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A Journal on Angiology
Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899
International Angiology 2000 December;19(4):345-50
Changes in signal transduction in the platelets of patients with peripheral occlusive arterial disease
Woinke M., Zeiger F., Ruehlmann C., Pfeiffer D., Koksch M.
From the Department of Cardiology-Angiology, Medical Hospital I, University of Leipzig, Leipzig, Germany
Background. The finding that platelets of patients with peripheral occlusive arterial disease (POAD) circulate in an activated state prompted us to study platelet signal transduction. We hypothesised that platelet hyper-reactivity is caused by changes in intracellular signalling.
Methods. Experimental design: a single blood sample was taken from the antecubital vein of each participant prior to the start of intravenous treatment with prostaglandins. Setting: patients were recruited from our inpatient Department of Cardiology and Angiology at the University Hospital. Participants: 15 hospitalised patients with symptomatic POAD were randomly selected. Patients receiving antiplatelet drugs and those with diabetes were excluded. The control group consisted of 15 healthy volunteers from the medical staff. Interventions: blood tests were performed on the day of admission before any therapeutic intervention. Measures: the platelet activation marker P-selectin was quantified on peripheral blood platelets before and after in vitro stimulation with platelet agonists (adenosine diphosphate, thrombin receptor activator peptide-6). The signal transduction cascade was also selectively blocked by preincubation with either: 1) forskolin, 2) phospholipase C inhibitor U-73122, or 3) bisindolylmaleimide.
Results. A stronger inhibitory effect on ADP-stimulated platelets was seen in patients with U-73122, as indicated by a decrease in mean fluorescence intensity of 51% versus 34% in controls (p<0.0005).
Conclusions. Our findings support the assumption that changes in platelet signal transduction in POAD lead to platelet hyper-reactivity.