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目的:比较传统液体复苏和限制性液体复苏对失血性休克大鼠炎性介质及其介导的肺损伤作用。方法:将72只大鼠建立控制性失血性休克模型后,随机分为未复苏组和45 mL/(kg.h)、30 mL/(kg.h)、15 mL/(kg.h)液体复苏组。于术后24、48和72 h处死大鼠,留取血液和肺组织。观察动脉血乳酸浓度、血浆肿瘤坏死因子α(TNF-α)浓度、肺湿/干重比、肺组织学和损伤评分。结果:未复苏组大鼠休克后2~12 h死亡,其余三组大鼠均存活。自30 m in复苏开始,15 mL/(kg.h)组大鼠平均动脉压(MAP)缓慢上升;而30 mL/(kg.h)组和45 mL/(kg.h)组迅速上升后又缓慢下降。45 mL/(kg.h)组大鼠24 h和72 h血浆TNF-α、24 h血乳酸值均高于30 mL/(kg.h)组和15 mL/(kg.h)组(P<0.05);15 mL/(kg.h)组大鼠48和72 h肺湿/干重比低于45 mL/(kg.h)和30 mL/(kg.h)组(P<0.05)。肺损伤程度随时间的推移逐渐减轻,45 mL/(kg.h)组大鼠肺病理损伤较30 mL/(kg.h)组和15mL/(kg.h)组严重(P<0.05)。结论:限制性液体复苏能显著降低失血性休克大鼠TNF-α的释放和酸中毒程度,减轻肺损伤。
Objective: To compare the effects of traditional liquid resuscitation and restrictive fluid resuscitation on inflammatory mediators and lung injury in hemorrhagic shock rats. Methods: 72 hemorrhagic shock rats were established and then randomly divided into non-recovery group and 45 mL / (kg.h), 30 mL / (kg.h), 15 mL / (kg.h) Recovery group. Rats were killed at 24, 48 and 72 h after surgery, and blood and lung tissue were collected. Arterial blood lactate concentration, plasma tumor necrosis factor alpha (TNF-α) concentration, lung wet / dry weight ratio, lung histology and injury score were observed. Results: The rats in the non-resuscitation group died 2 to 12 hours after shock, and the remaining three groups all survived. Mean arterial pressure (MAP) in 15 mL / (kg.h) group increased slowly after 30 m in resuscitation, while in 30 mL / (kg.h) group and 45 mL / (kg.h) group increased rapidly Slow down again. The serum levels of TNF-α and TNF-α in 24 h and 72 h after treatment in 45 mL / (kg · h) group were significantly higher than those in 30 mL / (kg.h) and 15 mL / (kg.h) groups <0.05). The lung wet / dry weight ratio of rats in 15 mL / (kg.h) group at 48 and 72 h were less than 45 mL / (kg.h) and 30 mL / (kg.h) . The degree of lung injury gradually decreased over time. The pathological lung damage of rats in 45 mL / (kg.h) group was more severe than that in 30 mL / (kg.h) group and 15 mL / (kg.h) group (P <0.05). Conclusion: Restrictive fluid resuscitation can significantly reduce the release of TNF-α and acidosis in hemorrhagic shock rats, and reduce lung injury.