Loidl C F, Capani F, Lopez-Costa J J, Lopez E, Selvin-Testa A, Pecci-Saavedra J
Instituto de Biología Celular y Neurociencias Eduardo De Robertis, LANAIS-MIE, Facultad de Medicine, Universidad de Buenos Aires.
Medicina (B Aires). 1996;56(2):169-72.
Neuropathological mechanisms triggered by excitatory aminoacids are known to involve nitric oxide (NO). Neurons containing NO are histochemically reactive to nicotinamide adenine dinucleotide phosphate diaphorase (NADPH-d), which labels NO synthase in CNS. Sprague-Dawley male rats subjected to perinatal asphyxia (PA) at 37 degrees C, and PA plus 15 degrees C hypothermia were evaluated when 6 months old by NADPH-d histochemical reaction. Computarized image analysis was used for quantification of stained sections. NADPH-d neurons in striatum from subsevere and severe PA showed a significant increment in soma size and dendritic process length versus control and hypothermic treated rats. Post-ischemic damage neurons are therefore involved in NO changes induced by PA that may be prevented by hypothermia treatment.
已知由兴奋性氨基酸触发的神经病理机制涉及一氧化氮（NO）。含有NO的神经元在组织化学上对烟酰胺腺嘌呤二核苷酸磷酸黄递酶（NADPH-d）有反应，该酶可标记中枢神经系统中的一氧化氮合酶。将斯普拉格-道利雄性大鼠在37摄氏度下进行围产期窒息（PA）处理，并对PA加15摄氏度低温处理的大鼠在6个月大时通过NADPH-d组织化学反应进行评估。使用计算机图像分析对染色切片进行定量分析。与对照组和低温处理的大鼠相比，亚重度和重度PA组纹状体中的NADPH-d神经元在细胞体大小和树突长度上有显著增加。因此，缺血后损伤神经元参与了PA诱导的NO变化，而低温治疗可能会预防这种变化。
