The endothelin antagonist @entity11344 reduces pulmonary vascular resistance after surgical intervention for XXXX .

@entity1 @entity2232 @entity26 @entity120 @entity534 @entity358 @entity842 @entity11344 @entity299
OBJECTIVE: @entity120 in @entity1 after surgical intervention for @entity299 has been attributed to failure of the pulmonary endothelium to provide adequate vasodilation. Although we have shown that the impaired vasodilatory component attributable to the @entity534 - @entity842 pathway is almost completely reversible, a nonrestorable component persists, implying an additional vasoconstrictive mechanism in @entity358 . In this study of @entity1 after surgical intervention for @entity299 , we measured @entity2232 levels and used @entity11344 , a selective endothelin-A receptor antagonist, together with inhaled @entity842 to discriminate dysfunctional pulmonary endothelial vasodilation from endothelin-mediated pulmonary vasoconstriction. METHODS: All @entity1 were examined early after surgical intervention in the intensive care unit. Pulmonary vascular resistance (with respiratory mass spectrometry), as well as arterial and venous @entity2232 levels (measured by means of a quantitative enzyme-linked immunosorbent assay), were determined in 7 @entity1 (age range, 3.3-13.7 months; median age, 6.3 months) with intracardiac shunting defects at baseline and during ventilation with a fraction of inspired @entity26 of 0.65, with additional @entity11344 (0.1 mg/kg infused over 20 minutes), and with inhaled @entity842 (20 ppm). RESULTS: Pulmonary vascular resistance decreased from 7.7 +/- 3.4 at baseline to 6.1 +/- 2.8 Woods units. m(-2) (P =.022) at a fraction of inspired @entity26 of 0.65 and to 4.7 +/- 2.7 Woods units. m(-2) (P =.013) during @entity11344 infusion. Inhaled @entity842 had no further effect on pulmonary vascular resistance. Left atrial @entity2232 levels (1.35-5.12 pg/mL; mean, 2.4 pg/mL) correlated significantly with the decrease in pulmonary vascular resistance in response to @entity11344 infusion (r(2) = 0.89, P =.003). CONCLUSION: Postoperative elevation of pulmonary vascular resistance in @entity1 after surgical intervention for @entity299 is responsive to endothelin-A blockade with @entity11344 . Increased levels of @entity2232 predict the response to this therapy, which might become an important addition to the clinical armamentarium in @entity120 .
