The Combined Effects of 2,3-Diphosphoglycerate and Phospholipase-A on Platelet Aggregation Induced by ADP, Epinephrine, Norepinephrine and Collagen

It has been shown recently, that under specific conditions, phospholipase-A (Phl-A) or 2,3-diphosphoglycerate (2,3-DPG) can inhibit human platelet aggregation induced by ADP, epinephrine, norepinephrine or collagen. In this report, by using a dual channel Payton Aggregometer, the effects of 2,3-DPG and Phl-A on platelet aggregation were further studied. When 2,3-DPG (2μM) was added in human platelet rich plasma with Phl-A (200μU), 30, 60, 120 or 300 sec. before the addition of ADP (0.5-2.0μM), epinephrine (2-5uM) or norepinephrine (2-5μM) an enhancement of platelet aggregation was observed, whereas the same concentration of 2,3-DPG alone or Phl-A alone, inhibited both the rate and extent of the second phase of platelet aggregation induced by the same aggregating substances. The combined effects of 2,3-DPG and Phl-A on collagen induced platelet aggregation remained inhibitory. Aspirin on the other hand abolished the enhancement of platelet aggregation induced by 2,3-DPG and Phl-A. These combined effects of 2,3-DPG and Phl-A were both a concentration and a time dependent response. The results indicate that the combined effects of 2,3-DPG and Phl-A were probably mediated through prostaglandin formation. Since Phl-A is a physiological platelet enzyme which releases arachidonic acid, then we may postulate that 2,3-DPG probably activates the synthetases and/or cyclooxygenases which are the enzymes necessary for the formation of the important platelet aggregating substances, namely the endoperoxides and thromboxanes. Supported by USPHS HL-15425.