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Obstetrics & Gynecology 2005;105:626-632
© 2005 by The American College of Obstetricians and Gynecologists
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ORIGINAL RESEARCH

Abnormal Endothelium-Dependent Microvascular Reactivity in Recently Preeclamptic Women

Judith Blaauw*{ddagger}, Reindert Graaff, PhD{ddagger}, Maria G. van Pampus, MD, PhD*, Jasper J. van Doormaal, MD, PhD{dagger}, Andries J. Smit, MD, PhD{dagger}, Gerhard Rakhorst, PhD{ddagger} and Jan G. Aarnoudse, MD, PhD*

From the Departments of *Obstetrics and Gynecology, {dagger}Internal Medicine, and {ddagger}Biomedical Engineering, Groningen University Medical Centre, Groningen, The Netherlands.

OBJECTIVE: To assess endothelial function at the level of skin microvasculature, using iontophoretic administration of acetylcholine (endothelium-dependent vasodilator) and sodium nitroprusside (endothelium-independent vasodilator), in women who recently had a preeclamptic pregnancy.

METHODS: Microvascular skin reactivity was assessed by laser Doppler perfusion monitoring and iontophoresis of acetylcholine (ACh) and sodium nitroprusside (SNP) in 25 women with a history of early onset preeclampsia and 23 women with previous uncomplicated pregnancies, all of whom were between 3 and 11 months postpartum.

RESULTS: Mean (± standard error of the mean) ACh-mediated vasodilatation, expressed as a percentage increase in flux, was higher in women who recently had a preeclampsia than in controls (535 ± 46% versus 314 ± 29%, P < .001). In contrast, SNP-mediated vasodilatation was not significantly different (560 ± 71% versus 483 ± 69%, P = .4) in both groups. Linear regression analysis revealed that the difference in ACh-mediated vasodilatation was explained by preeclampsia (P = .004), whereas vascular risk factors such as maternal age, diastolic blood pressure, and family history of premature cardiovascular diseases had no significant effect.

CONCLUSION: The increased ACh-mediated vasodilatation in the microcirculation of recently preeclamptic women indicates abnormal endothelial function. Furthermore, it may represent a compensatory response to an impaired vasodilatory response of the macrocirculation, thereby supporting the hypothesis of an underlying (micro)angiopathy.

LEVEL OF EVIDENCE: II-2




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J. Blaauw, M. G. van Pampus, J. J. Van Doormaal, M. R. Fokkema, V. Fidler, A. J. Smit, and J. G. Aarnoudse
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HypertensionHome page
J. Blaauw, R. Graaff, M. G. van Pampus, J. J. van Doormaal, A. J. Smit, G. Rakhorst, J. G. Aarnoudse, F. Khan, J. J.F. Belch, M. MacLeod, et al.
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Hypertension, March 1, 2006; 47(3): e14 - e15.
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