Abstract
Acute thrombosis can be induced in rabbits by a triggering protocol using Russell's viper venom and histamine given after 8 months of a 1% cholesterol diet and balloon desendothelization. In the present study, we tested the hypothesis that aortic desendothelization performed 4 months before the triggering protocol without a high cholesterol diet is a highly effective and less expensive way of producing arterial atherosclerosis and thrombosis. Nineteen male New Zealand white rabbits on a normal diet were studied. The control group (N = 9) received no intervention during the 4-month observation period, while the other group (N = 10) was submitted to aortic balloon desendothelization using a 4F Fogarty catheter. At the end of this period, all animals were killed 48 h after receiving the first dose of the triggering treatment. Eight of 10 rabbits (80%) in the balloon-trauma group presented platelet-rich arterial thrombosis while none of the animals in the control group had thrombus formation (P < 0.01). Thus, this model, using balloon desendothelization without dietary manipulation, induces arterial atherosclerosis and thrombosis and may provide possibilities to test new therapeutic approaches.
Highlights
Acute thrombosis can be induced in rabbits by a triggering protocol using Russell’s viper venom and histamine given after 8 months of a 1% cholesterol diet and balloon desendothelization
Plaque disruption and subsequent arterial thrombosis are currently considered to be the main mechanisms of acute ischemic coronary syndromes (1), and an animal model is needed for the study of these phenomena
Abela et al (3) reproduced this model and were able to increase the in vivo proportion of thrombosis after 8 months by adding arterial balloon desendothelization to the high-cholesterol diet intervention
Summary
Acute thrombosis can be induced in rabbits by a triggering protocol using Russell’s viper venom and histamine given after 8 months of a 1% cholesterol diet and balloon desendothelization. Plaque disruption and subsequent arterial thrombosis are currently considered to be the main mechanisms of acute ischemic coronary syndromes (1), and an animal model is needed for the study of these phenomena. Constantinides and Chakravarti (2) developed a model in which rabbits were fed a high cholesterol diet for 8 months to produce atherosclerosis, after which plaque disruption and thrombosis were triggered by intraperitoneal injection of Russell’s viper venom, a procoagulant and endothelial toxin, followed by the intravenous injection of histamine, which has a vasopressor effect in rabbits.
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