The effect of strenuous exercise on the clotting and fibrinolytic systems was studied on 1 Hageman-deficient and 59 normal subjects (males aged 18–37 years). In the normal subjects there was a significant shortening of the whole-blood clotting time and of the partial thromboplastin time both in glass and in siliconized tubes. Plasma factor VIII (AHF or AHG) assays rose to 188% (average), but the specificity of the test is questioned. Factor XII (HF) increased to 318% (average) unequivocally. A postexercise increased heparin tolerance was also noted. There was no significant increase in the levels of fibrinogen, prothrombin, factor V (AcG), or factor VII (proconvertin) and factor X (Stuart). Fibrinolytic activity as measured by the euglobulin lysis and plasma plate methods increased significantly in most of the normal subjects. The data suggest that the fibrinolytic factor which increases after exercise is not active plasmin, but is related to the “activator” mechanisms. A plasma lysokinase (indirect activator) seems to preponderate in over half the cases. In 20% of cases a plasminoplastin (direct activator) may be involved. In the Hageman-deficient subject there was no improvement in clotting, and the slight changes in some of the fibrinolysis tests were nonsignificant. Submitted on October 16, 1962 Submitted on October 16, 1962

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SummaryThe effect of wettable surfaces and Hageman factor on the activation of the fibrinolytic system was investigated.The fibrinolytic activity was estimated mainly by the euglobulin lysis test. Experiments were carried out with Normal and Hageman-deficient plasmas.The euglobulin lysis time of both plasmas was greatly affected by varying the surface exposure. Normal euglobulin suspension incubated at 37° C, and tested at intervals, showed an increase of fibrinolytic activity. The evidence suggests that this activity is related to the generation of endogenous activator. The rate of generation was a function of surface. Hageman-deficient euglobulin suspension, under the same conditions, did not generate endogenous activator.Evidence is presented to show that Hageman factor is different from proactivator and plasminogen.It is concluded that wettable surfaces and Hageman factor may have a role in the endogenous (or spontaneous) activation of the fibrinolytic system.

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SummaryPurified surface factor (SF or activation product) was prepared from canine plasma and its effect was studied on 22 dogs. It was shown that intravenous injection of SF increased the coagulability of the circulating blood (in vitro tests) and induced thrombosis in areas of vascular stasis (in vivo assay). The hypercoagulability was associated with the injected SF preparation and with no other known clotting factor increase. A second injection performed 61 minutes after the first was less effective. The survival period of injected SF seemed to be relatively short. This might be attributable, in part, to an inhibitory mechanism acting against SF (anti-SF) in plasma. Experimental evidence of the existence of such an inhibitor and its “progressive” mode of action is provided. Anti-SF has a variable titer normally, but appears to increase after the intravenous SF injection in dogs.