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Immunopharmacological Approach to Forssman Shock
Author(s) -
Nagai Hiroichi,
Kurimoto Yoshiyuki,
Koda Akihide
Publication year - 1980
Publication title -
microbiology and immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.664
H-Index - 70
eISSN - 1348-0421
pISSN - 0385-5600
DOI - 10.1111/j.1348-0421.1980.tb02866.x
Subject(s) - shock (circulatory) , lactate dehydrogenase , leukopenia , platelet , fibrinogen , immunology , pharmacology , colchicine , antibody , heparin , biology , coagulation , medicine , toxicity , biochemistry , enzyme
Forssman shock (FS) following the intravenous injection of antisheep erythrocyte antibody into guinea pigs resulted in fatal systemic shock with marked decrease in CH 50 values of complement, leucocyte, and platelet counts, and a prolongation of blood coagulation time. In addition, there was an increase in lactate dehydrogenase activity, and decreases in both esterase activity and fibrinogen levels were noted. F(ab′) 2 of antisheep erythrocyte IgG antibody was not capable of eliciting FS. Cobra venom factor showed a fairly potent inhibition of FS. Leukopenia induced by cytosine arabinoside given intraperitoneally for 5 days had no effect on FS. Colchicine, which decreased the leucocyte count, did not inhibit fatal systemic shock. Administration of heparin or trasyrol did not prevent FS. The present findings demonstrate that FS is inhibited by anticomplementary agents but not by drugs which affect leucocyte and platelet counts, the coagulation system or serum proteases.