Improved resuscitation minimizes respiratory dysfunction and blunts interleukin-6 and nuclear factor-κB activation after traumatic hemorrhage
Improved resuscitation minimizes respiratory dysfunction and blunts interleukin-6 and nuclear factor-κB activation after traumatic hemorrhage
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DOI：
10.1097/00003246-200208000-00024
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发表时间：
2002-08-01
影响因子：
8.8
通讯作者：
Young, JS
中科院分区：
文献类型：
--
作者：
Claridge, JA;Schulman, AM;Young, JS
目的：我们假设，修改复苏将改变失血性休克引起的呼吸功能障碍，并与核因子-κ B和细胞因子expression.Design相关：随机，对照，前瞻性研究。设置：大学医院创伤研究实验室。主题：女性，瑞士韦伯斯特小鼠，8-12 wks old.Interventions：失血性休克诱导通过颈动脉导管去除0.025毫升血液/克体重。30分钟后复苏动物。将小鼠随机分为四组：第一组插管但不流血的（假手术）;第二组接受生理盐水至其流出血量的三倍;第三组接受其流出血量;第四组接受流出血量+生理盐水至其流出血量的两倍。休克结束时和复苏后的血清乳酸盐，任何仪器之前和24小时后的肺功能，酶联免疫吸附测定的细胞因子浓度，电泳迁移率变动法测定核因子-κ B活性。在30分钟内，被隔离的组具有显著的低血压和血清乳酸盐的显著增加。复苏使所有组的血压恢复到基线水平，除第II组外，所有组的乳酸盐均有所改善。第二组还表现出肺功能显著下降，其特征是气道阻力增加，每分钟通气量、肺顺应性和肺泡功能下降。支气管肺泡液和血清白细胞介素-6和全肺核因子-kappaB活性也升高显着在组II。结论：组II表现出最少的改善，复苏后的血清乳酸，最显着的急性肺损伤，最大的白细胞介素-6和核因子-kappaB反应。组IV小鼠的急性肺损伤最少，没有检测到白细胞介素-6反应。用晶体液和放血改善复苏，最大限度地减少急性肺损伤。改善复苏后肺功能障碍的减少可能归因于核因子-κ B和白细胞介素-6对出血的反应减弱。
Objective: We hypothesized that modifying resuscitation would alter hemorrhagic shock-induced respiratory dysfunction and correlate with nuclear factor-kappaB and cytokine expression.Design: Randomized, controlled, prospective study.Setting: University hospital trauma research laboratory.Subjects: Female, Swiss Webster mice, 8-12 wks old.Interventions: Hemorrhagic shock was induced by removing 0.025 mL of blood/g of body weight via a carotid catheter. Animals were resuscitated 30 mins later. Mice were randomized into four groups: group I was cannulated but not bled (sham); group II received normal saline to three times their shed blood volume; group III received their shed blood; and group IV received shed blood + normal saline at two times shed blood volume.Measurements and Main Results: We measured the following: serum lactates at the end of shock and after resuscitation, pulmonary function before any instrumentation and after 24 hrs, cytokine concentrations by enzyme-linked immunosorbent assay, and nuclear factor-kappaB activity by electrophoretic mobility shift assay. Groups that were hemorrhaged had significant hypotension and a significant increase in serum lactates over 30 mins. Resuscitation returned the blood pressure to baseline in all groups, and lactates improved in all groups except group II. Group II also demonstrated a significant decrease in pulmonary function characterized by increased airway resistance and decreases in minute volume, lung compliance, and alveolar function. Bronchoalveolar fluid and serum interleukin-6 and whole lung nuclear factor-kappaB activity also were elevated significantly in group II.Conclusions: Group II demonstrated the least improvement in serum lactate after resuscitation, the most significant acute lung injury, and the greatest interleukin-6 and nuclear factor-kappaB response. Group IV mice had the least acute lung injury, with no detectable interleukin-6 response. Improved resuscitation with crystalloid and shed blood minimized acute lung injury. The reduction in pulmonary dysfunction after improved resuscitation may be attributable to a blunting of the nuclear factor-kappaB and interleukin-6 responses to hemorrhage.