (group 3). Immunohistochemistry was used to study the content and distribution of elastin in the pulmonary arterioles wall to understand the synthesis of elastin. The expression of elastase mRNA in pulmonary arterioles was investigated by in situ hybridization at the transcriptional level. Results: There was no difference in age between children in each group. Group 2, Group 3 pulmonary artery pressure was significantly different (P <0.01), Qp / Qs no difference (P> 0.05). In situ hybridization: no positive signal was observed in group 1 and group 2, while group 3 was expressed in varying degrees. The positive rate was positively correlated with pulmonary artery pressure (r = 0.89, P <0.01), but not pulmonary blood flow (r = -0.59, P = 0.08> 0.05). The expression sites mainly focus on the outer membrane of pulmonary arterioles and their surroundings. Immunohistochemistry: Group 1, group 2 each case of positive color mainly concentrated in the middle of the vascular wall inside and outside the elastic layer region, group 3 and around the outer membrane can also see the intensity and size of the positive signal area. CONCLUSIONS: Prolactin mRNA reappears and abnormal protein accumulation occurs in patients with left-to-right shunt congenital heart disease with pulmonary hypertension. High hyper tension (high pressure) in the pulmonary vascular wall is the major contributor to increased elastin synthesis. This elucidation of congenital heart disease pulmonary hypertension pulmonary vascular reconstruction plays an important role in the pathogenesis.