Figure 1.
Figure 1. Platelet adhesion and thrombus formation in α2-null mice. (A) Flow cytometric analysis of glycoprotein expression on wild-type (black line) and α2-null (shaded area) mice. (B) Platelet-vessel wall interactions after vascular injury were investigated in wild-type, α2-null, and GPVI-deficient mice by in vivo fluorescence microscopy of the common carotid artery in situ. The left and right graphs summarize platelet adhesion and aggregate formation, respectively, of 7 experiments per group. Results are shown as mean ± SEM. (C) The photomicrographs show representative in vivo fluorescence microscopy images 3 minutes after injury in wild-type, α2-null, and GPVI-deficient mice. (D) Representative histologic sections of carotid arteries 20 minutes after injury demonstrating large platelet-rich thrombi wild-type, α2-null, but not GPVI-deficient mice. Sections stained with toluidine blue/basic fuchsin; original magnification, × 5.

Platelet adhesion and thrombus formation in α2-null mice. (A) Flow cytometric analysis of glycoprotein expression on wild-type (black line) and α2-null (shaded area) mice. (B) Platelet-vessel wall interactions after vascular injury were investigated in wild-type, α2-null, and GPVI-deficient mice by in vivo fluorescence microscopy of the common carotid artery in situ. The left and right graphs summarize platelet adhesion and aggregate formation, respectively, of 7 experiments per group. Results are shown as mean ± SEM. (C) The photomicrographs show representative in vivo fluorescence microscopy images 3 minutes after injury in wild-type, α2-null, and GPVI-deficient mice. (D) Representative histologic sections of carotid arteries 20 minutes after injury demonstrating large platelet-rich thrombi wild-type, α2-null, but not GPVI-deficient mice. Sections stained with toluidine blue/basic fuchsin; original magnification, × 5.

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