Key result
eNOS deficiency does not accelerate arterial thrombosis or meaningfully alter platelet aggregation.
Why the study?
The role of endothelial nitric oxide synthase in platelet activation, aggregation, and arterial thrombosis in vivo was unclear.
Does eNOS deficiency affect platelet aggregation and arterial thrombosis in mice?
Population
Wild-type and eNOS-/- mice
Comparison
eNOS deficiency (genetic knockout) vs wild-type
Design
Preclinical experimental study
Authors
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eNOS deficiency does not accelerate thrombosis in this mouse model; leaves open its role in human platelet function and arterial thrombosis.
Does eNOS deficiency affect platelet aggregation and arterial thrombosis in mice?
Absolute Event Rate: 457% vs 501%
p-value: p=n.s.
Endothelial NO synthase deficiency minimally affects platelet aggregation and is not associated with accelerated arterial thrombosis in vivo in mice.
Özüyaman et al. (2005) studied Arterial thrombosis. eNOS deficiency vs. Wild-type mice was evaluated on Time to occlusion of the A.carotis after focal induction of thrombosis (seconds) (p=n.s.). eNOS-deficiency minimally affected platelet aggregation and was not associated with accelerated arterial thrombosis in vivo (time to carotid occlusion 457 vs 501 s, n.s.).
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