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Antibody ‐ Induced Platelet Injury: Its Potency as a Trigger of Intravascular Clotting
Author(s) -
EVENSEN STEIN A.,
ELGJO RAGNA FØLLING
Publication year - 1972
Publication title -
scandinavian journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0036-553X
DOI - 10.1111/j.1600-0609.1972.tb00914.x
Subject(s) - antiserum , platelet , thorotrast , fibrinogen , fibrin , chemistry , antibody , thrombin , antigen , clotting factor , immunology , medicine , endocrinology , pathology
Rabbits were injected with platelet antiserum to investigate whether antibody‐induced injury of platelets triggers intravascular clotting. More than 97 % of the circulating platelets were acutely removed, and profound thrombocytopenia persisted during an observation period of 6 hrs. The thrombocytopenic effect of platelet antiserum was associated with moderately increased consumption of 125 I‐fibrinogen and significant decreases in factors V and VIII, while the level of antigen reacting like fibrinogen (FR‐antigen) in serum did not increase. The antiserum produced a transient leucopenia, and the effects of platelet antiserum were therefore also evaluated in rabbits made severely leucopenic, but not thrombocytopenic, with nitrogen mustard. Similar results were obtained, indicating that the consumption of clotting factors did not result from leucocyte injury. Pretreatment with Thorotrast reduced rather than enhanced the clotting changes after platelet antiserum. In these animals non‐clottable degradation products of fibrinogen were found in serum. In neither group were fibrin thrombi observed in glomerular capillaries at autopsy. Our findings support the concept that antibody‐induced injury of the platelet membrane triggered moderate intravascular clotting in normal animals. Thorotrast modified the response probably in multiple ways.