Figure 4
Figure 4. Injured VWF−/− venules do not occlude. Fluorescently-labeled platelets representing approximately 2.5% of total platelets were observed in mesenteric venules of live mice after ferric-chloride injury. Representative photographs of the injured venules are shown. At 3 minutes, the number of single platelets deposited on the injured vessel wall (Figure 1) in the WT mice (top panels) was more than in VWF−/− venules (middle panels) even if the mice were infused with r-hu-FVIII (bottom panels). The thrombus growth was significantly delayed at 12 minutes in the VWF−/− mice with or without r-hu-FVIII when compared with WT. The vessel occluded at 18 minutes in WT, whereas in the VWF−/− mice with or without r-hu-FVIII injured venules remained opened for the entire 40-minute observation time. Blood flow was from left to right. White line delineates the venules, and time after ferric-chloride application is indicated. Bar = 100 μm.

Injured VWF−/− venules do not occlude. Fluorescently-labeled platelets representing approximately 2.5% of total platelets were observed in mesenteric venules of live mice after ferric-chloride injury. Representative photographs of the injured venules are shown. At 3 minutes, the number of single platelets deposited on the injured vessel wall (Figure 1) in the WT mice (top panels) was more than in VWF−/− venules (middle panels) even if the mice were infused with r-hu-FVIII (bottom panels). The thrombus growth was significantly delayed at 12 minutes in the VWF−/− mice with or without r-hu-FVIII when compared with WT. The vessel occluded at 18 minutes in WT, whereas in the VWF−/− mice with or without r-hu-FVIII injured venules remained opened for the entire 40-minute observation time. Blood flow was from left to right. White line delineates the venules, and time after ferric-chloride application is indicated. Bar = 100 μm.

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