Alterations of placental vascular function in asthmatic pregnancies

Asthma during pregnancy is associated with low-birthweight neonates at term but the mechanisms that cause this outcome are presently unknown. Changes in placental vascular function resulting from asthma or its treatment could contribute to altered fetal growth. We have prospectively followed women w ith asthma and a control group of women without asthma during their pregnan cies, classified them based on asthma severity and glucocorticoid intake, a nd monitored fetal development and placental blood flow using Doppler ultra sound at 18 and 30 wk gestation. The placentae from these women were collec ted after delivery and vascular responses to dilator and constrictor agonis ts assessed using an In vitro placental perfusion method. At 18 wk gestatio n, umbilical artery flow velocity waveforms were significantly reduced in t he moderate and severe asthmatic groups and in those women using high-dose inhaled glucocorticoid for the treatment of their asthma (ANOVA, p < 0.05). However, at 30 wk gestation there were no significant differences in umbil ical artery flow velocity between control and asthmatic women (ANOVA, p > 0 .05). Corticotropin-releasing hormone (CRH), a potent vasodilator that acts via the nitric oxide pathway, caused a dose-dependent vasodilatory respons e in all placentae in vitro. However, CRH-induced dilation was significantl y reduced in moderate and severe asthmatics (ANOVA, p < 0.05). Vasoconstric tor responses to potassium chloride and prostaglandin F-2 alpha were reduce d in placentae from moderate and severe asthmatic women (ANOVA, p < 0.05). These studies demonstrate significant differences in placental vascular fun ction in pregnancies complicated by asthma, which may relate directly to th e asthma or be a consequence of the associated glucocorticoid treatment. Th ese changes in vascular function in asthmatic pregnancies may contribute to the low-birthweight outcome observed in this condition.