Thromb Haemost 1977; 37(01): 170-176
DOI: 10.1055/s-0038-1649215
Original Article
Schattauer GmbH

Oxygen-Induced Consumptive Coagulopathy and its Enhancement by Lead Acetate

L. A Kiesow
1  Department of Experimental Medicine, Naval Medical Research Institute, Bethesda, Maryland 20014, U.S.A.
,
S Shapiro
1  Department of Experimental Medicine, Naval Medical Research Institute, Bethesda, Maryland 20014, U.S.A.
,
B. F Lindsley
1  Department of Experimental Medicine, Naval Medical Research Institute, Bethesda, Maryland 20014, U.S.A.
,
J. W Bless
1  Department of Experimental Medicine, Naval Medical Research Institute, Bethesda, Maryland 20014, U.S.A.
› Author Affiliations
Further Information

Publication History

Received 24 June 1976

Accepted 30 August 1976

Publication Date:
03 July 2018 (online)

Summary

The exposure of rats to 100% oxygen at 1 atmosphere leads to a prolongation of prothrombin times and activated partial thromboplastin times. This development is associated with a consumption of factor XII, VIII, and VII activities and with the appearance of fibrin monomers and fibrinogen degradation products. Lead acetate enhances all oxygen-induced changes of the coagulation systems drastically. The O2 survival time of chicks which are naturally deficient in factor XII is greatly increased over that of rats and is not affected by lead acetate. Oxygen survival times of rats suffering from chronic respiratory disease (CRD) are also significantly increased when compared with normal rats. It appears that consumptive coagulopathy and disseminated intravascular coagulation are early events in oxygen exposure, and that their development is accelerated by lead ions.