Neuronal nitric oxide synthase mutant mice show smaller infarcts and attenuated apparent diffusion coefficient changes in the peri-infarct zone during focal cerebral ischemia.
Neuronal nitric oxide synthase mutant mice show smaller infarcts and attenuated apparent diffusion coefficient changes in the peri-infarct zone during focal cerebral ischemia.
复制标题
神经元一氧化氮合酶突变小鼠在局灶性脑缺血期间表现出更小的梗塞和减弱的梗塞周围区域的表观扩散系数变化。
DOI：
10.1002/mrm.1910370204
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发表时间：
1997
影响因子：
3.3
通讯作者：
Rosen,BR
中科院分区：
文献类型：
--
作者：
Zaharchuk,G;Hara,H;Huang,PL;Fishman,MC;Moskowitz,MA;Jenkins,BG;Rosen,BR
Diffusion‐weighted MRI at 2 T was used to monitor and assess tissue damage after permanent middle cerebral artery occlusion (MCAO) in wild‐type (WT) and mice deficient in nitric oxide synthase gene expression (nNOS−). The ischemic lesion was evaluated 3 h after occlusion and subdivided into the lesion core and peri‐infarct zone based on the magnitude of the apparent diffusion coefficient (ADC) change. Infarct volume, measured by using histochemical staining 24 h after MCA occlusion, correlated best with MRI infarct volume as assessed by an ADC threshold of 25% decrease from baseline at 3 h. For ADC thresholds of greater than 25% decrease, lesion size was not significantly different in nNOS−and WT mice. However, brain tissue showing ADC decreases of 10–25% was significantly smaller in the ipsilateral hemisphere of mutants (27 · 2% and 21 · 2% in WT and nNOS−, respectively;P< 0.05). These findings occurred independently of infarct volume and are consistent with a smaller peri‐infarct zone in nNOS−mice. We postulate that the smaller peri‐infarct zone is a reflection of less severe metabolic disturbance after ischemia in nNOS−mice, possibly related to diminished production of nitric oxide (NO) or a related product. We conclude that magnetic resonance techniques previously used to assess ischemic damage in larger animals can be extended to the mouse, raising the possibility that the molecular mechanisms leading to ischemic damage can be examined by using genetically engineered mice.
