舱室内爆炸伤复合失血致休克大鼠液体复苏的研究

Fluid resuscitation in rats suffering from explosion injury in closed cabin combined with hemorrhagic shock

目的比较高渗盐溶液与生理盐水用于舱室内爆炸伤复合失血致休克大鼠液体复苏的治疗效果。方法健康成年雄性SD大鼠147只,固定于模拟舱室内,点爆源距大鼠胸腹部中心11~12cm瞬时引爆,迅速抽离舱内烟雾。炸后将大鼠静置于实验台上测量炸后10min平均动脉压（MAP）并以此为零时相点,由股动脉导管匀速放血造成中度休克。将108只大鼠随机分为无复苏组（对照组）、生理盐水组（NS组）及高渗盐溶液组（HSD组）,每组36只。对照组致伤后不予治疗;NS组于伤后90min由股静脉匀速输入失血量3倍的NS,30min输注完毕;HSD组以4ml/kg匀速输入7.5%高渗氯化钠/6%右旋醣酐高渗盐溶液,5min输注完毕。各组分别于150、210、270min时点在存活大鼠中随机处死8只大鼠,测量血气指标,并收集肺、脑组织标本检测含水量。另39只大鼠同上分组,每组13只,致伤复苏方法同前,记录30、90、150、210、270min时点各组血压变化及死亡状况。结果对照组13只大鼠有6只死亡,NS组有3只死亡,HSD组大鼠全部存活至270min时点,组间存活率比较差异有统计学意义（P〈0.05）。伤后150min时点,NS组及HSD组大鼠MAP显著增高,210、270min时点NS组MAP逐渐降低,而HSD组降低不明显,270min时点各组间比较差异显著（P〈0.05）。在150、210、270min时点,HSD组大鼠肺、脑含水量逐渐下降,而NS组则有上升趋势,组间比较差异有统计学意义（P〈0.05或P〈0.01）。与对照组比较,HSD与NS对血气指标均有一定的改善作用,且在210min及270min时间点,HSD组pH值、PO2高于NS组,乳酸水平低于NS组（P〈0.05或P〈0.01）。结论 HSD可维持爆炸伤复合失血致休克大鼠血流动力学稳定,且在改善血气指标及肺、脑水肿方面的作用优于NS。

Objective To compare the therapeutic efficacy of fluid resuscitation with hypertonic or normal saline on the rats suffering explosion injury in closed cabin combined with hemorrhagic shock. Methods One hundred and forty-seven anesthetized male SD rats undergoing explosion injury in a closed cabin where detonator was detonated instantaneously, while they were fixed at the site where the explosive was 11-12cm from the center of thoraco-abdominal junction of the rats. Smog was quickly removed from the cabin. The 10min time point after explosion was set as the zero point to record mean arterial pressure （MAP）, and moderate hemorrhagic shock was conducted by uniform femoral exsanguination. One hundred and eight rats were randomly divided into three groups （36 each）： control group （no resuscitation）, hypertonic saline solution （HSD, 75% NaC1/6% Dextran） group （4ml/kg） and normal saline （NS） group （NS：blood loss=3：l）. Fluid was given via femoral vein catheter 90rain after injury, and the infusion lasted for Smin in HSD group and 30min in NS group. Eight rats were randomly sacrificed in each group at the time points of 150, 210 and 270min to analyze the arterial blood gas and water content in the brain and lung tissues. The other 39 rats were also randomly and equally divided into 3 groups and the treatment was the same as above, but with recording of the MAP and survival rate at the time points of 30, 90, 150, 210 and 270min. Results Six rats died in control group, three died in NS group, and all rats of HSD group survived up to 270min. There were significant differences in survival rate among the 3 groups. The MAP rose obviously in NS and HSD groups at the time point of 150min, while it lowered gradually at 210min and 270min in NS group, but no obvious lowering was found in HSD group, and the difference was significant at 270min among the 3 groups （P〈0.0S）. The water contents in the lung and brain tissues decreased in HSD group but increased in NS group at 150min, 210min and 270min, and the differences were significant among the 3 groups （P〈0.0S or P〈0.01）. Arterial blood gas improvement was detected in both HSD and NS groups. At 210rain and 270min, pH and PO2 were higher but lactate level was lower in HSD group than in NS group （P〈0.05 or P〈0.01）. Conclusion HSD could maintain the hemodynamic stability of rats suffering from explosion injury combined with hemorrhagic shock, and its positive effect on arterial blood gas and edema of the lung and brain is superior to normal saline.