Mikael Norman1, Helena Martin. 1. Department of Women and Child Health, Karolinska Institute, Stockholm, Sweden. mikael.norman@ks.se
Abstract
BACKGROUND: Low birth weight predisposes to later coronary disease. To further elucidate the mechanisms behind this association and their timing, vascular endothelial function-a key factor in early pathophysiology of atherosclerosis-was studied in 54 infants born either before the third trimester or at term. METHODS AND RESULTS: All subjects were studied at 3 months of postnatal age. A laser-Doppler technique was used to measure skin perfusion before and after transdermal iontophoresis of acetylcholine (ACh; an endothelium-dependent vasodilator). In infants born at term (n=19; birth weight range: 2230 to 4205 g), maximum perfusion after ACh was 109+/-8 perfusion units (PU, mean+/-SEM) in normal-birth weight controls compared with 56+/-13 PU among those who had been small for gestational age at birth (P<0.01). In infants born preterm (n=35; birth weight range, 722 to 1868 g), ACh induced similar perfusion responses among subjects appropriate for gestational age (113+/-16 PU) and in those small for gestational age at birth (109+/-19 PU). CONCLUSIONS: Impairment in human endothelial function associated with low birth weight occurs or emerges late in pregnancy. Very preterm birth attenuates this association. Different gene-environment interactions in the third trimester may contribute to this finding.
BACKGROUND: Low birth weight predisposes to later coronary disease. To further elucidate the mechanisms behind this association and their timing, vascular endothelial function-a key factor in early pathophysiology of atherosclerosis-was studied in 54 infants born either before the third trimester or at term. METHODS AND RESULTS: All subjects were studied at 3 months of postnatal age. A laser-Doppler technique was used to measure skin perfusion before and after transdermal iontophoresis of acetylcholine (ACh; an endothelium-dependent vasodilator). In infants born at term (n=19; birth weight range: 2230 to 4205 g), maximum perfusion after ACh was 109+/-8 perfusion units (PU, mean+/-SEM) in normal-birth weight controls compared with 56+/-13 PU among those who had been small for gestational age at birth (P<0.01). In infants born preterm (n=35; birth weight range, 722 to 1868 g), ACh induced similar perfusion responses among subjects appropriate for gestational age (113+/-16 PU) and in those small for gestational age at birth (109+/-19 PU). CONCLUSIONS: Impairment in human endothelial function associated with low birth weight occurs or emerges late in pregnancy. Very preterm birth attenuates this association. Different gene-environment interactions in the third trimester may contribute to this finding.
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