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目的观察兔肢体火器伤合并海水浸泡时，伤肢骨骼肌组织过氧化脂质与抗氧化酶活力变化的特点，为早期救治提供依据。方法用滑膛枪发射钢珠致伤兔后肢，伤后将致伤兔分为两组：一组为海水浸泡组（ＳＩＧ），即将致伤兔浸泡于粗制海盐配制的人造海水中３０分钟；另一组为单纯致伤组（ＳＷＧ），伤后不浸泡海水。伤后３、６、１２、２４小时手术切取距伤道边缘０５、１５和２５ｃｍ处肌组织，测定丙二醛（ＭＤＡ）、ＡＴＰ含量和超氧化物歧化酶（ＳＯＤ）活力。取伤前骨骼肌组织作为对照。结果伤后ＳＩＧ兔伤肢骨骼肌ＭＤＡ含量明显较伤前升高，升高幅度与距伤腔距离呈反比，并呈伤后３、６小时升高，１２小时略有下降，２４小时再次升高的趋势。ＳＷＧ的ＭＤＡ变化与ＳＩＧ相似，但升高幅度低于ＳＩＧ，两组ＳＯＤ活力和ＡＴＰ含量的改变与ＭＤＡ变化呈相反趋势。结论肢体火器伤合并海水浸泡可加重伤道周围骨骼肌组织微循环障碍和能量代谢紊乱，导致氧自由基生成增加，过氧化脂质反应增强，继发损伤明显。
Objective To observe the changes of lipid peroxidation and antioxidant enzyme activity in skeletal muscle tissue of rabbits with firearm injury and seawater immersion in rabbits so as to provide basis for early treatment. Methods A steel ball was introduced into the hind limbs of the rabbits by using a muscular chamber gun. The injured rabbits were divided into two groups: one group is the seawater immersion group (SIG), which is immersed in artificial seawater prepared by crude sea salt for 30 minutes. A group of simple injury group (SWG), after injury does not soak seawater. Muscle tissues at 05, 15 and 25 cm away from the edge of the wound were surgically removed at 3, 6, 12, and 24 hours after injury. Malondialdehyde (MDA), ATP content and superoxide dismutase (SOD) vitality. Pre-injury skeletal muscle tissue as a control. Results The content of MDA in the skeletal muscle of injured limbs of SIG rabbits was significantly higher than that before injury, and the increasing amplitude was inversely proportional to the distance from the injured cavity. The content of MDA in skeletal muscle of SIG rabbits increased slightly at 3 and 6 hours, decreased slightly at 12 hours and rose again at 24 hours High trend. The change of MDA in SWG was similar to SIG, but the increase was lower than that of SIG. The change of SOD activity and ATP content in SWG showed opposite trend with the change of MDA. CONCLUSIONS: Firearm injury combined with seawater immersion can aggravate microcirculation disturbance and energy metabolism disorder in skeletal muscle around the wound, resulting in increased production of oxygen free radicals and peroxidation of lipid, with obvious secondary injury.