Figure 1.
Effect of FcRγ deficiency on occlusive thrombus formation in a “Folts-type” arterial thrombosis model. (A,C) Repetitive crush injury to stenosed carotid arteries was used to induce occlusive thrombus formation in wild-type and FcRγ–/– mice as described in “Materials and methods.” Vascular injury (indicated by *) led to the formation of repetitive cyclic flow reductions (CFRs) in both the wild-type and FcRγ–/– mice. The blood flow traces are from single-mouse experiments representative of 9 and 8 independent wild-type and FcRγ–/– experiments, respectively. (B,D) Histologic analysis of longitudinally sectioned carotid arteries from wild-type mice and FcRγ–/– mice demonstrating the presence of vaso-occlusive platelet-rich thrombi (PT) in the arterial lumen following the development of CFRs.

Effect of FcRγ deficiency on occlusive thrombus formation in a “Folts-type” arterial thrombosis model. (A,C) Repetitive crush injury to stenosed carotid arteries was used to induce occlusive thrombus formation in wild-type and FcRγ–/– mice as described in “Materials and methods.” Vascular injury (indicated by *) led to the formation of repetitive cyclic flow reductions (CFRs) in both the wild-type and FcRγ–/– mice. The blood flow traces are from single-mouse experiments representative of 9 and 8 independent wild-type and FcRγ–/– experiments, respectively. (B,D) Histologic analysis of longitudinally sectioned carotid arteries from wild-type mice and FcRγ–/– mice demonstrating the presence of vaso-occlusive platelet-rich thrombi (PT) in the arterial lumen following the development of CFRs.

Close Modal

or Create an Account

Close Modal
Close Modal