Pulmonary hypertension is a major source of morbidity and mortality in infants born with
congenital diaphragmatic hernia (CDH). Increased pulmonary vascular resistance leads to right-to-left shunting, which is evident as decreases in the PaO2 measured in postductal arterial blood.
Thromboxane A2 (TXA2), a
vasoconstrictor, and
prostacyclin (
prostaglandin I2, PGI2), a
vasodilator, have been studied as possible mediators of
pulmonary hypertension in certain conditions of the newborn, including
congenital diaphragmatic hernia (CDH). The goal of our study was to determine the association of TXA2 and PGI2 levels with
hypoxemia in infants born with CDH. Eleven newborn infants with severe
respiratory insufficiency (
birth weight 2.0-4.1 kg; gestational age 32-42 weeks) were studied 0-5 days after surgical repair of CDH. Umbilical artery samples were collected for arterial blood gas determinations and radioimmunoassay of
thromboxane B2 (TXB2) and 6-keto
prostaglandin F1 alpha (6-keto-PGF1 alpha), stable metabolites of TXA2 and PGI2, respectively. Postductal arterial
hypoxemia (reflected by a low a-A ratio, the ratio of
oxygen tension in arterial blood to that in the alveolus) was associated with increases in TXB2 (r = -0.71, P = 0.004) and 6-keto-PGF1 (r = -0.65, P = 0.017). The a-A ratio also correlated inversely with TXB2/
6-keto-PGF1 alpha (r = -0.50, P = 0.01), suggesting an increased influence of the
vasoconstrictor TXA2.(ABSTRACT TRUNCATED AT 250 WORDS)