Fujii H, Berliner L J
Department of Inflammation Research, Tokyo Metropolitan Institute of Medical Science, Tokyo, Japan.
Magn Reson Med. 1999 Sep;42(3):599-602. doi: 10.1002/(sici)1522-2594(199909)42:3<599::aid-mrm24>3.0.co;2-y.
The concentration of nitric oxide (NO) was measured in the brain of septic-shock animals by electron paramagnetic resonance spectrometry (EPR). NO was spin trapped and quantitated in several regions of the brain (cortex, hippocampus, hypothalamus, cerebellum, and olfactory bulb) as well as other organs (liver, kidney, and heart) of rats induced with lipopolysaccharide (LPS) using Fe(II)/dithiocarbamate complexes containing diethyldithiocarbamate (DETC) or N-methyl-D-glucamine (MGD). The spin trap, (DETC)(2)-Fe(II), complexed NO generated in all tissues examined, but (MGD)(2)-Fe(II) complex was ineffective in detecting NO in the brain of septic-shock rats, although identical amounts of NO were detected in the liver with either spin trap. A triplet EPR spectrum of (DETC)(2)-Fe(II)-NO with a(N) = 12.8 gauss and g = 2.04 was observed in the cortex, hippocampus, hypothalamus, cerebellum, but not the olfactory bulb. The amount of NO in the brain was about 20% of that found in the liver. The (DETC)(2)-Fe(II)-NO signal in all the tissues of septic-shock rats was markedly suppressed by preadministration of the nitric oxide synthase (NOS) inhibitors, N(G)-monomethyl-L-arginine (L-NMMA) or 3-bromo-7-nitroindazole, suggesting that the NO detected from brain tissue was produced enzymatically by NOS. In contrast to previous studies on the liver and other organs, phenyl-N-tert-butyl nitrone (PBN), did not suppress iNOS expression in brain tissue of LPS-treated rats. This could be due to a totally different regulation system for iNOS in liver versus brain tissue. Magn Reson Med 42:599-602, 1999.
采用电子顺磁共振波谱法（EPR）测定脓毒症休克动物脑内一氧化氮（NO）的浓度。使用含有二乙基二硫代氨基甲酸盐（DETC）或N-甲基-D-葡糖胺（MGD）的Fe（II）/二硫代氨基甲酸盐复合物，对用脂多糖（LPS）诱导的大鼠的脑（皮质、海马、下丘脑、小脑和嗅球）以及其他器官（肝脏、肾脏和心脏）中的NO进行自旋捕获和定量分析。自旋捕获剂（DETC）2-Fe（II）能与所有检测组织中生成的NO结合，但（MGD）2-Fe（II）复合物在检测脓毒症休克大鼠脑内的NO时无效，尽管使用任一自旋捕获剂在肝脏中检测到的NO量相同。在皮质、海马、下丘脑、小脑中观察到（DETC）2-Fe（II）-NO的三重态EPR谱，其a（N）=12.8高斯，g = 2.04，但在嗅球中未观察到。脑内NO的量约为肝脏中NO量的20%。预先给予一氧化氮合酶（NOS）抑制剂N（G）-单甲基-L-精氨酸（L-NMMA）或3-溴-7-硝基吲唑可显著抑制脓毒症休克大鼠所有组织中的（DETC）2-Fe（II）-NO信号，这表明从脑组织中检测到的NO是由NOS酶促产生的。与先前对肝脏和其他器官的研究不同，苯基-N-叔丁基硝酮（PBN）并未抑制LPS处理大鼠脑组织中诱导型NOS（iNOS）的表达。这可能是由于肝脏和脑组织中iNOS的调节系统完全不同。《磁共振医学》42:599 - 602，1999年。
