RUC-1 protects hαIIb/mβ3 mice, but not WT mice from FeCl₃-induced carotid artery thrombotic occlusion. Mice expressing the hybrid hαIIb/mβ3 receptor were injected intraperitoneally with vehicle control [1% (n = 2) or 10% DMSO (n = 6)], or RUC-1 (n = 8; 26.5 mg/kg) approximately 25 minutes before carotid artery injury. Carotid arteries were isolated by blunt dissection and treated with 20% FeCl₃ for 3 minutes using a piece of filter paper. The surgical area was flushed with water, and blood flow through the carotid artery was monitored for 30 minutes with a Doppler flow probe. (A) Representative blood flow tracings from 2 mice treated with DMSO and 2 mice treated with RUC-1. Time to occlusion was calculated from the time the filter paper containing the FeCl₃ was applied to the artery until the time when the arterial flow rate became undetectable. (B) Kaplan-Meier analysis of time to occlusion data in hαIIb/mβ3 mice receiving either RUC-1 (n = 8) or DMSO vehicle control (n = 8). (C) Kaplan-Meier analysis of time to occlusion data from RUC-1-treated mice comparing WT mice (n = 10) and hαIIb/mβ3 mice (n = 8, data repeated from panel B). (D,E) Hematoxylin and eosin stains of fixed cross-sections of carotid arteries in a mouse treated with DMSO as a control (left) and a mouse treated with RUC-1 (right). An extensive platelet thrombus nearly completely fills the lumen of the control animal's carotid artery, whereas there is minimal platelet thrombus formation in the carotid artery of RUC-1-treated animal. Most of the material in the lumen of the RUC-1-treated animal is trapped erythrocytes. The bar in panel D is 50 μm, and both panels D and E were photographed and reproduced at the same magnification.