Blood coagulation is a basic physiological defense mechanism that occurs in all vertebrates to prevent blood loss following vascular injury. In all species the basic mechanism of clot formation is similar; when endothelium is damaged a complex sequence of enzymatic reactions occurs that is localized to the site of trauma and involves both activated cells and plasma proteins. The reaction sequence is initiated by the expression of tissue factor on the surface of activated cells and results in the generation of thrombin, the most important enzyme in blood clot formation. Thrombin converts soluble fibrinogen, via soluble fibrin monomers, into the insoluble fibrin that forms the matrix of a blood clot as well as exerting positive-feedback regulation that effectively promotes additional thrombin generation that facilitates the rapid development of a thrombus. Both spontaneous and trauma-induced haemorrhagic episodes can develop in all mammals with inherited or acquired abnormalities in one or more of the coagulant proteins. Experimental studies with plasma from a wide range of species have led to the conclusion that there are extensive differences in the rates of thrombin generation and fibrin formation among species. However, current evidence suggests that at least some of these quantitative differences are likely due to the use of non-species specific laboratory reagents. Although the individual proteins involved in the procoagulant pathways exhibit similar functions in all animals, differences in amino acid sequence cause incomplete homology and varying degrees of immunological cross-reactivity for the same protein across species.