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本研究由上海第三人民医院
本研究采用30%体表面积重度烧伤大鼠模型,5ml/kg体重腹腔注射氢气生理盐水,阳性对照采用9 mg/kg Edaravone腹腔注射,模型组损伤后6小时给Ringer's液复苏。实验结果发现,氢气生理盐水和Edaravone均可显著改善烧伤后肺损伤,同时烧伤动物肺组织氧化损伤指标和炎症因子显著下降。结果表明,氢气对烧伤休克引起的肺组织氧化损伤和炎症反应有治疗作用,对烧伤休克引起的肺损伤有明确的治疗作用。提示氢气对烧伤休克具有潜在的治疗作用。
Hydrogen-Rich Saline Protects against Acute Lung Injury Induced by Extensive Burn in Rat Model
Abstract
Objectives Hydrogen has been reported to selectively quench detrimental reactive oxygen species, particularly hydroxyl radical, and to prevent myocardial or hepatic ischemia/reperfusion injury in multiple models. The aim of this study is to investigate whether hydrogen protects against severe burn-induced acute lung injury in rats.
Methods Rats were divided into four groups: sham plus normal saline, burn injury plus normal saline, burn injury plus hydrogen-rich saline, and burn injury plus Edaravone. Animals were given full-thickness burn wounds (30% total body surface area) using boiling water, except the sham group which was treated with room-temperature water. The rats in hydrogen group received 5 ml/kg of hydrogen-rich saline, sham and burn controls obtained the same amount of saline, and the Edaravone group was treated with 9 mg/kg of Edaravone in saline. Lactated Ringer's solution was given at 6 h post-burn. Lungs were harvested at 12 h post-burn for laboratory investigations.
Results Severe burns with delayed resuscitation rapidly caused lung edema and impaired oxygenation in rats. These dysfunctions were ameliorated by administration of hydrogen-rich saline or Edaravone. Compared with the burn injury plus normal saline group, hydrogen-rich saline or Edaravone significantly attenuated the pulmonary oxidative products, such as malondialdehyde, carbonyl, and 8-hydroxy-2'-deoxyguanosine. Furthermore, administration of hydrogen-rich saline or Edaravone dramatically reduced the pulmonary levels of pulmonary inflammation mediators and myeloperoxidase.
Conclusion Intraperitoneal (i.p.) administration of hydrogen-rich saline improves pulmonary function by reducing oxidative stress and inflammatory response in severe burn-induced acute lung injury.
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