2. Academic Validation
  3. Attenuated cyclooxygenase-mediated vasodilation in cutaneous microvasculature with no difference in platelet aggregation in women with endometriosis

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

  • J Appl Physiol (1985). 2026 Mar 1;140(3):652-663. doi: 10.1152/japplphysiol.00865.2025.
Auni C Williams 1,  Marta Martinez Yus 2 3,  Lakshmi Santhanam 2 4 3,  Lacy M Alexander 1 5 6
Affiliations

Affiliations

  • 1 Noll Laboratory, Department of Kinesiology, The Pennsylvania State University, University Park, Pennsylvania, United States.
  • 2 Department of Anesthesiology and Critical Care Medicine, The Pennsylvania State University, University Park, Pennsylvania, United States.
  • 3 Department of Chemical and Biomolecular Engineering, Whiting School of Engineering, The Johns Hopkins University, Baltimore, Maryland, United States.
  • 4 Department of Biomedical Engineering, The Johns Hopkins University School of Medicine, Baltimore, Maryland, United States.
  • 5 Center for Healthy Aging, The Pennsylvania State University, University Park, Pennsylvania, United States.
  • 6 Department of Obstetrics and Gynecology, Penn State College of Medicine, Hershey, Pennsylvania, United States.
PMID: 41615377 DOI: 10.1152/japplphysiol.00865.2025
Abstract

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.NEW & NOTEWORTHY We demonstrate attenuated cyclooxygenase-mediated vasodilation in women with endometriosis. In addition, we show no differences in platelet aggregation between women with and without endometriosis despite increased platelet count in the endometriosis group.

Keywords

current-induced vasodilation; cyclooxygenase; endometriosis; platelet aggregation; thromboxane.

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