Fig. 1.
Fig. 1. Effect of PAR3 deficiency on ferric chloride–induced thrombosis in mesenteric arterioles. / Offspring of PAR3 heterozygote crosses were studied. Shown is the fraction of arterioles remaining patent as a function of time after ferric chloride application. The mice were not genotyped until the completion of each experiment. Par3 genotypes and the number of mice studied for each genotype are indicated at right. The effect of genotype on patency was significant by log-rank test (P < .02), and the fraction of vessels patent at 30 minutes in Par3−/− mice versusPar3+/− orPar3+/+ mice was different by χ2 (P < .035).

Effect of PAR3 deficiency on ferric chloride–induced thrombosis in mesenteric arterioles.

Offspring of PAR3 heterozygote crosses were studied. Shown is the fraction of arterioles remaining patent as a function of time after ferric chloride application. The mice were not genotyped until the completion of each experiment. Par3 genotypes and the number of mice studied for each genotype are indicated at right. The effect of genotype on patency was significant by log-rank test (P < .02), and the fraction of vessels patent at 30 minutes in Par3−/− mice versusPar3+/− orPar3+/+ mice was different by χ2 (P < .035).

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