Hum. Reprod. Advance Access originally published online on July 21, 2005
Human Reproduction 2005 20(11):3219-3224; doi:10.1093/humrep/dei199
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Microvascular dysfunction in women with polycystic ovary syndrome
1 Ultrasound Department, North Middlesex Hospital, London, 2 University Department of Obstetrics and Gynaecology, Royal Free and University College Medical School, University College London, London and 3 Vascular Haemodynamic Unit, University Department of Surgery, Royal Free Hospital, London, UK
4 To whom correspondence should be addressed at: University Department of Obstetrics and Gynaecology, RFUCMS The Royal Free Hospital, Pond Street, London NW3 2PF, UK. E-mail: p.hardiman{at}medsch.ucl.ac.uk
BACKGROUND: Polycystic ovary syndrome (PCOS) is associated with multiple cardiovascular risk factors and an increased prevalence of arterial dysfunction. However, microvascular dysfunction in PCOS has not been assessed. METHODS: Subjects comprised 12 women with PCOS and 12 age-matched controls with normal ovaries. Microvascular function was assessed by observing forearm skin microvascular erythrocyte flux responses, to cumulative iontophoretic doses of 1% (w/v) acetylcholine (ACh) and 1% (w/v) sodium nitroprusside (SNP), using laser Doppler imaging. RESULTS: Basal microvascular perfusion was comparable in PCOS and controls. The increase in skin microvascular perfusion in response to ACh was however generally blunted in PCOS women (P = 0.018). Peak ACh-induced erythrocyte flux was also less (p < 0.04) in PCOS women (125.1 6 21.7, i.e. 5.3-fold basal flux) than in controls (200.8 6 28.5, i.e. 8.3-fold basal flux). Analysis of covariance indicated this effect was unrelated to differences in body mass index or serum testosterone but serum insulin may be a weak confounder. No differences were noted between the PCOS and control groups in their response to SNP. CONCLUSION: Despite its limited sample size studied, this is the first demonstration that women with PCOS exhibit microvascular endothelial dysfunction, indicated by an inhibited vasodilatory response to ACh.
Key words: acetylcholine/endothelium/erythrocyte flux/microcirculation/polycystic ovary syndrome
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