Figure 7
Figure 7. Increased bleeding and diminished thrombosis are observed in mice in the absence of NK1 receptor function. The time to cessation of bleeding following transection of the tail tip of NK1 receptor–deficient mice and littermate controls was measured. The assay was terminated after 10 minutes. Data represent individual mice (n = 10) with mean value indicated. **P < .01 (A). Collagen-induced thromboembolism was measured in Balb/c mice infused with 111Indium oxine–labeled platelets by measurement of the accumulation of radiolabeled platelets in the pulmonary region (B). Mice were treated with the NK1 receptor antagonist L733060 (10 mg/kg) or vehicle alone prior to stimulation of thromboembolism through intravenous administration of collagen (100 μg/kg). Data were acquired as percentage change in basal counts and expressed as maximal percentage response (embolic response, mean ± SEM) where measurements acquired for vehicle alone treated mice were taken as 100%.

Increased bleeding and diminished thrombosis are observed in mice in the absence of NK1 receptor function. The time to cessation of bleeding following transection of the tail tip of NK1 receptor–deficient mice and littermate controls was measured. The assay was terminated after 10 minutes. Data represent individual mice (n = 10) with mean value indicated. **P < .01 (A). Collagen-induced thromboembolism was measured in Balb/c mice infused with 111Indium oxine–labeled platelets by measurement of the accumulation of radiolabeled platelets in the pulmonary region (B). Mice were treated with the NK1 receptor antagonist L733060 (10 mg/kg) or vehicle alone prior to stimulation of thromboembolism through intravenous administration of collagen (100 μg/kg). Data were acquired as percentage change in basal counts and expressed as maximal percentage response (embolic response, mean ± SEM) where measurements acquired for vehicle alone treated mice were taken as 100%.

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