內(nèi)皮素、降鈣素基因相關肽與先天性心臟病肺動脈壓、肺血流量關系的研究

1、內(nèi)皮素、降鈣素基因相關肽與先天性心臟病肺動脈壓、肺血流量關系的研究 2009-12-14 徐寶元李渝芬* 【摘要】目的探討先天性心臟病(CHD)肺動脈高壓(PH)的發(fā)病機理。方法采用非平衡放射免疫分析法測定52例肺高壓(同伴Qp增加)和30例肺循環(huán)血流量(Qp)增加的先心病患兒上腔靜脈(SVC)、右心房(RA)、右心室(RV)、肺動脈(PA)、肺靜脈(PV)部位血漿ET-1濃度和SVC部位CGRP濃度，18例健康兒童作為對照。結(jié)果血漿ET-1濃度隨著PH程度的加重和Qp的增加而升高，ET-1與肺動脈收縮壓(SPAP)、全肺阻力(PVP)和Qp呈正相關(r=0.93,0.79,0.65;P0.0

2、1)，CGRP則相反(r=-0.90,-0.82, -0.55; P0.01)。SVC、RA、RV部位間ET-1濃度無顯著差異(P0.05)，而RV、PA、PV間ET-1濃度都有顯著差異(P0.01或0.05)。ET-1與CGRP呈負相關(r=-0.93,P0.01)。結(jié)論先心病PH和Qp增加皆可導致血漿ET-1濃度升高，PH時更著，升高之來源為肺循環(huán)。ET-1促進了先心病PH的形成和發(fā)展。Qp增加是PH形成的啟動因子。CGRP的濃度下降和CGRP/ET-1的失衡可能是PH發(fā)病的另一因素。 【關鍵詞】先天性心臟病內(nèi)皮素-1降鈣素基因相關肽肺動脈高壓肺循環(huán)血流量 Correlations of

3、plasma endothelin-1 and calcitonin gene-related peptide concentrations to pulmonary arterial pressure and flow in children with congenital heart defects Xu Baoyuan, Li Yufen. Guangdong Provincial Cardiovascular Institute, Guangzhou 510100 【Abstract】ObjectiveTo study the pathogenesis of pulmonary hyp

4、ertension (PH) associated with congenital heart defects (CHD). MethodsPlasma endothelin-1 (ET-1) concentrations at superior vena cava (SVC), right atrium (RA), right ventricle (RV), pulmonary artery (PA) and pulmonary vein (PV), and calcitonin gene-related peptide (CGRP) concentration at SVC were me

5、asured by using the non-balanced radioimmunoassay in 52 patients with PH and 30 patients with the increased pulmonary blood flow (Qp) caused by CHD.ResultsThe plasma ET-1 concentrations elevated along with an increase in degree of PH and in Qp. ET-1 concentration correlated positively with systolic

6、pulmonary artery pressure (SPAP), total pulmonary resistance (PVR) and Qp(r=0.93, 0.79, 0.65; P0.01), respectively, while the plasma CGRP was correlated negatively with SPAP, PVR and Qp(r=-0.90,-0.82,-0.55; P0.01), respectively. There was no significant difference among SVC, RA and RV (P0.05), but w

7、ere significant differences among RV, PA and PV(P0.01 or P0.05). There was a negative correlation between ET and CGRP concentrations (r=-0.93, P0.01). ConclusionsPlasma ET-1 concentrations in patients with PH and increased Qp secondary to CHD are elevated, especially in patients with PH; the elevati

8、on is due to the increased production of ET-1 in pulmonary circulation. ET-1 promotes the formation and development of PH in patients with CHD, and is a major factor for the pathogenesis of PH. Increased Qp is also a factor inducing PH. Insufficient secretion of plasma CGRP and severe imbalance of C

9、GRP/ET-1 also were possiblely involved in the pathophysiology of PH. 【Key words】Congenital heart defects Endothelin-1 Calcionin geneRelated peptide Pulmonary hypertension Pulmonary blood flow 肺動脈高壓(簡稱肺高壓或PH)是先天性心臟病(簡稱先心病或CHD)常見并發(fā)癥，是關系手術適應癥及預后的重要因素之一，但其發(fā)病機理尚不清楚。內(nèi)皮素-1(ET-1)是血管內(nèi)皮細胞分泌的最強的縮血管肽1，而降鈣素基因相關肽

10、(CGRP)則是肽能神經(jīng)纖維釋放的最強的舒血管肽2。本文探討二者的消長變化及在PH發(fā)病中的意義。 對象和方法 一、研究對象 1.CHD組：82例，均為1998年2月1999年1月在我所住院的左向右分流型CHD患兒。其中男48例，女34例；年齡6個月14歲(4.8±3.6）歲。全部病例行心導管檢查及選擇性心血管造影確診，包括室間隔缺損(VSD)47例，房間隔缺損(ASD)9例，動脈導管未閉(PDA)1例，ASD+VSD 4例，VSD+PDA 14例，ASD+PDA 1例，完全型房室隔缺損(CAVC)3例，部分型房室隔缺損(PAVC)2例，冠狀動脈瘺(CAF)1例。全部病例均除外嚴重心律

11、失常、高血壓、肺部感染及肝腎功能障礙等。 CHD組患兒分為肺高壓組(PH組，52例)(同伴Qp的增加)和肺循環(huán)血量增加組(HQp組,30例)。PH組又分為三個亞組：輕度PH組，30 mmHg肺動脈收縮壓(SPAP)50 mmHg(6.7 kPa),18例；中度PH組，50 mmHgSPAP70 mmHg(9.3 kPa),16例；重度PH組，SPAP70 mmHg，18例。HQp組又按肺/體循環(huán)血流量(Qp/Qs)分為兩個亞組：少量左向右分流組(LF組)，Qp/Qs2.0， 15例；大量左向右分流組(HF組)，Qp/Qs2.0，15例。 PH組和HQp組之間，性別、年齡均相匹配，主動脈收縮壓(

12、SABP)、Qs、體循環(huán)阻力(Rs)、體表面積、血紅蛋白等均無顯著差異。 2.對照組：18例，男10例，女8例，年齡8個月12.5歲(5.5±3.5）歲，均為健康體檢者。 二、研究方法 1.血流動力學參數(shù)測定和計算：CHD組在右心導管檢查中，經(jīng)導管分別在上腔靜脈(SVC)、下腔靜脈(IVC)、右心房(RA)、右心室(RV)、肺動脈(PA)、肺靜脈(PV)和主動脈(Ao)部位采血0.5 mL，用血氧分析儀測定這些部位血氧飽和度。同時接電生理記錄儀測量右房平均壓(MPAP)、SPAP、肺動脈平均壓(MPAP)、SABP、主動脈平均壓(MABP)。計算出血氧含量(mL/dL)、氧消耗量(mL/min),按Fick公式計算出QpL/（min.m2)、QsL/（min.m2)，繼而算出Qp/Qs、全