Thrombogenic Properties of Surface Factor; Evidence for an Anti-Surface Factor Activity in Canine Plasma.

Abstract

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.

Aspirin Inhibition of In Vivo Effects of Intestinal Alkaline Phosphatase on Platelets

“…Thus it is possible that, in the present experiments, HF was unable to be activated on the surface of the aspirinized platelets since these platelets remained intact and consequently no hypercoagulation observed. In the non-aspirinized animals, however, AlPh aggregated the platelets upon the altering surfaces of which HF is probably activated to induce t he hypercoagulation noted in the present experiments as well as in previous studies (10,12).…”

“…Since aspirin has no direct effect on any of the known clotting factors (14,16) it is possible that the hypercoagulation observed in the non-aspirinized animals was due to the increased platelet aggregation and adhesion after ALPh injection. It has been shown previously (12) that SF (XIa + XIIa) is one of the main clotting factors for inducing hypercoagulation. Also it has been shown (8,9) that Hageman factor (HF or factor XII) could be activated on the surface of the altering platelets and consequently could trigger the clotting mechanism and induce a hypercoagulable state.…”

Blood Factor XI after Fat-Rich Meals

“…In the extensive studies of Wessler and his co-workers it has been shown that their serum thrombotic accelerator, STA, defined responsible for the initiation of thrombosis in isolated venous segments, is more or less dependent on HF, AHC and AHB and on surface activation of the injected serum fractions ( 41,42). The thrombosis-inducing property of a concentrate of AHC' in stasis conditions in experimental animals was later also confirmed by others (11,16,17). These results are in good accordance with the experiments of Connor et al (5,14) producing thrombosis in dogs by infusions of long-chain saturated fatty acids which were known to activate HF.…”

Effect of Alkaline and Acid Phosphatases on Clotting:

“…III, IV, V) to suggest that the "beta" fraction contains the factor responsible for the stated acceleratory effect of alkaline phosphatase on clotting. In previous studies, as well as others [cited (14)], a key role of SF is emphasized in the induction of a hypercoagulable state which, in the presence of other contributory factors (such as local stasis of the circulation), strongly favors the incidence of thrombosis. Thomas et al ( 27) also emphasize the importance of factor IX in hypercoagula ble states.…”

“…The important protective role of the plasmatic inhibitor of SF (anti-SF) is emphasized by Iatridis et al (14,17). In a recent study (10) evidence was presented that ATP-ase (Apyrase form) is a specific in vitro inhibitor of active SF.…”