高张溶液复苏对“失血性休克-内毒素”二次打击所致肺和血管内皮细胞损伤的影响

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目的探讨高张溶液复苏对“失血性休克-内毒素”二次打击所致肺和血管内皮细胞损伤的影响。方法将62只SD大鼠随机分为假失血性休克组(Sham组)、乳酸钠林格氏液/6%羟乙基淀粉液复苏组(RLH组)和7.5%氯化钠溶液/6%羟乙基淀粉溶液复苏组(HTH组)。RLH和HTH组复制大鼠失血性休克的动物模型,两组用相应液体进行复苏,复苏成功后腹腔注入内毒素,Sham组注入0.9%氯化钠溶液。分别在注射内毒素和0.9%氯化钠溶液后24h和48h采集血液和肺组织标本,测定大鼠肺组织内细胞间黏附分子-1(ICAM-1)mRNA表达水平、肺髓过氧化物酶(MPO)活性、肺组织的湿重/干重(W/D)和循环内皮细胞(CEC)数量。结果HTH组大鼠腹腔注射内毒素后24h肺组织ICAM-1mRNA表达水平、MPO活性、W/D、CEC计数分别为(37.8±2.5)、(4.15±0.93)U/g、(4.59±0.18)、(9.1±2.7)/0.9μl与RLH组(46.9±4.1)、(6.04±1.50)U/g、(5.25±0.23)、(11.8±3.2)/0.9μl比较,差异均有统计学意义(P<0.01);HTH组大鼠腹腔注射内毒素后48h上述指标(45.6±6.7)、(4.62±0.78)U/g、(4.84±0.16)、(13.4±3.5)/0.9μl与RLH组(54.5±6.2)、(7.59±0.88)U/g、(5.31±0.22)、(16.8±4.2)/0.9μl比较,差异亦有统计学意义(P<0.01)。HTH组24h和48h时肺损伤程度评分分别为(3.17±0.98)分和(3.19±1.20)分,RLH组24h和48h肺损伤程度评分分别为(4.41±1.13)分和(4.63±1.48)分,相应时间点的评分比较差异有统计学意义(t值分别为2.3448和2.2731,P<0.05)。结论采用高张溶液加6%羟乙基淀粉溶液复苏可抑制“失血性休克-内毒素”二次打击时ICAM-1mRNA在肺内的表达、中性粒细胞在肺内的浸润和聚集以及相关炎症反应,并因此减轻肺和血管内皮细胞的损伤程度。 Objective To investigate the effects of hypertonic solution resuscitation on lung and vascular endothelial cell injury induced by secondary hemorrhagic shock-endotoxin challenge. Methods Sixty two Sprague Dawley rats were randomly divided into Sham group, Lactated Ringer’s solution / 6% hydroxyethyl starch solution group (RLH group) and 7.5% sodium chloride solution / 6% Ethyl starch solution resuscitation group (HTH group). Rat models of hemorrhagic shock were replicated in RLH and HTH groups. Both groups were resuscitated with the corresponding fluids. After successful resuscitation, endotoxin was injected intraperitoneally, and 0.9% sodium chloride solution was injected into Sham group. Blood and lung tissue samples were taken at 24h and 48h after injection of endotoxin and 0.9% sodium chloride solution respectively. The expression of intercellular adhesion molecule-1 (ICAM-1) mRNA in lung tissue of rats was measured. The levels of pulmonary myeloperoxidase (MPO) activity, wet / dry weight (W / D) and circulating endothelial cells (CEC) in lung tissue. Results The expression of ICAM-1mRNA, MPO activity, W / D and CEC in HTH group were (37.8 ± 2.5), (4.15 ± 0.93) U / g and (4.59 ± 0.18) , (9.1 ± 2.7) /0.9μl and RLH group (46.9 ± 4.1), (6.04 ± 1.50) U / g, (5.25 ± 0.23) and (11.8 ± 3.2) /0.9μl respectively. The difference was statistically significant (4.62 ± 0.78) U / g, (4.84 ± 0.16), (13.4 ± 3.5) /0.9μl, respectively, compared with the RLH group (P <0.01) at 48h after intraperitoneal injection of endotoxin in HTH group 54.5 ± 6.2, 7.59 ± 0.88, U / g, (5.31 ± 0.22) and (16.8 ± 4.2) /0.9μl respectively. There was also a significant difference between the two groups (P <0.01). The scores of lung injury in HTH group were (3.17 ± 0.98) and (3.19 ± 1.20) points at 24h and 48h, respectively. The scores of lung injury in HTH group at 24h and 48h were (4.41 ± 1.13) and (4.63 ± 1.48) points respectively (T = 2.3448 and 2.2731, respectively, P <0.05), the scores of the corresponding time points were statistically significant. Conclusions The recovery of ICAM-1mRNA in the lungs and the infiltration and aggregation of neutrophils in the lungs after “hemorrhagic shock-endotoxin” second-strike treatment with hypertonic solution and 6% hydroxyethyl starch solution As well as the associated inflammatory response, and thus lessening the degree of damage to lung and vascular endothelial cells.
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