Higuchi Y, Hattori H, Kume T, Tsuji M, Akaike A, Furusho K
Department of Pediatrics, Faculty of Medicine, Kyoto University, Japan.
Eur J Pharmacol. 1998 Jan 19;342(1):47-9. doi: 10.1016/s0014-2999(97)01524-0.
We measured the changes in nitric oxide (NO) metabolites in the brains of neonatal rats with hypoxic-ischemic damage. There were two peaks of NO metabolites in the lesioned side of the cortex without treatment: one during hypoxia and the other during the re-oxygenation period. Prehypoxic treatment with 7-nitroindazole, a selective neuronal NO synthase inhibitor, suppressed both peaks of NO metabolites, whereas prehypoxic treatment with aminoguanidine, a selective inducible NO synthase inhibitor, partially suppressed only the peak in the re-oxygenation period. These data suggest different roles of neuronal and inducible NO synthases in the pathogenesis of hypoxic-ischemic encephalopathy.
我们检测了缺氧缺血性脑损伤新生大鼠脑内一氧化氮（NO）代谢产物的变化。未经治疗时，皮质损伤侧的NO代谢产物出现两个峰值：一个在缺氧期，另一个在复氧期。用选择性神经元型NO合酶抑制剂7-硝基吲唑进行缺氧前处理可抑制NO代谢产物的两个峰值，而用选择性诱导型NO合酶抑制剂氨基胍进行缺氧前处理仅部分抑制复氧期的峰值。这些数据提示神经元型和诱导型NO合酶在缺氧缺血性脑病发病机制中发挥不同作用。
