血浆ET-1和AT-Ⅱ与室间隔缺损肺动脉高压关系的研究

Plasma endothelin-Ⅰ and angiotensin-Ⅱ concentrations in children with ventricular septal defects

为探讨血浆内皮素一l（ET-1）和血管紧张素-Ⅱ（AT一Ⅱ）与室间隔缺损肺动脉高压的关系以及围手术期两者的动态变化。30例室间隔缺损患儿，超声心动图检查诊断明确，并根据跨室间隔压差分成肺动脉压力正常组（组Ⅰ，n=12）和肺动脉高压组（组Ⅱ，n=18）。ET-Ⅰ和AT-Ⅱ均用放射免疫法测定。其中20例行右心导管检查以取得血流动力学资料。结果：全组肺动脉和主动脉血浆ET-l分别为68．8土10．4ng／L和77．4土11．2ng／L，高于放射免疫法的正常值50．8土7．58ng／L（P＜0．01）；AT-Ⅰ值分别为182．5土34．7ng／L和207·8士40．4ng／L，明显高于放射免疫法正常值40．2士12．ong／L（P＜0．01）。转流前组Ⅱ的ET-l和AT-Ⅱ值明显高于组Ⅰ（P〈0.01），组Ⅱ主动脉血ET-l和AT-Ⅱ含量均高于肺动脉血，有显著差异，P＜0．05；组Ⅰ也是如此，但无显著差异，P＞0．05。相关分析发现ET-Ⅰ与肺循环流量、肺动脉压力呈直线正相关，而AT-Ⅰ含量则与肺动脉压力和肺循环阻力呈直线正相关。体外循环结束时ET-Ⅰ和AT-Ⅱ含量较转流前明显升高，术后24小时则明显下降。本文结果提示：血浆ET-Ⅰ和AT-Ⅱ与室间隔缺损肺动脉高压明显相关，提示可能与肺动脉高压的发生有关。

To investigate the changes of plasma endothelin- Ⅰ and angiotensin-Ⅱ, concentrations in children withventricular septal defects. We measured plasma endothelin- Ⅰ (ET- Ⅰ )and angiotensin- Ⅱ (AT- Ⅱ ) concentrations by us-ing radioimmunoassay in 30 patients with ventricular septal defects(VSD). According to pulmonary artery pressure fromechocardiography, we divided the patients into groupⅠ (non-pulmonary hypertension,n= l2) and group Ⅱ (phlmonary hypertension, N= l8). 20 cases were subjected to cardiac catheterization. Blood samples were obtained from pulmonary artery, aorta and radial artery. Plasma ET- Ⅰ and AT-Ⅱ concentrations in group Ⅰ were significantly higher than those in group Ⅰ. ET- Ⅰ and AT- Ⅱ concentrations at aorta were also slightly higher than those at pulmonary artery in two groups. ET- I concentration had a linear positive correlation with pulmonary blood flow and pulmonary artery pres-sure, and plasma AT- Ⅱ concentration had a linear positive correlation with pulmonary artery pressure and pulmonary resistance. After surgical repair of VSD, plasma ET- Ⅰ and AT-Ⅱ, concentrations decreased except for 6 cases with the pulmonary resistance more than 500 dyne. sec. cm-5. Plasma ET- Ⅰ and AT- Ⅱ concentrations are elevated in patients with ventricular septal defects associated with left-to-right shunt and may have an important role in the pathogenesis of pulmonary hypertension.