Carbon monoxide: Anticoagulant or procoagulant?
Vance G Nielsen1, Etheresia Pretorius2
1The Department of Anesthesiology, The University of Arizona College of Medicine, Tucson, AZ, USA.
Thrombosis Research
|December 24, 2013
Summary
Carbon monoxide has a dual effect on blood clotting, potentially inhibiting or enhancing it. Research indicates species-specific differences in hemostatic responses to carbon monoxide exposure.
Area of Science:
- Biochemistry
- Hematology
- Toxicology
Background:
- Carbon monoxide (CO) exposure, both exogenous and endogenous, has been investigated for its effects on hemostasis.
- Conflicting findings exist regarding CO's impact, with some studies suggesting anticoagulation and others procoagulation.
Purpose of the Study:
- To define the impact of carbon monoxide exposure on hemostasis.
- To investigate potential species-specific differences in hemostatic responses to carbon monoxide.
Main Methods:
- Review of existing literature on carbon monoxide and hemostasis.
- Analysis of in vitro and in vivo studies in humans, rodents, rabbits, mice, and rats.
- Examination of thrombus ultrastructure following carbon monoxide exposure.
Main Results:
- Carbon monoxide can inhibit platelet aggregation, leading to anticoagulation in vitro (human) and in vitro/in vivo (rodents).
- CO interaction with heme groups can enhance coagulation and decrease fibrinolysis in vitro (human, other species) and in vivo (rabbits).
- Thrombus ultrastructure analysis revealed species-specific differences in fine fiber formation and matting.
Conclusions:
- Carbon monoxide exhibits a Janus-faced role in hemostasis, capable of both attenuating and exacerbating thrombotic disease.
- Species-specific variations in hemostatic responses to carbon monoxide warrant further investigation.
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