A novel nitric oxide scavenger decreases liver injury and improves survival after hemorrhagic shock
A novel nitric oxide scavenger decreases liver injury and improves survival after hemorrhagic shock
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DOI：
10.1152/ajpgi.1999.277.1.g144
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发表时间：
1999-07-01
影响因子：
4.5
通讯作者：
Harbrecht, BG
中科院分区：
文献类型：
--
作者：
Menezes, J;Hierholzer, C;Harbrecht, BG
我们测试了一氧化氮（NO）清除剂减少啮齿动物失血性休克模型中组织损伤的能力。将大鼠的平均动脉血压（MAP）降至40 mmHg，然后在30%的失血量恢复时（组I）或连续休克100 min后（组2）复苏。用NO清除剂NOX（30 mg.kg（-1）.h（-1））处理选定的动物，输注4小时。与假休克对照组大鼠相比，出血大鼠复苏后MAP较低。NOX治疗显著增加了出血复苏后的MAP。出血性休克也增加了肝损伤，如升高的鸟氨酸氨甲酰转移酶（OCT）血浆水平所反映的，NOX治疗显著降低了OCT的释放。此外，NOX与显著减少肝脏中性粒细胞浸润和改善24小时存活率相关（n. = 8/9）与盐水处理的休克动物（n 3/9）相比。这些数据表明，过量的NO介导的休克诱导的组织损伤和抑制NO可用性与NO清除剂可能会减少严重出血的病理生理后遗症。
We tested the ability of a nitric oxide (NO) scavenger to reduce tissue injury in a rodent model of hemorrhagic shock. Rats were hemorrhaged to a mean arterial blood pressure (MAP) of 40 mmHg and then resuscitated when either 30% of their shed blood had been returned (group I) or after 100 min of continuous shock (group 2). Selected animals were treated with the NO scavenger NOX (30 mg.kg(-1).h(-1)) infused over 4 h. Hemorrhaged rats had a lower MAP after resuscitation compared with sham-shock control rats. NOX treatment significantly increased MAP after resuscitation from hemorrhage. Hemorrhagic shock also increased liver injury as reflected by elevated ornithine carbamoyltransferase (OCT) plasma levels, and NOX treatment significantly reduced OCT release. In addition, NOX was associated with significantly decreased hepatic neutrophil infiltration and improved 24-h survival (n. = 8 of 9) compared with saline-treated shock animals (n 3 of 9). These data suggest that excess NO mediates shock-induced tissue injury and that suppression of NO availability with NO scavengers may reduce the pathophysiological sequelae of severe hemorrhage.