In vitro models demonstrate that platelet-endothelium interactions under stress lead to endothelial injury and reduced nitric oxide sensitivity, contributing to atherothrombotic risk.
Normal platelet-endothelium interplay is a key mechanism for the prevention of intravascular thrombosis. Endothelial injury and a loss of normal endothelial function lead to platelet activation and cardiovascular events. We have proposed two models for altered platelet-endothelium interaction, i.e. endothelial injury by activated platelets and exercise-mediated 'desensitization' of platelets to endothelial anti-thrombotic substances. Cultured aortic endothelial cells exposed to aggregated platelets showed mitochondrial damage with ATP depletion and a reduction in nitric oxide (NO) release. Attenuated NO release was accompanied by impaired anti-thrombotic function, which was restored by L-arginine supplementation. Platelets, on the other hand, were desensitized to NO in a stressful condition like acute strenuous exercise. Although the mechanisms involved in the exercise-induced attenuation of platelet sensitivity to NO remain unclear, our in vitro study showed that both mechanical stress and epinephrine may contribute to the attenuation, at least in part. In conclusion, platelet-endothelium interaction is not simply an alliance of mutual benefits, but also a 'tense' relationship, especially in a diseased or stressful situation.
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Kishi et al. (1998) studied Healthy (n=16). Acute vigorous exercise (treadmill test) vs. At rest (before exercise) was evaluated on Platelet aggregation by collagen (EC50) (p=0.011).
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