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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
Online ISSN 1827-1839
Clinical Pathophysiology, Division of Human Comprehensive Medicine, Graduate School of Medicine Sapporo Medical University, Japan
Background. Many thrombotic angiopathies are known to originate from abnormalities in platelet-blood vessel interaction. The present study focuses on the platelet activating factor (PAF)-induced platelet aggregating mechanism and the arachidonate metabolic pathways activated by it in platelets from a male rabbit.
Methods. Blood vessel contractility was examined using perfused arterial segments dissected from rabbit ear central arteries. Autologous platelet rich plasma (PRP) was infused into the perfusion system. Vascular contractilities were examined during infusion of PRP with a platelet agonist such as collagen or PAF. Platelet aggregation was measured with a platelet aggregometer.
Results. Vasocontractile response to noradrenaline (NA) during infusion of PRP with PAF was initially augmented but gradually became attenuated, whereas repetitive vasocontractile responses to NA in the presence of PRP with collagen gradually increased. Platelet aggregation in response to PAF was moderately inhibited by both nordihydroguaiaretic acid (NDGA) and baicalein, 12-lipoxygenase (LOX) inhibitors, was unaffected by indomethacin (IM), a cyclo-oxygenase (COX) inhibitor, and was markedly diminished by EGTA, a calcium chelator.
Conclusions. PAF-induced platelet aggregation may participate in the activation of the 12-LOX pathway rather than the COX pathway in platelets, and is remarkably sensitive to intracellular Ca2+ levels.