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.