| Popis: |
Interactions between platelets and vascular endothelial cells play a key role in hemostasis and particularly primary hemostasis. In this context, the metabolism of arachidonic acid is believed to be an important point. When platelets are triggered with aggregating agents like collagen or thrombin, arachidonic acid is liberated from membrane phospholipids and then subsequently oxygenated by two pathways. One of these pathways is the cyclooxygenase which leads to PGH2, readily converted into TXA2. Both compounds are pro-aggregatory molecules and have also a vasocontracting activity. TXA2 is quite labile and it is degraded into TXB2 which is not active. PGH2 is also transformed into small amounts of primary prostaglandins PGE2, F2α, and D2. The second pathway is the lipoxygenase one, which catalyzes specifically the oxygenation of carbon 12, leading to 12-hydroperoxy-eicosatetraenoic acid (12-HPETE) or 12-hydroperoxy-arachidonic acid, which is further reduced into its 12 hydroxy products, 12-HETE, by a glutathione-dependent peroxydase. PGH2 of platelet origin may also be transformed into prostacyclin (PGI2), a very potent antiaggregating and vasodilating agent produced by vascular endothelium. PGI2 may also be formed from endogenous arachidonic acid when liberated from endothelial phospholipids by specific agonists like bradykinin or thrombin. |
