Fig. 1.
Fig. 1. Quantitative analysis of thrombi formation in wild-type and GP V−/− arterioles. / Wild-type mice (n = 16; ▩) were compared to GP V−/−mice (n = 17; ▪). The diameter of the mesenteric arterioles was 103 ± 3 μm in wild-type mice and 104 ± 3 μm in GP V−/− mice, P = .95. The shear rates were 1529 ± 46/s in wild-type and 1441 ± 58/s in knockout mice,P = .24. Experiments were performed without knowledge of the mice genotypes. (A) The number of fluorescently labeled platelets that came in contact with the vessel walls in the first minute after FeCl3 injury was counted over a 410-μm length of vessel. (B) The time required for the appearance of the first thrombus (diameter > 20 μm) after injury was measured. Thrombi appeared about 4 minutes sooner in GP V−/− mice than in wild-type mice. (C) The number of large emboli (diameter > 30 μm), generated in the period before vessel occlusion and embolized away from the viewing field, was determined. Although this period was shorter in GP V−/− mice (panel D), the number of emboli formed in these mice was higher. (D) The time before blood flow completely stopped for more than 10 seconds was determined. If blood flow did not cease during the 40-minute observation period, 40 minutes was used as the occlusion time. The vessel occlusion time in GP V−/− mice was shorter than in wild-type mice, but only a small number of GP V−/− vessels were occluded by the original thrombus (35%). The majority of vessels were occluded by large emboli, which caused occlusion either within the injured region (24%) or downstream of injured region (41%). All occlusions in wild-type vessels were caused by one of the original thrombi within the injured area.

Quantitative analysis of thrombi formation in wild-type and GP V−/− arterioles.

Wild-type mice (n = 16; ▩) were compared to GP V−/−mice (n = 17; ▪). The diameter of the mesenteric arterioles was 103 ± 3 μm in wild-type mice and 104 ± 3 μm in GP V−/− mice, P = .95. The shear rates were 1529 ± 46/s in wild-type and 1441 ± 58/s in knockout mice,P = .24. Experiments were performed without knowledge of the mice genotypes. (A) The number of fluorescently labeled platelets that came in contact with the vessel walls in the first minute after FeCl3 injury was counted over a 410-μm length of vessel. (B) The time required for the appearance of the first thrombus (diameter > 20 μm) after injury was measured. Thrombi appeared about 4 minutes sooner in GP V−/− mice than in wild-type mice. (C) The number of large emboli (diameter > 30 μm), generated in the period before vessel occlusion and embolized away from the viewing field, was determined. Although this period was shorter in GP V−/− mice (panel D), the number of emboli formed in these mice was higher. (D) The time before blood flow completely stopped for more than 10 seconds was determined. If blood flow did not cease during the 40-minute observation period, 40 minutes was used as the occlusion time. The vessel occlusion time in GP V−/− mice was shorter than in wild-type mice, but only a small number of GP V−/− vessels were occluded by the original thrombus (35%). The majority of vessels were occluded by large emboli, which caused occlusion either within the injured region (24%) or downstream of injured region (41%). All occlusions in wild-type vessels were caused by one of the original thrombi within the injured area.

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