Effect of GPV deficiency in an intravital arterial thrombosis model.

GPV knockout (−/−, open bars) or WT (+/+, gray bars) mice were injected with calcein-labeled platelets of matching phenotype. After exposure of mesenteric arteries and FeCl3 injury, the arteries were observed for up to 20 minutes by fluorescence videomicroscopy. Time to vessel closure was determined (A), and vessels still permeable at the end of the experiment were scored as occluded in 20 minutes. Occlusion times in GPV-deficient mice (n = 10) were statistically prolonged (P = .01; 2-tailed t test) compared to those of littermate (+/+) controls (n = 12). During the first 2 minutes after injury, single platelets tethering to the vessel wall were randomly assigned and timed for detachment after frame-by-frame analysis (B) (n = 34 platelets from 5 arteries for WT mice and n = 24 platelets from 5 arteries for GPV null mice). Platelets detached significantly faster (P < .0001; 2-tailed ttest) in GPV null (0.47 ± 0.05 seconds) than in WT mice (2.97 ± 0.48 seconds). Results in panels A and B are expressed as mean values ± SEMs.