Chronic exposure to cigarette smoke extract impairs endothelium-dependent relaxation of chicken embryo pulmonary arteries

Maternal smoking may increase the risk for various adverse neonatal outcome s including persistent pulmonary hypertension of the newborn (PPHN). We inv estigated whether chronic prenatal cigarette smoke extract (CSE) exposure c ould produce abnormal vasoreactivity in pulmonary arteries. Daily injection s of CSE (diluted in phosphate buffered saline) or vehicle were added to th e air cells of fertilized eggs starting on day 5 of the 21-day incubation p eriod of the chicken embryo. On day 19, pulmonary arteries were dissected o ut and their contractile properties were assessed using small vessel myogra phy. Endothelium-dependent and endothelium-independent vasorelaxations were examined by using acetylcholine (ACh, 10(-8) to 10(-4) M) and sodium nitro prusside (SNP, 10(-8) to 10(-4) M), respectively. The drug concentration in ducing 50% of the maximal relaxation was determined for each concentration- response curve and expressed as negative log molar (pD(2)). Exposure to CSE significantly decreased the sensitivity of pulmonary arteries to ACh (pD2 control group: 7.29 +/- 0.24; pD(2) CSE-exposed group 6.24 +/- 0.12, p < 0. 05). SNP elicited similar responses in vessels of both groups at all tested concentrations. In conclusion, chronic prenatal exposure to CSE impaired e ndothelium-dependent but not endothelium-independent vasodilation in chicke n embryo pulmonary arteries. This observation suggests that cigarette smoke components may produce deleterious effects on fetal vascular endothelial v asorelaxant pathways, leading to the development of adverse outcomes such a s PPHN. Copyright (C) 2001 S. Karger AG, Basel.