Abstract
Direct and filmed observations of events during intravascular hemagglutination have been made using our Living Extracorporeal Eye preparation.
Agglutinated erythrocyte masses in the arterioles are separated by plasma gaps but tied to one another in short chains by fibrin threads and have a surface deposition of fibrin. This fibrin forms under circumstances that make autocatalytic coagulation unlikely. This seems to indicate that if thrombin evolution occurs, it must be localized to the areas of exposed erythrocyte stroma and adjacent endothelial cell surfaces altered by deoxygenation.
These masses plug some of the microcirculatory channels and venous many-tailed casts build from multicentric sites at the exits of venules with stilled flow. The light and electron microscopic structure of such casts shows a core of aggregated erythrocytes with surface fibrin and platelet deposition.
The above events are not prevented by prothrombinopenic, leukopenic or thrombocytopenic reacting bloods but are abolished by resuspending from each of the reacting bloods, the autologous erythrocytes, leukocytes, and platelets in the supernate of its centrifuged heat-defibrinated plasma.
Hydrocortisone, benadryl and 6 per cent clinical dextran do not alter the reaction.
When calcium ion binding agents are also present, heparin abolishes the fibrin formation and sharply reduces the magnitude of erythrocyte aggregates so that vigorous perfusion of the microcirculation continues. Heparin alone is ineffective in suppressing interspecies hemagglutination and erythothrombus formation when non-anticoagulated bovine blood is intermixed with heparinized diluted human blood.
The obstructing arteriolar masses and the many-tailed venous cast induced by hemagglutination, are promptly and completely disaggregated by plasma plus streptokinase or by urokinase or by 5M urea solution perfusion.
Osmotically lysed erythrocytes lead to similar erythrothrombosis only when stasis is induced by interrupting arterial perfusion for a minute or more.
