Arterial vessel wall injury results in thrombotic occlusion in mice but not in birds. The carotid arteries of anesthetized mice and Australian budgerigars were exposed to filter pads soaked in the indicated concentrations of FeCl₃ for 5-20 minutes. (A) Time to occlusion after removal of the FeCl₃ pad was determined by measuring arterial blood flow using a Doppler flow probe. N/O indicates no occlusion, defined as normal blood flow after 20 minutes afterFeCl₃ pad removal, the termination point of the experiment. Zero minutes indicates occlusion before the time of Doppler probe measurement. Diamonds and circles represent individual mouse and budgerigar carotids, respectively. Horizontal bars indicate the mean time to occlusion for mouse carotid vessels at a given concentration and time of FeCl₃ administration. Budgerigar carotid occlusion was observed only after repeated administration of the highest concentration of FeCl₃ (40% FeCl₃ for 10 minutes × 2). (B) Histologic examination of thrombus formation in FeCl₃-injured mouse and budgerigar carotid arteries. Transverse sections of injured carotid arteries were stained with H&E or Prussian blue (to detect FeCl₃). The occlusive mass of eosin-staining anuclear cells that occlude the mouse arterial lumen is composed of platelets (PLTs). Budgerigar thrombocytes (TCs) are elongated nucleated cells that do not stain strongly for Prussian blue. Occlusive thrombi failed to form in injured budgerigar carotids in the absence of FeCl₃ penetration into the vessel lumen. Scale bar = 50 μm. n = 1-5 experiments for each condition, as indicated by the number of diamonds and circles in panel A.