May 1, 1997Journal of Cerebral Blood Flow & MetabolismOpen Access

[ ³ H]L- N G -Nitroarginine Binding after Transient Focal Ischemia and NMDA-Induced Excitotoxicity in Type I and Type III Nitric Oxide Synthase Null Mice

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Structured PICO

Population

Wild-type (SV-129 and C57black/6) and type I (neuronal) and type III (endothelial) nitric oxide synthase (NOS)-deficient mice

Intervention

Transient focal ischemia (middle cerebral artery occlusion for 3 h) or intrastriatal injection of N-methyl-D-aspartate (NMDA)

Comparator

Baseline conditions

Outcome

Density and distribution of nitric oxide synthase (NOS) binding by quantitative autoradiography using [3H]L-NG-nitroarginine ([3H]L-NNA)surrogate

Ischemic and excitotoxic insults up-regulate type I NOS gene expression and binding, suggesting a pivotal role in the pathogenesis of ischemic/excitotoxic diseases.

Discussion

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Implication

Type I NOS upregulation may contribute to ischemic injury; this animal data leaves open its therapeutic targeting in stroke.

Cite This Study

Hara et al. (1997) studied this question.

synapsesocial.com/papers/6a873379ed1c9801b3cfa5c8 https://doi.org/10.1097/00004647-199705000-00005

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[ ³ H]L- N G -Nitroarginine Binding after Transient Focal Ischemia and NMDA-Induced Excitotoxicity in Type I and Type III Nitric Oxide Synthase Null Mice

Structured PICO

Discussion

Implication

Cite This Study

[ ³ H]L- N G -Nitroarginine Binding after Transient Focal Ischemia and NMDA-Induced Excitotoxicity in Type I and Type III Nitric Oxide Synthase Null Mice

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Also Consider