Changes of Endothelin-1 Level after the Closure of Patent Ductus Arteriosus

Pulmonary hypertension is characterized by an increase in vascular tone of an abnormal proliferation of muscle cells in the wall of small pulmonary arteries. Endothelin-1(ET-1) is a potent endothelium-derived vasoconstrictor peptide with important mitogenic properties. It has been recognized that endothelin-1 may contribute to increase in pulmonary arterial tone or smooth muscle proliferation in congenital heart disease patients with pulmonary hypertension. To explore the role of endothelin-1 in patent ductus arterious, we measured endothelin-1 before and after closure of ductus in artery and vein plasma.

Seven patients of patent ductus arteriosus underwent thoracoscopic clipping of dustus in 1997 June-August. Their age was 1-24 months and male 4, female 3. Blood samples were drawn from radial artery and inferior vena cava before, 30 minutes and 90 minutes after closure of ductus. Endiothelin-1 was measured by radioimmunoassay method.

Arterial endothelin-1 was 17.96±8.09pg/ml at before closure of ductus, 13.47±3.14pg/ml at 30 minutes after closure of ductus and 11.43±2.9pg/ml at 90 minutes after closure of ductus. Venous endothelin-1 was 9.34±3.55pg/ml at before closure, 8.9±3.74pg/ml at 30 minutes after closure and 8.4±3.71pg/ml at 90minutes after closure of ductus. Arterial endo-thelin-1 was significantly higher than venous one at before and 30 minutes after ductus closure(p<0.05). Arterial endothelin-1 at 90 minutes after ductus closure was significantly lower than that at before the closure(p<0.05).

Patients pf patent ductus arteriosus have substantial alterations in plasma endo-thelin-1 which is decreased after closure of ductus. Comparing with venous plasma, the higher levels of ET-1 in arterial plasma suggest pulmonary production of endothelin-1, which may contribute to induce pulmonary hypertension.