Figure 7
Figure 7. ceacam1−/− mice are more susceptible to type I collagen–induced pulmonary thromboembolism. (A) The percent reduction in platelet count over 3 minutes for wild-type (●), ceacam1+/− (■), and ceacam1−/− (▴) mice after intravenous injection of 350 μg/kg type I fibrillar collagen was determined. Note that the mice of each genotype showed a similar reduction in platelet count over time (77.24 ± 2.25% vs 73.49 ± 3.16% vs 74.21 ± 3.51%, respectively; P > .05; n = 20 mice/group). (B) The time until restrained breathing, quantified by a breathing interval of 10 seconds, for wild-type (●), ceacam1+/− (■), and ceacam1−/− (▴) mice after intravenous injection of 350 μg/kg of type I fibrillar collagen. Compared with the wild-type and ceacam1+/− mice, the ceacam1−/− mice showed greater susceptibility to type I collagen-induced pulmonary thromboembolism (343.5 ± 23.7 vs 327.0 ± 28.3 vs 252.1 ± 15.4 seconds, respectively; **P < .001; n = 20 mice/group). (C) The percent reduction in platelet count over 3 minutes for wild-type (●) and ceacam1−/− (▴) mice after intravenous injection of 0.200 μL/g tissue thromboplastin Thromborel S was determined. Note that wild-type and ceacam1−/− mice showed a similar reduction in platelet count over time (94.30 ± 2.16% vs 93.22 ± 1.76%, respectively; P > .05; n = 10 mice/group). (D) The time until restrained breathing, quantified by a breathing interval of 10 seconds, for wild-type (●) and ceacam1−/− (▴) mice after intravenous injection of 0.200 μL/g tissue thromboplastin Thromborel S was determined. Note that wild-type control mice and ceacam1−/− mice showed similar susceptibility to tissue thromboplastin induced pulmonary thromboembolism (223.8 ± 8.0 vs 214.2 ± 4.1 seconds; P > .05; n = 10 mice/group).

ceacam1−/− mice are more susceptible to type I collagen–induced pulmonary thromboembolism. (A) The percent reduction in platelet count over 3 minutes for wild-type (●), ceacam1+/− (■), and ceacam1−/− (▴) mice after intravenous injection of 350 μg/kg type I fibrillar collagen was determined. Note that the mice of each genotype showed a similar reduction in platelet count over time (77.24 ± 2.25% vs 73.49 ± 3.16% vs 74.21 ± 3.51%, respectively; P > .05; n = 20 mice/group). (B) The time until restrained breathing, quantified by a breathing interval of 10 seconds, for wild-type (●), ceacam1+/− (■), and ceacam1−/− (▴) mice after intravenous injection of 350 μg/kg of type I fibrillar collagen. Compared with the wild-type and ceacam1+/− mice, the ceacam1−/− mice showed greater susceptibility to type I collagen-induced pulmonary thromboembolism (343.5 ± 23.7 vs 327.0 ± 28.3 vs 252.1 ± 15.4 seconds, respectively; **P < .001; n = 20 mice/group). (C) The percent reduction in platelet count over 3 minutes for wild-type (●) and ceacam1−/− (▴) mice after intravenous injection of 0.200 μL/g tissue thromboplastin Thromborel S was determined. Note that wild-type and ceacam1−/− mice showed a similar reduction in platelet count over time (94.30 ± 2.16% vs 93.22 ± 1.76%, respectively; P > .05; n = 10 mice/group). (D) The time until restrained breathing, quantified by a breathing interval of 10 seconds, for wild-type (●) and ceacam1−/− (▴) mice after intravenous injection of 0.200 μL/g tissue thromboplastin Thromborel S was determined. Note that wild-type control mice and ceacam1−/− mice showed similar susceptibility to tissue thromboplastin induced pulmonary thromboembolism (223.8 ± 8.0 vs 214.2 ± 4.1 seconds; P > .05; n = 10 mice/group).

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