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Thromb Haemost 1972; 27(03): 543-553
DOI: 10.1055/s-0038-1649394
Originalarbeiten — Original Articles — Travaux Originaux
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Activation of Hageman Factor by Cardiac Arrest

J. G. Latour Ph.D   *)
1   Department of Pathology, University of California School of Medicine, San Francisco General Hospital, San Francisco, Cal., U.S.A
,
D. G. McKay M. D.
1   Department of Pathology, University of California School of Medicine, San Francisco General Hospital, San Francisco, Cal., U.S.A
,
Mary H. Parrish B. S.
1   Department of Pathology, University of California School of Medicine, San Francisco General Hospital, San Francisco, Cal., U.S.A
› Author AffiliationsSupported by United States Public Health Service NIH Grant No. HE-12033 and GM-18470-01. Dr. Latour is a fellow of the “Medical Research Council of Canada55.
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Publication Date:
24 July 2018 (online)

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Summary

The induction of cardiac arrest in rabbits for a period of 3min, followed by reestablishment for the circulation, resulted in a 27 % decrease in circulating Hageman factor. The maximum depletion occurred within 30 to 60 min and normal levels were restored by 4 h. Anti-contact product activity remained unchanged. Circulating platelets dropped by 17 % and small arterial thrombi were found predominantly in the lungs. It is concluded that cardiac arrest followed by re-circulation of the blood causes activation of Hageman factor. The proximate mechanism of this activation in experimental generalized anoxemia remains to be determined. Administration of a potent glucocorticoid prior to cardiac arrest markedly inhibited activation of the clotting mechanism.

*) Present adress: Institut de Cardiologie de Montreal, 5000 Est, Rue Belanger, Montreal 410, Quebec, Canada.


 

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