Experimental and epidemiologic studies have identified several potential genetic components for increased thrombotic risk. Studies of thrombosis often use rat models without considering the effect of strain differences on thrombotic propensity. A comparison of in vivo thrombotic occlusion after small-vessel anastomosis was made between age/weight-matched male Copenhagen and Lewis rats. One-day thrombotic occlusion rates were significantly higher in Copenhagen arteries (67%) and veins (100%) compared to Lewis arteries (8%) and veins (50%), respectively. Single-bolus intravenous heparin (150 units/kg body weight) had a slight effect on reducing occlusion rates in Copenhagen rats (50% and 67% for arteries and veins, respectively), while occlusion was totally prevented by heparin in both vessel types of Lewis rats (0% occlusion). In vitro assays for platelet aggregation and coagulation revealed no apparent differences between these two rats strains, although AT-III levels were slightly higher in Copenhagen rats, contrary to the prothrombotic state. These findings indicate a profound prothrombotic tendency in the Copenhagen rat strain and support a broader investigation of the genetic basis of this thrombotic potential.
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- Copenhagen rat
- Lewis rat