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目的 :探讨影响先天性心脏病 ( CHD)患儿血浆内皮素 - 1( ET- 1)水平的因素及临床意义。方法 :选择69例左向右分流的 CHD患儿 ,其中伴肺动脉高压 ( PH) 5 0例 ,轻度 PH17例 ,中度 PH16例 ,重度 PH17例 ;不伴PH 19例。分别采股静脉血 ,伴有中、重度 PH 3 3例患儿随机给予前列腺素 E1 ( PGE1 ,16例 ) 2 0 ng/ ( kg· min)静脉滴注或卡托普利 ( 17例 ) 1mg/ ( kg· d)口服治疗 15 d后再采血 ,用放射免疫法测定样品中 ET- 1含量。结果 :1肺血流量增加 ,血浆 ET- 1水平亦增加 ,达正常对照 2倍多 ( P <0 .0 0 1) ;2 CHD并 PH者血浆 ET- 1水平较无PH者明显增高 ( P<0 .0 0 1) ,ET- 1含量随肺动脉压力的升高而增加 ;3 PGE1 可显著降低 PH患儿的平均肺动脉压 ( P <0 .0 5 )及血浆 ET- 1水平 ( P <0 .0 5 ) ;4卡托普利可使患儿的平均肺动脉压及血浆 ET- 1水平下降 ,但与治疗前比较差异无显著性意义 ( P >0 .0 5 )。结论 :PGE1 和卡托普利可能延缓 PH的发展。
Objective: To investigate the factors and clinical significance of plasma endothelin - 1 (ET - 1) in children with congenital heart disease (CHD). Methods: Sixty-nine children with left-to-right shunting CHD were enrolled. Among them, 50 with pulmonary hypertension (PH), 17 with mild PH, 16 with moderate PH, 17 with severe PH, and 19 without PH. Blood samples were taken from femoral vein, and 3 cases of moderate and severe PH 3 were randomly assigned to receive intravenous infusion of 20 ng / (kg · min) of prostaglandin E1 (PGE1, 16 cases) or 1 mg of captopril (17 cases) Blood samples were collected 15 days after oral administration and the content of ET-1 in the samples was determined by radioimmunoassay. Results: 1 pulmonary blood flow increased plasma ET-1 levels also increased to more than twice the normal control (P <0.01); 2 CHD and PH plasma ET-1 levels were significantly higher than those without PH (P (P <0.01). The content of ET-1 increased with the increase of pulmonary artery pressure. 3 PGE1 significantly decreased the mean pulmonary arterial pressure (P <0.05) and plasma ET-1 level in PH children (P < 0.05). 4 Captopril decreased the mean pulmonary arterial pressure and plasma ET-1 level in children with no significant difference compared with that before treatment (P> 0.05). Conclusion: PGE1 and captopril may delay the development of PH.