Reduced brain edema and infarction volume in mice lacking the neuronal isoform of nitric oxide synthase after transient MCA occlusion
Reduced brain edema and infarction volume in mice lacking the neuronal isoform of nitric oxide synthase after transient MCA occlusion
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DOI：
10.1097/00004647-199607000-00010
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发表时间：
1996-07-01
影响因子：
6.3
通讯作者：
Moskowitz, MA
中科院分区：
文献类型：
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作者：
Hara, H;Huang, PL;Moskowitz, MA
在缺乏神经元型一氧化氮合酶（NOS）基因表达的小鼠短暂局灶性缺血后，评估脑体积和水肿。使用8-0涂覆的单丝，将突变型（n = 32）和野生型小鼠[SV-129（n = 31），C57 Black/6（n = 18）]的大脑中动脉（MCA）闭塞3小时并再灌注长达24小时。在所有三种品系中检查局部CBF（rCBF）、神经缺陷、水含量和梗塞体积，再灌注后1小时测量时，两组之间的心率没有差异。大脑中动脉闭塞后，突变小鼠的神经功能缺损不那么严重。野生型小鼠再灌注后3小时的脑含水量和再灌注后24小时的梗死体积更大。这些数据表明，在再灌注模型中，神经元NOS的基因缺失赋予对局灶性缺血损伤的抵抗力。这一结果与以往的研究结果一致，即在缺乏神经元NOS基因表达的小鼠中，大脑中动脉永久性闭塞和全脑缺血后组织损伤的范围较小，因此，NO可能在缺血性脑损伤的发病机制中起关键作用。
Infarct volume and edema were assessed after transient focal ischemia in mice lacking neuronal nitric oxide synthase (NOS) gene expression. With use of an 8-0 coated monofilament, the middle cerebral artery (MCA) of mutant (n = 32) and wild-type mice [SV-129 (n = 31), C57Black/6 (n = 18)] were occluded for 3 h and reperfused for up to 24 h, Regional CBF (rCBF), neurological deficits, water content, and infarct volume were examined in all three strains, rCBF, blood pressure, and heart rate did not differ between groups when measured for 1 h after reperfusion. Neurological deficits were less severe in mutant mice after MCA occlusion. Brain water content at 3 h after reperfusion and infarct volume at 24 h after reperfusion were greater in wild-type mice. These data indicate that genetic deletion of neuronal NOS confers resistance to focal ischemic injury in a reperfusion model. The findings agree with previous studies showing that tissue injury is less extensive after both permanent MCA occlusion and global ischemia in mice lacking neuronal NOS gene expression, Hence, NO may play a pivotal role in the pathogenesis of ischemic brain damage.