Key result
eNOS-deficient mice exhibited a paradoxical prolongation of time to occlusion following carotid arterial injury compared with wild-type mice (P<0.001).
Why the study?
Does eNOS deficiency alter hemostasis and thrombosis in a mouse model of carotid arterial injury?
Population
eNOS-deficient and wild-type mice
Comparison
eNOS deficiency (genetic knockout model) vs Wild-type mice
Design
Preclinical
Authors
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Should not guide human antithrombotic therapy; leaves open eNOS roles in clinical arterial thrombosis.
Does eNOS deficiency alter hemostasis and thrombosis in a mouse model of carotid arterial injury?
p-value: p=<0.001
eNOS deficiency paradoxically prolongs time to occlusion in arterial injury due to enhanced fibrinolysis resulting from a lack of NO-dependent inhibition of Weibel-Palade body release.
Iafrati et al. (2004) studied carotid arterial injury and thrombosis. eNOS deficiency vs. wild-type mice was evaluated on time to occlusion (p=<0.001). eNOS-deficient mice exhibited a paradoxical prolongation of time to occlusion following carotid arterial injury compared with wild-type mice (P<0.001).
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