Blood platelets from reserpinized rabbits produced a larger amount of malondialdehyde (M DA) in response to thrombin than the platelets from control rabbits. The MDA production was almost completely inhibited by aspirin and indomethacin, indicating that the MDA was produced through the cyclooxygenase pathway. When intracellular free Ca" was diminished by tetracaine or dibutyryl cyclic AMP, thrombin could not induce MDA production in the reserpinized or in the control platelets. When

more »

... r Ca" was raised by ionophore A23l87 plus Ca", MDA was produced in the absence of thrornbin. No difference in MDA production, however, was observed between the reserpinized and the control platelets. The measurement of intracellular bound calcium with chlortetracycline showed that the fluorescence after thrombin addition in the reserpinized platelets was decreased more than in the controls, suggesting an enhancement of intracellular liberation of Ca" from the binding sites of the reserpinized platelets. The augmentation of MDA production in the reserpinized platelets can be explained as a result of a stimulation of the cyclooxygenase pathway. The stimulation might be due to an excess supply of the substrates caused by Ca"-dependent degradation of platelet phospholipids, which is enhanced by intracellular Ca" mobilization in response to thrombin.