Within the past decade there have been several investigations attempting to define the impact of exogenous and
endogenous carbon monoxide exposure on hemostasis. Critically, two bodies of literature have emerged, with
carbon monoxide mediated platelet inhibition cited as a cause of in vitro human and in vitro/in vivo rodent
anticoagulation. In contrast, interaction with heme groups associated with fibrinogen, α2-antiplasmin and plasmin
by carbon monoxide has resulted in enhanced coagulation and decreased fibrinolysis in vitro in human and
other species, and in vivo in rabbits. Of interest, the ultrastructure of platelet rich plasma thrombi demonstrates
an abnormal increase in fine fiber formation and matting that are obtained fromhumans exposed to carbonmonoxide.
Further, thrombi obtained from humans and rabbits have very similar ultrastructures, whereas mice and
rats have more fine fibers and matting present. In sum, there may be species specific differences with regard
to hemostatic response to carbon monoxide. Carbon monoxide may be a Janus-faced molecule, with potential
to attenuate or exacerbate thrombophilic disease.