PLATELET MALONDIALDEHYDE PRODUCTION AND AGGREGATION RESPONSES INDUCED BY ARACHIDONATE, PROSTAGLANDIN-G-2, COLLAGEN, AND EPINEPHRINE IN 12 PATIENTS WITH STORAGE POOL DEFICIENCY

  • 1 January 1981
    • journal article
    • research article
    • Vol. 58  (1) , 27-33
Abstract
The integrity of the prostaglandin synthetic pathway was assessed by measuring malondialdehyde (MDA) production and studied platelet aggregation responses to arachidonic acid and PGG2 [prostaglandin G2] in 12 patients with storage pool deficiency (SPD). Eight patients were deficient only in dense granules (.delta.-SPD) and 4 were deficient in both dense and .alpha.-granules (.alpha..delta.-SPD). Production of MDA in response to arachidonic acid (AA), epinephrine and collagen suggested that the transformation of AA to prostaglandin metabolites was normal in .delta.-SPD but abnormal in .alpha..delta.-SPD and that the liberation of AA from phospholipids was abnormal in the majority of patients with SPD. Since the content of secretable ADP is diminished in SPD platelets, the aggregation responses of these platelets to AA and PGG2 were studied to help answer the question whether these agents aggregate platelets directly or through release of endogenous ADP. Among patients with .delta.-SPD, aggregation by both AA and PGG2 was decreased in 4 albinos whose platelets were markedly deficient in ADP. Normal, or less strikingly abnormal, responses were observed in patients whose platelets either contained higher levels of platelet ADP or showed increased sensitivity to ADP. The more markedly impaired responses to AA and PGG2 in patients with .alpha..delta.-SPD suggest that substances derived from .alpha.-granules may also play a role in platelet aggregation by these agents. The aggregation responses in these patients with various types of SPD is consistent with a theory that granule-derived ADP mediates platelet aggregation by AA and PGG2.