Trial reportJournal of applied physiology (Bethesda, Md. : 1985)2026
Attenuated cyclooxygenase-mediated vasodilation in cutaneous microvasculature with no difference in platelet aggregation in women with endometriosis.
Trial report in Journal of applied physiology (Bethesda, Md. : 1985), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Attenuated cyclooxygenase-mediated vasodilation in cutaneous microvasculature with no difference in platelet aggregation in women with endometriosis.Journal of applied physiology (Bethesda, Md. : 1985) · 2026Trial
Corrections and comments
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Authors and funding
4 authors.
Funding
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 (
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Registered trials
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