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目的观察兔肢体火器伤合并海水浸泡时伤道周围骨骼肌组织Ｎａ＋－Ｋ＋－ＡＴＰ酶（Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ）活性变化及其影响因素，为防治继发损伤提供依据。方法以高速钢珠射击兔后肢，伤后将实验兔随机分为海水浸泡和单致伤组。将浸泡组（１４只）兔浸泡于人工配制的海水中３０分钟，于伤前及伤后３，６，１２，２４小时分别切取距伤道壁０．５ｃｍ（Ａ区）、１．５ｃｍ（Ｂ区）、２．５ｃｍ（Ｃ区）处组织，测定Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ和超氧化物歧化酶（ＳＯＤ）活性、ＡＴＰ和丙二醛（ＭＤＡ）含量。单致伤组（１０只）除不浸泡外，处理同海水浸泡组。结果海水浸泡组各区骨骼肌组织Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ活性、ＡＴＰ含量均呈伤后３小时较伤前明显下降（Ｐ＜０．０１），６～１２小时回升，２４小时再次下降的趋势，下降幅度为Ａ区＞Ｂ区＞Ｃ区。ＭＤＡ含量与Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ活性变化呈负相关（ｒ＝－０．７７Ｐ＜０．０１）。单致伤组上述指标变化趋势同海水浸泡组，但变化幅度小。结论肢体火器伤合并海水浸泡时，可加剧伤道周围骨骼肌组织过氧化脂质反应，抑制抗氧化物酶活性，从而导致能量代谢障碍和细胞膜酶活性下降，加剧继发损伤。
Objective To observe the change of Na + -K + -ATPase (Na + -K + -ATPase) activity and its influencing factors in skeletal muscle tissue of rabbit limbs with firearm injury and seawater immersion, so as to provide basis for prevention and treatment of secondary injury. Methods High-speed steel balls were used to shoot the hindlimbs of rabbits. After the injury, the rabbits were randomly divided into seawater immersion and single injury group. The rabbits in the soak group (14 rabbits) were immersed in the artificial seawater for 30 minutes. The wounds were excised from the injured wall 0.5cm (area A), 1.5cm (before wounding) and 3,6,12,24hours (Area B) and 2.5cm (area C). The activities of Na + -K + -ATPase and superoxide dismutase (SOD), ATP and malondialdehyde (MDA) were measured. Single injury group (10) except not immersed, the same seawater immersion treatment group. Results The activities of Na + -K + -ATPase and ATP in skeletal muscle tissue of seawater immersion group decreased significantly (P <0.01) 3 h after injury, recovered from 6 to 12 h, then decreased again 24 h Amplitude for the A zone> B zone> C zone. The content of MDA was negatively correlated with the change of Na + -K + -ATPase activity (r = -0.77P <0.01). Single injury group the trend of the above indicators with the seawater immersion group, but the change range of small. Conclusion When the firearm limbs are immersed in sea water, the lipid peroxidation reaction in skeletal muscle tissue around the injured wound can be aggravated, and the activity of antioxidant enzymes can be inhibited. As a result, the energy metabolism disorder and the activity of cell membrane enzymes decrease, which aggravates the secondary injury.