Studies in Intravascular Coagulation

Lipemia-Induced Acceleration of Intravascular Clotting.

“…Wessler (6) has drawn attention to the fact that reduced coagulability, as demonstrated by test tube methods, such as the one-stage (Quick) prothrombin time, does not necessarily mean decreased tendency to thrombosis. The observed acceleration of clot formation in stagnant venous blood in dogs resulting from intravenous infusion of a fat emulsion correlates with the increased iii z~itro coagulability previously found in association with either intravenous or oral administration of fat in humans (3).…”

Kontaktfaktorinduzierte experimentelle Thrombose

“…Ebenso wie mit ungereinigten Kontaktfaktoren (Wessler, 1960;Henderson u. Rapaport, 1962 ;Botti u. Rattnoff, 1964;Iatridis, 1966) konnten wir --alle Experimente zusammengenommen --in 7 yon 10 F&llen bei alleiniger KAP-Injektion und in 7 yon 10 F~llen bei KAP-Injektion nach Pr/~paration mit Endotoxin Thrombosen in der V. jugularis nach Unterbindung der Zirkulation erzeugen. Der direk~e Nachweis einer sog.…”

“…5Iaeh heutiger Auffassung seheint eine ErhShung der Gerinnbarkeit des Blutes nieht ausreichend zu sein, um Thrombosen entstehen zu lassen (Wessler, 1952(Wessler, , 1960. Aueh eine Unterbrechung des Kreislaufs bewirkt unter physiologischen Bedingungen allein keine Entstehung yon intravasalen Thromben (MeLachlin et al, 1960).…”

“…Zu Substanzen, die in vivo zu einer Hypercoagulabilit/it fiihren und unter Stasebedingungen thrombogenetisch wirken, gehSren die aktivierten Kontaktfaktoren (Wessler, 1960;Henderson u. Rapaport, 1962), der aktivierte Faktor X (Wessler, 1968) sowie Substanzen, die nieht dem Gerinnungssystem angehSren, jedoch wie Ellags~ure (Botti u. Rattnoff, 1964;Iatridis, 1966) und Celite (Ashkinazi u. Klemina, 1970) die Kontaktphase des Gerinnungssystems aktivieren.…”

Oral and Intravenous Estrogens in the Treatment and Prevention of Bleeding Associated With Long‐term Anticoagulant Therapy

“…This is best explained by variations iii local blood flow, capillary beds, platelets, and alterations itivolviiig aspects of the coagulation mechanism other than prothromhin coriceiitratiori. Wessler aiid his colleagues (8) properly called attention to the fact that changes in prothrombin time and related determinations which specifically reflect a coagulation defect heretofore have been assumed t,o parallel the antithrombotic effect. In experimeiit>s involving t'he administration of serum fractions from dotior dogs (in which the plasma prothrombic activity had hceii reduced by Dicumarol) to ot,her animals in which the prothrombic activity was comparably depressed by Dicumarol, these iiwestigators were able to demonstrate that : a ) there was a clear-cut distinction between the coagulation defect arid the antithrombotic effect of Dicumnrol, aiid 6) neither the one-stage prothrombic activity nor the prothromhin aiid corivertiii concentrations acaurat,ely reflected such antithrombotic activity.…”