Abstract
It is well known that 0.0025 M solution of sodium oxalate does not delay blood coagulation, even when in stoichiometric concentration with calcium. Three times more sodium oxalate than calcium present in blood is required to prevent blood coagulation (Quick 1 ). On the other hand the prothrombin time of oxalated human plasma is prolonged because destruction of the plasmatic cofactor of thromboplastin (P.C.T.) starts a few hours after storage. 3 Quick believes that calcium protects this factor because hemophilic plasma from which calcium has not been removed does not alter its prothrombin time after 48 hours. 2 These experiments do not explain satisfactorily why an excess of sodium oxalate is needed to render blood incoagulable and why oxalated stored plasma destroys by oxidation its cofactor of thromboplastin. 3
We do not believe that the prothrombin time of oxalated human stored plasma is prolonged because calcium is eliminated. Another possibility must be considered. Sodium oxalate may have more affinity for another substrate than calcium and only when an excess has been added does this last reaction take place. It seems logical to suppose the existence of a substance in blood which protects the P.C.T. against oxidation. It must be a strong reductor. Its destruction by sodium oxalate would explain the slow but effective alteration of stored plasma.
To test this hypothesis the following experiments were carried out. Human blood with-drawn in silicon syringes (Jaques5) was passed through Amberlite IR-100-H (Quick6 to eliminate all the calcium without using oxalate. Then 0.1 cc of 0.1 M. Sodium oxalate or 0.125 M sodium citrate to 0.9 cc of plasma were added. A third sample passed through Amberlite (without addition of any other substance) was stored at 5°C. For prothrombin time determination a modified one-stage method of Quick4 was used.
Get full access to this article
View all access options for this article.
