Background. Secondhand smoke exposure increases cardiovascular risk. Secondhand smoke–induced endothelial dysfunction has been demonstrated in older teenagers and young adults. We have previously shown in adult rabbits that SHS induces atherogenesis and endothelial dysfunction. The effects of SHS on vascular function in the offspring of SHS-exposed mothers and in infants are unknown.

Methods. In this study the effects of in-utero (21 days) and neonatal (28 days) exposure to SHS were examined in 80 rats, 4 weeks of age, in a 2-by-2 design study. Rats were exposed to sidestream smoke in smoking chambers. Aortic rings were excised and isometric force responses to phenylephrine, acetylcholine, A23187 and nitroglycerin were studied in organ baths.

Results. Neonatal SHS exposure reduced animal weight (p = 0.009). In-utero exposure increased the sensitivity (decreased the EC50) of aortic rings to phenylephrine (p < 0.0005), as did neonatal exposure (p = 0.01). Maximal contraction to phenylephrine was reduced by in-utero exposure (p = 0.04). In-utero SHS exposure reduced maximal endothelium-dependent relaxation to acetylcholine (p = 0.04) and increased the EC50 (p = 0.05), suggesting impaired sensitivity to acetylcholine. In-utero exposure decreased the sensitivity (increased the EC50) to the endothelium-independent vasodilator nitroglycerin (p = 0.003).

Conclusions. Secondhand smoke has detrimental effects on vascular smooth muscle function in the newborn.