LIPOXYGENASE PRODUCTS CHANGES IN ‘IN VITRO’ AND ‘IN VIVO’ ASPIRINISED PLATELETS UNDER THE INFLUENCE OF PAF AND EPINEPHRINE

We aimed to investigate the changes of lipoxygenase products in platelets and the simultaneous behaviour of ‘in vivo’ or ‘in vitro’ aspirinised platelets, stimulated by two agonists, PAF and epinephrine (EPI). 12 healthy were included. 6 received 20mg of aspirin (ASA) per os for 7 days (group A), and in 6 (group B) platelets were aspirinised ‘in vitro’ (5 or lOmin incubation at 37°C with ASA 1M). In group A blood was drawn once at the beginning and once at the end of the trial, while in group B just ome. First, platelet aggregation was studied using two agonists simultaneously (0.6 ¼M EPI and 20 nM PAF). We incubated then all platelet samples with 0.5 M of the substance BW755C (kind offer of Dr Moncada) far 3 min at 37°C. Second we measured PL0 products according to Takayama et al (1980), in platelets with or without ASA, and in platelets with ASA and after treatment with BW755C, always after addition of both agonists. Our results showed: a) Irreversible aggregation was slightly enhanced by the simultaneous addition of PAF and EPI in both groups and in non-aspirinised platelets. After ASA treatment, each agonist alone did not induce irreversible aggregation, whereas their combination overcame this inhibition, a fact not noticed under BW755C (a known PLO inhibitor). b) PLO products were measured in nmol TBRS/10 platelets:

Our results agree with Cerletti et al (1986) and confirm that the two agonists combined are capable of overcoming the inhibition caused by ASA, possibly by activating the PLO pathway (Cerletti et al, 1986). Respectively the quantitative determination of PLO products (about which we did not notice any other report insofar) confirm the above assumption, since inhibition by BW755C coincides with the steep fall of PLOlevels, which for group A is statisticallysignificant (p≺0.01, paired t-test) and for group B entirely significant (p ≺0.001).