The interaction of blood platelets with surfaces coated with human type I, III, IV, and V collagen (CI, CIII, CIV, and CV) has been studied. Using scanning electron microscopy it was demonstrated that the reactivity of the collagen substrates for platelets varies widely. In contrast to CV and CIV, on surfaces coated with CI and CIII, along with spreading, the formation of thrombi-like platelet aggregates occurs. Previously, it was demonstrated that this thrombogenesis in vitro correlates well with the synthesis of platelet prostanoids, and is sensitive to inhibitors of TXA2-synthesis. Therefore, we have investigated the influence of the TXA2/PGH2 receptor-antagonists, 13-azaprostanoic acid (13-APA) and the BM 13.177 compound, on the formation of thrombi-like platelet aggregates on CI and CIII-coated surfaces. It was demonstrated that both 13-APA and BM 13.177 cause a dose-dependent inhibition of the thrombogenesis without any effect on the initiation of the thrombogenesis without any effect on the initial attachment and the spreading of platelets on collagen-coated surfaces. The obtained data suggest that (1) the formation of platelet aggregates on CI and CIII-coated surfaces is triggered by platelet prostanoids; (2) TXA2/PGH2 receptor-antagonists may be useful as antithrombotic drugs.
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J Mol Cell Cardiol
January 2025
Department of Physiology, University of Kentucky, Lexington, KY, USA; Department of Internal Medicine, University of Kentucky, Lexington, KY, USA. Electronic address:
Cardiologists have analyzed daily patterns in the incidence of sudden cardiac death to identify environmental, behavioral, and physiological factors that trigger fatal arrhythmias. Recent studies have indicated an overall increase in sudden cardiac arrest during daytime hours when the frequency of arrhythmogenic triggers is highest. The risk of fatal arrhythmias arises from the interaction between these triggers-such as elevated sympathetic signaling, catecholamine levels, heart rate, afterload, and platelet aggregation-and the heart's susceptibility (myocardial substrate) to them.
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