Figure 5
Figure 5. In vivo thrombosis. Thrombosis in a carotid artery occlusion model is presented. After damage via FeCl3 to an exposed carotid artery, blood flow in an anesthetized animal was followed for approximately 40 minutes. hTgWT animals display a rapid and stable reduction in blood flow initiated approximately 5 minutes after chemical damage (top graph). Three representative tracings are shown but are indicative of results obtained from 10 different animals. In contrast, hTgG233V mice were unable to occlude the carotid artery as evidenced by only small changes in the blood flow during the 40-minute experiment (bottom graph). Again, only 3 representative tracings are shown, but similar results were obtained with all hTgG233V animals tested (n = 10). The patent carotid artery of hTgG233V animals is in stark contrast to the occlusive thrombi that form with hTgWT animals.

In vivo thrombosis. Thrombosis in a carotid artery occlusion model is presented. After damage via FeCl3 to an exposed carotid artery, blood flow in an anesthetized animal was followed for approximately 40 minutes. hTgWT animals display a rapid and stable reduction in blood flow initiated approximately 5 minutes after chemical damage (top graph). Three representative tracings are shown but are indicative of results obtained from 10 different animals. In contrast, hTgG233V mice were unable to occlude the carotid artery as evidenced by only small changes in the blood flow during the 40-minute experiment (bottom graph). Again, only 3 representative tracings are shown, but similar results were obtained with all hTgG233V animals tested (n = 10). The patent carotid artery of hTgG233V animals is in stark contrast to the occlusive thrombi that form with hTgWT animals.

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