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一氧化氮(NO)参与了肢体缺血再灌注后肺损伤,一方面内皮型NO减少参与了肺动脉高压的形成、引起器官的灌注量不足、促进“无复流”现象的发生,另一方面诱导型NO升高则可能通过降低血管的反应性维持器官的灌注,抗血小板和白细胞聚集,参与中性粒细胞的呼吸爆发,发挥非特异性的免疫功能、清除氧自由基、抑制脂质过氧化等而起代偿性的保护作用。NO生成过多或不足也会对机体产生不利的影响。
Nitric oxide (NO) is involved in lung injury following limb ischemia-reperfusion. On the one hand, the decrease of endothelial NO is involved in the formation of pulmonary hypertension, resulting in insufficient perfusion of organs and promoting the occurrence of “no-reflow” phenomenon. On the other hand Elevated inducible NO may maintain the organ perfusion, anti-platelet and leukocyte aggregation by reducing the reactivity of blood vessels, participate in the respiratory burst of neutrophils, exert non-specific immune function, scavenge oxygen free radicals and inhibit lipid peroxidation And so on and compensatory protection. NO generated too much or too little will have a negative impact on the body.