Association of gestational diabetes with abnormal maternal vascular endothelial function |
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Authors: | Gregory A. Knock Research Assistant rew L. McCarthy Consultant Clara Lowy Consultant Lucilla Poston Professor |
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Affiliation: | Fetal Health Research Group, Division of Obstetrics and Gynaecology, St. Thomas' Hospital, London;Division of Endocrinology and Chemical Pathology, United Medical and Dental Schools, St. Thomas' Hospital, London;Division of Obstetrics and Gynaecology, Wycombe General Hospital, High Wycombe |
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Abstract: | Objective To evaluate vascular endothelial function in isolated small arteries from women with gestational diabetes. Methods Small subcutaneous arteries (mean luminal diameter ∼ 250μm) were dissected from biopsies obtained at caesarean section in 14 normotensive women with gestational diabetes and in 18 normotensive nondiabetic pregnant women. Vascular function was determined after mounting the arteries on a small vessel myograph. Results Pre-constricted arteries from gestational diabetic pregnant women demonstrated poor relaxation to acetylcholine, an endothelium-dependent vasodilator (pEC50, mean [SE], 6.98 [0.10] vs normal pregnant, 7.28 [0.08], P < 0.03 ; % maximum relaxation, median [range], 88.2 [42.4–994] vs normal pregnant 94.2 [71.8–100.0], P < 0.01 ). In the presence of indomethacin relaxation to acetylcholine was similar in both groups suggesting a deficiency in dilator prostaglandin synthesis in the arteries from the diabetic women. The nitric oxide synthase inhibitor N -monomethyl-L-arginine further reduced sensitivity of arteries to acetylcholine but to a similar degree in both normal pregnant and gestational diabetic women. Relaxation to sodium nitroprusside, an indicator of sensitivity of the vascular smooth muscle to nitric oxide, was similar in both groups. Conclusions Maternal vascular endothelial dysfunction may contribute to the increased incidence of cardiovascular disorders in women with gestational diabetes. |
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