Extracorporeal Thrombosis Models

These models employ passing blood over a section of damaged vessel (or other selected substrates) and 

Badimon L, Badimon JJ (1989) Mechanism of arterial thrombosis in non-parallel streamlines Platelet thrombi grow on the apex of stenotic severely injured vessel wall. J Clin Invest 84 1134-1144 

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A method for the direct observation of extracorporal thrombus formation has been introduced by Rowntree and Shionoya (1927). These first studies could provide evidence that anticoagulants like heparin and hirudin do inhibit thrombus development in arteriovenous shunts. Since today, the A-V-shunt thrombosis models have been often used to evaluate the antithrombotic potential of new compounds in different species including rabbits (Knabb et al. 1992), rats (Hara et al. 1995), pigs (Scott et al. 1994), dogs and cats (Best et al. 1938), and non-human primates (Yokoyama et al. 1995). 

Using an arteriovenous shunt model of thrombosis in the rat, compounds 4 and 7 were evaluated for their ability to maintain patency of the extracorporeal circuit which serves as a thrombogenic surface [76]. Table 2 shows that on a gravimetric basis r-hirudin and inhibitor 4, were equipotent [r-hirudin EDis = 1.4 mg/kg 4 EDi5= 1.2 mg/kg i.v. bolus]. The thrombin inhibitor 7 was less effective in this assay having an EDi5= 6.3 mg/kg. 

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