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氫氣和一氧化氮聯合治療急性肺損傷

發布時間:2017-08-26 瀏覽次數:次 字號:  【關閉】
氫氣不僅能中和強毒性羥基自由基,也能中和亞硝酸陰離子,亞硝酸陰離子是一氧化氮和超氧陰離子反應產生。一氧化氮對肺損傷也具有治療作用,在治療的同時,會因為一氧化氮和肺組織中的超氧陰離子反應產生亞硝酸陰離子帶來危害。如果聯合使用一氧化氮和氫氣,則不僅可以發揮兩者對氧化損傷和肺損傷的治療作用,而且可以減少一氧化氮治療導致的亞硝酸陰離子增加,應該是一種比較理想的治療策略。
 最近,中國天津醫科大學麻醉學研究小組,在《休克》雜志上發表最新研究論文,證明聯合呼吸一氧化氮和氫氣能有效治療急性肺損傷
  Acute lung injury (ALI)is still a leading cause of morbidity and mortality in critically ill patients.Inhaled nitric oxide (NO) has been reported to ameliorate ALI. However,reactive nitrogen species (RNS) produced by NO can cause lung injury. Since hydrogengas (H2) is reported to eliminate peroxynitrite, it is expected to reduce theadverse effects of NO. Moreover, we have found that H2 inhalation can attenuatelung injury. Therefore, we hypothesized that combination therapy with NO and H2might afford more potent therapeutic strategies for ALI. In the present study,a mouse model of ALI was induced by intratracheal administration oflipopolysaccharide (LPS). The animals were treated with inhaled NO (20 ppm), H2(2%), or NO+H2, starting 5 min after LPS administration for 3 hours. We foundthat LPS-challenged mice exhibited significant lung injury characterized by thedeterioration of histopathology and histologic scores, wet-to-dry weight ratio,oxygenation index (PaO2/FiO2) as well as total protein in the bronchoalveolarlavage fluid (BALF), which was attenuated by NO or H2 treatment alone.Combination therapy with NO and H2 had a more beneficial effect withsignificant interaction between the two. While the nitrotyrosine level in lungtissue was prominent after NO inhalation alone, it was significantly eliminatedafter breathing a mixture of NO with H2. Furthermore, NO or H2 treatment alonemarkedly attenuated LPS-induced lung neutrophils recruitment and inflammation,as evidenced by down-regulation of lung myeloperoxidase activity, total cellsand polymorphonuclear neutrophils in BALF, as well as pro-inflammatorycytokines (TNF-α, IL-1β, IL-6 and HMGB1) and chemokines (KC, MIP-1α, MIP-2, andMCP-1) in BALF. Combination therapy with NO and H2 had a more beneficial effectagainst lung inflammatory response. Moreover, combination therapy with NO andH2 could more effectively inhibit LPS-induced pulmonary early and late NF-κBactivation as well as pulmonary cell apoptosis. In addition, combinationtreatment with inhaled NO and H2 could also significantly improve the lunginjury in polymicrobial sepsis. Combination therapy with sub-thresholdconcentrations of NO and H2 still had a significantly beneficial effect againstlung injury induced by LPS and polymicrobial sepsis. Collectively, theseresults demonstrate that combination therapy with NO and H2 provides enhancedtherapeutic efficacy for ALI.
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