Platelet and Fibrinogen Survival in Normal and Abnormal States of Coagulation

Abstract

1. Platelet and fibrinogen survival have been studied by isotope tagging in normal and abnormal states of coagulation in humans and dogs. 2. By our technic, the normal curve of platelet survival is exponential. Evidence is given that such a curve is obtained because of random utilization of the platelets in the continuous process of coagulation. 3. In the postoperative subject and in the subject receiving epinephrine injections, platelet survival is shortened because the process of coagulation is speeded up. In the hypocoagulable, the curve of platelet survival becomes more nearly linear because random platelet destruction ceases. 4. When a massive thrombus forms, platelet survival is shortened. Evidence is given that this may be due to escape of thrombin from the clot into the systemic circulation—with a resultant hypercoagulable state. 5. Fibrinogen survival was not altered in those states in which increased platelet utilization occurred. This is explained by the theory that the alteration in the hemostatic mechanism had not penetrated to the fibrinogen-fibrin stage. 6. Hypercoagulability is defined as that state in which platelet utilization is accelerated—whether or not thrombosis occurs.

Effects of Bacterial Endotoxin on Rabbit Platelets

“…Thus, in states characterized by alterations in the rate of formation or activation of thromboplastin or thromboplastin precursors the normal reticuloendothelial system is competent to remove the proeoagulant substance and prevent thrombin formation and conversion of fibrinogen to fibrin. In this regard, Adelson and associates (28) have demonstrated that hypercoagulable states accompanying thrombus formation, operative procedures, and epinephrine injection considerably modify the half-life of labeled platelets but have no effect on the rate of utilization of labeled fibrinogen.…”

Platelet Survival in Man

“…The survival time of isotopically labelled platelets has by most authors been expressed as platelet half-life time (TYz), or as the time of disappearance of labelled platelets from the circulation (Adelson et al 1961, Davey & Lander 1964, O'Neill & Firkin 1964, Najean et al 1967, Abrahamsen 1968a, Kotilainen 1969, Murphy & Gardner 1969.…”

Adrenaline and Experimental Thrombosis*

“…Other investigators have prescnted evidence that adrenaline may accelerate blood coagulation by increasing the activity of clotting components such as Factor VIII (Ingrain, 1961). Adrcnaline increases the platelet count and this increase may be sustained over a pcriod of weeks in rabbits givcn daily injections (Ozge and Mustard, 1962) ; we and others have also found that it can shorten platelet survival and increase platelet turnover (Adelson et a/., 1961 ;Ozgc and Mustard, 1962). Thus three competing views on thc site of action of adrenaline on thrombosis can be considcrcd at this stagc: first, rhe artcrial wall; secondly, clotting factors; and thirdly, the…”