The Comparative Effect of Platelets on Prothrombin Utilization from Dogs in the Degenerative and Regenerative Phase of Irradiation Bone Marrow Aplasia

Abstract

Under specific conditions, a quantitative relationship between platelet concentration and amount of prothrombin utilized in the coagulation of shed blood in glass tubes was demonstrated by Buckwalter et al. (1). In their studies, canine and human blood was collected into cold, siliconed glassware without the aid of anticoagulants. Platelet-rich plasma was obtained by slow centrifugation in the cold, and the platelet count was adjusted by differential centrifugation and dilution with plateletpoor plasma. The coagulation was initiated by transfer of platelet plasma mixture to chemically clean Pyrex glassware at room temperature, coagulation stopped at intervals by the addition of sodium citrate, and the residual prothrombin assayed by a two-stage prothrombin determination (2). This procedure was modified and applied by Jackson et al. (3) in the investigation of the relation of the platelet count to prothrombin utilization and the hemorrhagic tendency in dogs exposed to lethal whole-body irradiation. In these studies, it was not necessary to resort to differential centrifugation because the platelet count progressively decreases to almost zero by the tenth day as a result of irradiation aplasia of the marrow. In general, there was a parallelism in the decrease in the platelet count and the diminished utilization of prothrombin. However, it appeared that, under these conditions, the utilization of prothrombin diminished more rapidly than the platelet count. In further studies, Cronkite et al. (4) confirmed these observations and found that in the prothrombin utilization returned much more rapidly to normal than did the platelet count. In addition, Ferguson et al. (5), using injected radiogold, has reported that prothrombin utilization is depressed before there is a significant decrease in the platelet count. The above observations can be interpreted as indicating that platelets are less active than normal in accelerating prothrombin utilization in the degenerative phase and more active than normal in the regenerative phase. An alternative explanation in the degenerative phase would be the presence of abnormal anticoagulant or increased amounts of normally occurring lipid antithromboplastins.