Experimental and clinical evidence has suggested that vasoconstrictor substances released from activated platelets could play a role in mediating the pulmonary hypertension of hypoxemic patients with chronic obstructive pulmonary disease. In order to extend previous knowledge on platelet function in such patients, platelet production of malondialdehyde and plasma levels of beta-thromboglobulin were assayed in 12 patients before and after a short-term treatment with the platelet-inhibiting drug, dipyridamole. The impairment of platelet malondialdehyde generation concomitant with the increase of plasma levels of beta-thromboglobulin suggests that in patients with chronic obstructive pulmonary disease, blood platelets undergo chronic overstimulation and become exhausted. Dipyridamole can antagonize this platelet activation and thus may prove useful in reducing the pulmonary hypertension of these patients.