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目的观察海水浸泡肢体火器伤时，骨骼肌组织内一氧化氮（NO）水平变化，探讨与组织继发损伤的关系。方法以高速钢球射击兔后肢，伤后将兔颈以下浸泡于人工海水中30分钟，伤前及伤后6、12、24小时分别切取伤道周围骨骼肌组织，测定组织内NO氧化产物亚硝酸盐、Na+－k+－ATP酶活性、肿瘤坏死因子（TNF）以及过氧化脂质产物丙二醛（MDA）含量。结果海水浸泡火器伤骨骼肌组织NO水平明显较伤前升高（P＜0．01），并与伤后下降的Na+－k+－ATP酶活性呈负相关（γ＝－0．76，P＜0．O1），与伤后含量升高的TNF以及MDA呈正相关（γ＝0，46P＜0．05；γ＝0．82P＜0．01）。结论肢体火器伤合并海水浸泡时，伤道周围骨骼肌组织NO水平升高是膜脂质过氧化反应增强，膜酶活性抑制，骨骼肌组织继发损伤的重要生化因素。
Objective To observe the changes of nitric oxide (NO) level in skeletal muscle after immersion in seawater and to discuss the relationship with secondary injury of tissues. Methods The hind limbs of rabbits were shot with high speed steel balls. The rabbits were immersed in artificial seawater for 30 minutes after injury, and the skeletal muscle tissues around the injured wounds were harvested at 6, 12 and 24 hours after injury. The NO oxidation products Nitrate, Na + -k + -ATPase activity, tumor necrosis factor (TNF) and malondialdehyde (MDA) content as lipid peroxidation products. Results The level of NO in skeletal muscle of firearm-infested fire was significantly higher than that before injury (P <0.01), and negatively correlated with the decreased Na + -k + -ATPase activity after injury (γ = -0.76, P < 0.O1), which was positively correlated with TNF and MDA levels after injury (γ = 0, 46P <0.05; γ = 0.82P <0.01). Conclusions When limb firearm injury combined with seawater immersion, the increase of NO level in the skeletal muscle tissue around the injured wounds is an important biochemical factor for enhanced lipid peroxidation, inhibition of membrane enzyme activity and secondary injury of skeletal muscle.