The Clot Accelerating Effect of Dilution on Blood and Plasma. Relation to the Mechanism of Coagulation of Normal and Hemophilic Blood

Abstract

Dilution with physiologic saline solution and other fluids accelerates the coagulation of properly collected normal and hemophilic blood and plasma in silicone coated vessels, with or without the aid of activating agents such as platelets, thromboplastin, cephalin, glass particles or plasma euglobulin fractions. When normal plasma is diluted under a concentration of about 20 per cent, its rate of clotting is prolonged, principally because of diminution in prothrombin. Regardless of the activating agent used, the rate of coagulation of hemophilic plasma can be made equal to that of normal plasma by appropriate dilution. These findings speak against the existence in hemophilic blood or plasma of a deficiency in any procoagulant factor, and support the concept of the presence in excess of a stabilizing inhibitor which slows the conversion of prothrombin to thrombin by one or both of the following mechanisms: (1) reducing or inactivating the effect of released coagulants (antithromboplastin activity) (2) conjugation with a procoagulant thereby maintaining it in an inactive form (anti Ac-globulin activity).

Initiation of blood coagulation by glass and related surfaces

“…of strands of insoluble material as well as by the gradual loss of activity. It is possible that these observations represent the phenomenon of dilution activation (Tocantins et al 1951), but in the absence of further evidence the euglobulin fractions cannot be included in the same category as the other plasma derivatives studied. Contact activation of pathological plasma…”

“…Lozner, Taylor & MacDonald (1942) showed that glass contact shortens the clotting time of platelet-poor plasma and concluded that this reaction is associated with the plasma euglobulin fraction. Tocantins (1945) and his coworkers (Tocantins, Carroll & Holburn, 1951) made an extensive study of the effect of different surfaces on the clotting of plasma and decided that the basis of the reaction was the adsorption of a lipid inhibitor of clotting ('anticephalin'). Conley and collaborators (Conley, Hartmann & Morse, 1949;Hartmann, Conley & Lalley, 1949;Ratnoff & Conley, 1951;Hartmann & Conley, 1952;Dick, Jackson & Conley, 1954) studied the effect of glass contact on human and canine platelet-free plasma and its euglobulin fraction.…”

Activation of plasma by contact with glass: evidence for a common reaction which releases plasma kinin and initiates coagulation

“…An allied problem which still awaits investigation is the relation between the phenomena described in this paper and the activation of plasma by dilution, trypsin, saliva, urine and some snake venoms (Rocha e Silva et al 1949;Tocantins, Carroll & Holburn, 1951;Miles & Wilhelm, 1955;Hilton & Lewis, PLASMA FOREIGN SURFACE REACTION 1955;Werle, 1955;Schachter, 1956;Holdstock, Mathias & Schachter, 1957;Stewart & Bliss, 1957). The observation that plasmin is a potent releaser of plasma kinin (Lewis, 1958) deserves special attention, since plasmin has also been shown to activate coagulation (Travis & Ferguson, 1951).…”

Complete free flap loss due to extensive hemodilution

“…An increased coagulability is described due to 20% to 30% saline hemodilution (in vitro and in vivo). [10][11][12][13] Tocantins et al 14 10 detecting an increased coagulability after 20% hemodilution with saline solution. Egli et al 11 compared clotting parameters after hemodilution by saline, HES, gelatin, and albumin and reported that 30%-saline hemodilution produced a hypercoagulable state by affecting all variables of blood coagulation and clot lysis.…”