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作 者:赵翠芬[1] 夏伟[1] 王玉玮[1] 杨杰[1] 杨兴季[1]
出 处:《临床儿科杂志》2006年第5期374-376,共3页Journal of Clinical Pediatrics
摘 要:目的研究左向右分流先心病肺动脉高压(肺高压)患儿肺组织内皮素-1(ET-1)与肺组织Ⅰ、Ⅲ型胶原合成的关系,探讨左向右分流先心病患儿肺高压形成的机理。方法选择左向右分流先心病患儿18例,根据肺动脉收缩压分为肺高压组(n=10),非肺高压组(n=8)。所有患儿在外科手术体外循环开始前,取右肺中叶组织(1cm×1cm×1cm),放射免疫法测定患儿血浆及肺组织ET-1含量;RT-PCR法检测肺组织Ⅰ、Ⅲ型胶原mRNA表达。结果先心病肺高压患儿血浆及肺组织ET-1含量明显高于肺动脉压正常者(P<0.01)。肺高压患儿肺组织Ⅰ、Ⅲ型前胶原mRNA的表达与肺动脉压正常者相比明显增加(P<0.05)。结论ET-1可能通过刺激肺动脉平滑肌细胞胶原合成增加参与肺高压的形成。Objective To explore the pathogenesis of pulmonary hypertension in children with left to right shunt congenital heart disease (CHD) and the relationship of endothelin-1 (ET-1) and typeⅠ and type Ⅲ collagen synthesis in pulmonary tissue. Methods 18 children with CHD were enrolled in this study, and the right middle lung tissue (1cm×1cm×1cm) were dissected before extrasystolic circulation. The plasma and pulmonary tissue ET-1 were detected with radioimmunoassay, and the expression of the mRNA of type Ⅰ and type Ⅲ procollagen in lung tissue was measured with RT-PCR. Results The plasma and pulmonary tissue ET-1 levels as well as the expression levels of the mRNA of type Ⅰ and type Ⅲ procollagen in lung tissue were significantly higher in pulmonary hypertension group than those in non-pulmonary hypertension group (P〈0.05). Conclusions ET-1 can increase the collagen level of lung tissue that maybe involved in the pathogenesis of pulmonary hypertension through stimulating the collagen synthesis of pulmonary arterial smooth muscle cells.
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