[Effect of influenza virus infection on arachidonic acid cascade in mouse thrombocytes].

Prostaglandins (PGs) are essential for many physiological and pathological processes. As they are not stored in tissue, their presence and actions therefore result from de novo synthesis and release. Although platelets themselves appear to have the ability to synthesize TxA2, PGD2, arachidonic acid may also be metabolized in the lipoxygenase pathway in platelets, producing 12-hydroperoxy/12-hydroxy-5,8,10,14-eicosatetraenoic acid (12-HPETE/12-HETE). CFLP mice were infected intranasally with A/H3N2/Hong Kong (1/68) influenza virus. Platelets were isolated from the control (saline treated) and infected mice 3-13 days after virus application. Platelets were isolated from the diluted arterial blood of the mice. Metabolites of arachidonate cascade were determined using 1-14C-arachidonic acid (2035 MBq/mM spec. act.) as substrate. All incubations were carried out in TC Medium 199 (pH 7.4) at 37 degrees C for 10 min. Radiolabelled products were separated and quantitatively determined. The synthesis of TxA2 in the platelets of animals was found to be significantly increased 7 days after the virus infection. The 12-hydroxy-heptadecatrienoic acid level was higher on the 10th and 13th days of infection, as were the products of the lipoxygenase pathway.