Wednesday, February 4, 2009
WEDNESDAY, Feb. 4 (HealthDay News) -- The reduced fetal growth seen in the offspring of maternal smokers may be due in part to lower endothelial nitric oxide synthase (eNOS) activity in fetal umbilical and chorionic vessels, according to research published online Feb. 2 in Circulation: Journal of the American Heart Association.
Malene R. Andersen, Ph.D., of the Gentofte University Hospital in Hellerup, Denmark, and colleagues analyzed data from 266 healthy singleton pregnancies, in which 43 women were smokers, 41 stopped at roughly six weeks into the pregnancy, and 182 were non-smokers. The researchers took women's blood samples during the pregnancy, as well as a blood sample from the fetal umbilical vein upon delivery. They also collected endothelial cells from umbilical and chorionic vessels.
Compared with newborns of non-smokers and former smokers, the offspring of smokers were significantly smaller in weight, height and head circumference, the researchers report. Non-smokers and former smokers had similar eNOS activity in umbilical veins and eNOS concentration, but these values were 36 percent and 47 percent lower, respectively, in smokers, the investigators found. Roughly 25 percent of the difference in newborn weight between smokers and non-smokers may be due to differences in eNOS activity, they write.
"The reduction in size and in eNOS activity and concentration in umbilical and chorionic endothelium of the newborns of women who smoke may be prevented by smoking cessation early in pregnancy. The findings suggest that smoking in pregnancy reduces the endothelial production of NO in the fetal vessels, contributing to restricted fetal growth caused by an impaired vasodilatory capacity," the authors conclude.
Diabetes & Endocrinology
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