Angle N, Hoyt D B, Coimbra R, Liu F, Herdon-Remelius C, Loomis W, Junger W G
Department of Surgery, University of California San Diego Medical Center, 92103, USA.
Shock. 1998 Mar;9(3):164-70. doi: 10.1097/00024382-199803000-00002.
Hypertonic saline (HS) resuscitation after hemorrhage and sepsis has been shown to markedly reduce the development of lung injury in animals, compared with traditional resuscitation with lactated Ringer's (LR). These experiments examined the effect of HS on lung injury after hemorrhage without sepsis. The effects of HS and LR resuscitation on neutrophil trafficking, neutrophil adhesion, and neutrophil oxidative burst were studied.
BALB/c mice were hemorrhaged to a mean arterial pressure of 40 torr for 1 h. Animals were resuscitated with shed blood and either 4 mL/kg of 7.5% HS or LR in twice the volume of the shed blood. Lung histology was examined 24 h after hemorrhage. Lung myeloperoxidase content and bronchoalveolar lavage fluid neutrophil counts were obtained. Peripheral blood smears were obtained to determine the neutrophil percentage. Peripheral blood neutrophil CD11b expression and neutrophil H2O2 production were assayed by flow cytometry.
HS animals had less lung injury than LR animals. The mean myeloperoxidase activity in HS versus LR animals was 1.79+/-1.33 U/100 mg versus 3.0+/-1.33 U/100 mg, respectively. The percentage of neutrophils in the bronchoalveolar lavage fluid of HS animals (3.8%+/-.8) was significantly less than that of LR animals (10.8%+/-2.1). This corresponded to a significantly higher peripheral blood neutrophil count in HS animals compared with LR animals, 41% vs. 20%, respectively. There was no difference in neutrophil expression of the CD11b integrin between the HS and LR groups. The neutrophils of LR animals had basal H2O2 production that was 107% greater than that of controls; HS suppressed this hemorrhage-induced activation by > 60%. HS resuscitation after hemorrhagic shock protects against the development of lung injury. This protection is due, in part, to suppression of the hemorrhage-induced neutrophil oxidative burst. HS resuscitation offers immunomodulatory potential after hemorrhagic shock.
与用乳酸林格氏液（LR）进行传统复苏相比，出血和脓毒症后用高渗盐水（HS）复苏已显示可显著减少动物肺损伤的发生。这些实验研究了HS对无脓毒症出血后肺损伤的影响。研究了HS和LR复苏对中性粒细胞运输、中性粒细胞黏附和中性粒细胞氧化爆发的影响。
将BALB/c小鼠出血，使平均动脉压维持在40托1小时。用失血及4 mL/kg的7.5%HS或两倍失血量的LR对动物进行复苏。出血24小时后检查肺组织学。测定肺髓过氧化物酶含量和支气管肺泡灌洗液中性粒细胞计数。获取外周血涂片以确定中性粒细胞百分比。通过流式细胞术检测外周血中性粒细胞CD11b表达和中性粒细胞H2O2产生。
HS组动物的肺损伤比LR组动物少。HS组与LR组动物的平均髓过氧化物酶活性分别为1.79±1.33 U/100 mg和3.0±1.33 U/100 mg。HS组动物支气管肺泡灌洗液中中性粒细胞百分比（3.8%±0.8）显著低于LR组动物（10.8%±2.1）。这与HS组动物外周血中性粒细胞计数显著高于LR组动物相对应，分别为41%和20%。HS组和LR组之间中性粒细胞CD11b整合素的表达无差异。LR组动物的中性粒细胞基础H2O2产生比对照组高107%；HS可将这种出血诱导的激活抑制>60%。失血性休克后用HS复苏可预防肺损伤的发生。这种保护部分归因于对出血诱导的中性粒细胞氧化爆发的抑制。HS复苏在失血性休克后具有免疫调节潜力。
