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.