1. The formation of thromboxane B2 and malondialdehyde was studied in human platelet-rich plasma, in gel-filtered platelets and in bovine platelet microsomes.

2. Exogenous sodium arachidonate was converted into thromboxane B2 and malondialdehyde in a concentration-dependent manner. Pre-incubation of platelets with aspirin inhibited the production of both thromboxane B2 and malondialdehyde, although malondialdehyde could apparently be detected in the absence of thromboxane B2.

3. The aggregating agents, thrombin, collagen and the ionophore A23187 also caused production of thromboxane B2 and malondialdehyde. ADP and adrenaline produced a smaller rise whilst the endoperoxide analogue U 46619 had only a slight influence on thromboxane and malondialdehyde, even though they all induced aggregation.

4. Pre-incubation of platelets with imidazole or 1-N-butylimidazole, which inhibit thromboxane synthetase, resulted in an inhibition of both thromboxane B2 and malondialdehyde formation in response to collagen.

5. The results indicate that thromboxane B2 and malondialdehyde are formed in parallel, in comparable quantities. However, under the conditions used in these studies, the apparent amounts of malondialdehyde exceed those of thromboxane B2, especially in the presence of exogenous arachidonate. Thus the thiobarbiturate reaction used to assay malondialdehyde may detect other products of lipid peroxidation.

6. Platelet thromboxane B2 concentrations did not always relate to the extent of aggregation. In particular, platelet aggregation could occur in the absence of detectable thromboxane B2 production.

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