The role of the liver in serum-induced hypercoagulability.

The infusion of normal human serum into animals engenders a transient period of hypercoagulability characterized by profound shortening of the whole blood clotting time in both glass and silicone-coated tubes (2). During this period of hypercoagulability, blood trapped in isolated venous segments rapidly coagulates, forming a thrombotic cast of the isolated venous segment (3). In previous experiments it has been demonstrated that the ability of serum to induce thrombosis in the recipient animal is dependent on the presence of activated coagulation Factors IX (plasma thromboplastin component) and XI (plasma thromboplastin antecedent) in the infused serum (4). It was suggested that the presence of activated Factor XI was essential for the activation of Factor IX, and that activated Factor IX accelerated a rate-limiting step in the coagulation mechanism in the recipient animal to a degree that exceeded the capacity of a postulated cellular clearance mechanism, similar to that previously demonstrated in the rat by Spaet (5). In the present study the duration of the hypercoagulability produced by the infusion of serum was examined in the intact rabbit by measuring thrombus formation in venous segments isolated immediately and at intervals after serum infusion. These experiments demonstrate that in the intact animal the liver plays a central role in the attenu-