Attenuated cyclooxygenase-mediated vasodilation in cutaneous microvasculature with no difference in platelet aggregation in women with endometriosis

Endometriosis is a systemic inflammatory disease known to increase the risk of cardiovascular disease. The inducible form of cyclooxygenase (COX), COX-2, is an inflammatory enzyme upregulated in endometriosis (Endo) with COX metabolites having potent effects on platelet aggregation and neurovascular control. The purpose of this study was to determine if COX activity modulates mechanisms of platelet aggregation and neurovascular control in patients with endometriosis. We hypothesized that women with endometriosis (Endo) would demonstrate augmented platelet aggregation and anodal current-induced vasodilation (a method of inducing COX-mediated vasodilation) compared with similarly aged healthy control women (HC) and that this difference would be mediated, at least in part, by COX activity. In a randomized, placebo-controlled design, 12 Endo and 9 HC participants underwent an anodal current-induced vasodilation protocol with following placebo or aspirin (650 mg). Laser Doppler flowmetry continuously recorded red blood cell flux and cutaneous vascular conductance (CVC = flux/mean arterial pressure) was quantified. A blood sample was taken for impedance aggregometry analysis and quantification of the COX metabolite thromboxane in plasma with enzyme-linked immunosorbent assay. The Endo group demonstrated attenuated increases in CVC compared with HC (P < 0.01). There were no differences between groups in platelet aggregation characteristics (P ≥ 0.10, all reagents, all characteristics). There were no differences between groups in COX metabolites (Thromboxane B₂, P = 0.27; prostaglandin E2, P = 0.70). Our findings suggest that COX-mediated vasodilation is attenuated in women with endometriosis and that platelet activity is not different between women with endometriosis and healthy women.