Formation of free radicals and nitric oxide derivative of hemoglobin in rats during shock syndrome.
Formation of free radicals and nitric oxide derivative of hemoglobin in rats during shock syndrome.
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休克综合征期间大鼠血红蛋白自由基和一氧化氮衍生物的形成。
DOI：
--
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发表时间：
1990
期刊：
影响因子：
--
通讯作者：
O. Trentz
中科院分区：
文献类型：
--
作者：
Ulrich Westenberger;Siegfried Thanner;Hans Heinrich Ruf;Klaus Gersonde;Günter Sutter;O. Trentz
自由基被认为在休克综合征和多器官衰竭的发病机制中发挥着重要的介导作用。我们试图用电子自旋共振（ESR）直接检测休克动物模型（即内毒素（ETX）休克或大鼠失血性休克）中自由基形成的增加。在冷冻夹持的肺组织中，在应用ETX后检测到自由基信号的小但显著的增加。在内毒素休克大鼠的血液中，观察到具有三重超精细结构的显著ESR信号。后一种ESR信号在应用ETX后数小时内出现，并定位于红细胞中。该信号被归属于血红蛋白的一氧化氮（NO）加合物，其暂定结构为[α 2+ NO）β 3+）2。形成的血红蛋白-NO的量高达总血红蛋白的0.8%，表明在ETX休克下，在血管系统中产生了相当数量的NO。精氨酸类似物NG-单甲基精氨酸（NMMA）强烈抑制NO的产生。在重度失血性休克后也可观察到Hb-NO的ESR信号。存在三个问题，即（i）血管细胞的类型和在ETX休克期间形成如此大量的NO的过程的调节，（ii）所形成的NO的病理生理学意义，其作用已被描述为细胞毒性介质、内皮衍生的舒张因子（EDRF）或血小板聚集的抑制剂，和（iii）Hb-NO用于监测休克综合征阶段的可能用途。
Free radicals have been postulated to play an important role as mediators in the pathogenesis of shock syndrome and multiple-organ failure. We attempted to directly detect the increased formation of radicals by Electron Spin Resonance (ESR) in animal models of shock, namely the endotoxin (ETX) shock or the hemorrhagic shock of the rat. In freeze-clamped lung tissue, a small but significant increase of a free radical signal was detected after ETX application. In the blood of rats under ETX shock, a significant ESR signal with a triplet hyperfine structure was observed. The latter ESR signal evolved within several hours after the application of ETX and was localized in the red blood cells. This signal was assigned to a nitric oxide (NO) adduct of hemoglobin with the tentative structure [alpha 2+ NO)beta 3+)2. The amount of hemoglobin-NO formed, up to 0.8% of total hemoglobin, indicated that under ETX shock a considerable amount of NO was produced in the vascular system. This NO production was strongly inhibited by the arginine analog NG-monomethyl-arginine (NMMA). The ESR signal of Hb-NO was also observed after severe hemorrhagic shock. There are three questions, namely (i) the type of vascular cells and the regulation of the process forming such a large amount of NO during ETX shock, (ii) the pathophysiological implications of the formed NO, effects which have been described as cytotoxic mediator, endothelium-derived relaxing factor (EDRF) or inhibitor of platelet aggregation, and (iii) the possible use of Hb-NO for monitoring phases of shock syndrome.
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DOI：
10.1016/0006-291x(89)92615-6
发表时间：
1989-06
影响因子：
3.1
作者：
D. Stuehr;Nyoun Soo Kwon;Steven S. Gross;Bonnie A. Thiel;Roberto Levi;Carl Nathan
通讯作者：
D. Stuehr;Nyoun Soo Kwon;Steven S. Gross;Bonnie A. Thiel;Roberto Levi;Carl Nathan
影响因子：
2.9
作者：
MARLETTA, MA;YOON, PS;WISHNOK, JS
通讯作者：
WISHNOK, JS
DOI：
10.1073/pnas.85.8.2786
发表时间：
1988-04-01
影响因子：
11.1
作者：
BAKER, JE;FELIX, CC;KALYANARAMAN, B
通讯作者：
KALYANARAMAN, B
红细胞中亚硝酸盐转化为一氧化氮及其作为血红蛋白亚硝基化价杂合体的稳定性。
DOI：
--
发表时间：
1987
期刊：
The Journal of pharmacology and experimental therapeutics
影响因子：
--
作者：
Kruszyna,R;Kruszyna,H;Smith,RP;Thron,CD;Wilcox,DE
通讯作者：
Wilcox,DE