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Pediatr Res. 1988 Aug;24(2):186-90.

Acute hemodynamic effects of nifedipine in infants with bronchopulmonary dysplasia and pulmonary hypertension.

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1
Division of Pediatric Cardiology, C.S. Mott Children's Hospital, University of Michigan, Ann Arbor 48109.

Abstract

The acute hemodynamic effects of nifedipine were evaluated and compared to the effects of 95% oxygen in six children with bronchopulmonary dysplasia and pulmonary artery hypertension. The children ranged in age from 7-26 months and all were oxygen dependent. In the cardiac catheterization laboratory, hemodynamic data were collected in 95% oxygen, room air, and 15 and 30 min after nifedipine administration (0.5-0.6 mg/kg per nasogastric tube). Compared to values in room air, nifedipine resulted in a 34% decrease in pulmonary artery mean pressure (from 69.3 +/- 2.4 to 45.8 +/- 1.2 mm Hg, p = 0.03) and a 49% decrease in pulmonary vascular resistance (from 14.8 +/- 1.4 to 7.5 +/- 0.9 U/m2, p = 0.03). A linear relationship was found between the arterial pO2 and the change in the ratio of pulmonary to systemic resistance after nifedipine (% decrease in Rp/Rs ratio = 86.3 - 1.3 x pO2, r = -0.95, p = 0.004) suggesting that nifedipine may act to oppose the vascular effects of arterial hypoxemia. There was no significant change in heart rate, arterial pO2, or pCO2 with nifedipine, but cardiac output increased significantly. Compared to 95% oxygen, nifedipine achieved a lower pulmonary vascular resistance (7.5 +/- 0.9 versus 10.9 +/- 1.2 U/m2, p = 0.03) and a greater cardiac output (5.25 +/- 0.71 versus 3.54 +/- 0.35 liter/min/m2, p = 0.03) with comparable systemic oxygen delivery (699 +/- 85 ml versus 698 +/- 91 ml O2/min/m2, p = 1.0). Thus, nifedipine is an acute pulmonary vasodilator in some children with bronchopulmonary dysplasia.(ABSTRACT TRUNCATED AT 250 WORDS).

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