不同液体复苏对未控制失血性休克大鼠肺损伤及肺水通道蛋白表达的影响

目的 观察不同液体复苏对未控制失血性休克大鼠肺损伤和肺水通道蛋白l(AQP1)和AQP5表达的影响.方法 SD大鼠被随机分为假手术组(C组)、无液体复苏组(NF组)、乳酸林格液组(LRS组)、高渗盐水组(HS组)和羟乙基淀粉组(HES)5组,每组12只.建立未控制失血性休克大鼠模型,模拟临床分为4期;动态观察各期的平均动脉压(MAP)变化.①失血性休克期(时间为60 min):在15 min内将MAP降至40 mm Hg(1mm Hg=0.133 kPa)并维持60 min;然后向气管内注射内毒素2 mg/kg,并用断尾法造成大鼠未控制失血性休克.②液体复苏期(时间为30 min):LRS、HS、HES组分别用3倍放血量的LRs、4 ml/kg的7.5%NaCl和1倍放血量的6%HES 130/0.4进行复苏,C组和NF组不处理.③综合复苏期(时间为1 h):在1 h内回输全部失血及1:1失血量的生理盐水.④复苏后观察期:输血、输液结束后继续观察3.5 h. 实验结束后测定肺组织湿/干重(W/D)比值;用免疫组化测定肺组织AQPl和AQP5表达,用苏木素一伊红(HE)染色,光镜下观察肺损伤程度.结果 在C组和HES组,肺血管内皮细胞AQP1和肺泡上皮AQP5均呈阳性表达;HS组仅AQP1呈阳性表达,AQP5则呈微弱表达;NF组和LRS组AQP1、AQP5均呈微弱表达.各组MAP、肺W/D比值和肺组织损伤程度比较显示,HS组和HES组显著优于NF组和LRS组(P<0.05或P<0.01).结论 遭受"二次打击"失血性休克大鼠并发肺损伤时,肺AQP1和AQP5表达下调;采用6%HES 130/0.4进行休克复苏可有效抑制AQP1和AQP5下调,并使肺损伤明显减轻;采用7.5%NaCI复苏仅能抑制AQPl表达下调和在一定程度上减轻肺水肿;而采用LRS复苏既不能保持AQP1、AQP5的表达,也不能有效防止肺损伤的发生.     

HES200溶液复苏失血性休克对肺损伤保护作用的实验研究

目的探讨羟乙基淀粉200/0.5(HES200)溶液复苏失血性休克对大鼠肺损伤保护作用及其机制。方法制作SD大鼠失血性休克模型,分别用HES200、羟乙基淀粉40溶液(HES40)、乳酸林格液(RL)复苏大鼠,观察复苏后1、2、4 h动脉氧分压(PaO2)、血清TNF-α、肺组织核因子κB(NF-κB)、细胞间粘附分子-1(ICAM-1)的表达、肺组织髓过氧化物酶(MPO)活性、肺组织湿干重比值(W/D)。结果失血性休克大鼠复苏后各生物学指标HES200组较其它液体复苏组低,肺损伤程度减轻。结论羟乙基淀粉200溶液通过减轻失血性休克大鼠复苏后炎症反应从而对肺损伤具有保护作用。     

不同液体复苏对颅脑外伤并发急性失血性休克大鼠脑保护作用比较

目的比较不同种类液体复苏对大鼠颅脑外伤并发急性失血性休克模型的局部脑血流（rCBF）、脑水肿和血脑屏障（BBB）的影响.方法SD大鼠60只随机分为5组：①假手术组（Ⅰ组）;②脑外伤＋休克组（Ⅱ组）;③生理盐水组（Ⅲ组）;④10%羟乙基淀粉（HES）组（Ⅳ组）;⑤小容量高晶体-高胶体渗透压混合液（HHS,7.5%NaCl与10%HES按1：1混合）（Ⅴ组）.记录外伤、休克和复苏前后平均动脉压（MAP）和rCBF的变化,测定复苏后3 h脑组织含水量以及脑组织伊文思蓝（EB）含量.结果在复苏后即刻,Ⅲ、Ⅳ、Ⅴ组MAP和rCBF均恢复正常,分别在15 min、30 min和45 min后开始下降,至120 min时,Ⅴ组显著高于Ⅲ、Ⅳ组（P＜0.05）.复苏后3 h,Ⅴ组脑组织含水量双侧正常,Ⅲ组双侧均显著高于Ⅰ、Ⅴ组（P＜0.05）;Ⅱ、Ⅲ组损伤侧脑组织EB含量显著高于Ⅳ、Ⅴ组（P＜0.05）.结论小容量HHS复苏能够有效、持久地恢复颅脑外伤并发失血性休克大鼠的MAP和rCBF,减轻脑水肿,改善BBB.NS恢复MAP和rCBF的时间较短,加重脑水肿和BBB破坏.10%HES的作用介于小容量HHS和NS之间.     

Effect of different resuscitation fluids on cytokine response in a rat model of hemorrhagic shock

This study was designed to determine the effects of different resuscitation fluids on the production of proinflammatory and anti-inflammatory cytokines in an animal model of hemorrhagic shock. Wistar male rats (n = 24; 8/group) were subjected to a volume-controlled hemorrhagic shock for 30 minutes and resuscitated as follows: (1) sham group without resuscitation, (2) lactated Ringer solution (LR), 3:1; (3) 4% hydroxyethyl starch (HES) solution, 1:1; and (4) 4% modified fluid gelatin (GEL), 1:1. Hemodynamic parameters were recorded, and blood samples were collected at 0 min and 30, 90, 150, 210, 270, and 330 min after hemorrhage for plasma levels of IL-6, IL-10, and TNFalpha. The circulating concentrations of IL-6 at 90, 150, 210, 270, and 330 min and TNFalpha levels at 150, 210, and 270 min after hemorrhage were significantly elevated in animals resuscitated with GEL compared with HES or LR (P < 0.05). At 210, 270, and 330 min, IL-10 concentration was decreased significantly in GEL-resuscitated rats compared with rats resuscitated with LR or HES (P < 0.05). Mean blood pressure and serum levels of lactate after resuscitation were not different among three kinds of fluids. LR, HES, and GEL are comparable in volume efficacy for resuscitation of hemorrhagic shock but are associated with different postresuscitation immune responses. Resuscitation with GEL may be associated with cytokine production favoring a proinflammatory response. The marked elevation of IL-6 observed in the GEL-treated animals may play a role in the relatively high frequency of anaphylactoid reaction in clinical use of GEL.     

腹腔复苏对失血性休克大鼠小肠黏膜的保护作用

目的 探讨腹腔复苏对失血性休克大鼠小肠黏膜的保护作用.方法 健康雄性SD大鼠50只随机(随机数字法)分成5组:假手术组(Ⅰ组)、失血性休克组(Ⅱ组)、静脉复苏组(Ⅲ组)、静脉复苏加生理盐水腹腔复苏组(Ⅳ组)、静脉复苏加PD-2液腹腔复苏组(Ⅴ组).Ⅰ组依次行右颈总动脉、右股静脉、左股动脉插管及全身肝索化;Ⅱ组在Ⅰ组基础上经左股动脉放血制备失血性休克大鼠模型;Ⅲ组在造模后经右股静脉补入放出的血量及2倍量林格氏液进行复苏;Ⅳ组和Ⅴ组分别在Ⅲ组基础上经腹腔内注入生理盐水、2.5%PD-2液各30 mL.各组分别于造模及复苏后60～120 min取材.测定血浆二胺氧化酶(DAO)活性、D-乳酸(D-LA)含量及内毒素(LPS)含量,光镜和电镜下观察大鼠小肠黏膜组织学和超微结构变化.采用单因素方差分析对数据进行统计学处理.结果 Ⅱ组血浆DAO活性、D-LA及LPS含量均较Ⅰ组明显升高,差异具有统计学意义(P<0.01);Ⅴ组分别与Ⅱ、Ⅲ及Ⅳ组比较,血浆DAO活性、D-LA及LPS含量差异有统计学意义(P<0.05 or P<0.01).各组小肠黏膜组织病理学及黏膜超微结构比较,Ⅱ组较Ⅰ组有明显损伤,Ⅴ组较Ⅱ、Ⅲ及Ⅳ组损伤明显减轻.结论 PD-2液腹腔复苏可减轻失血性休克大鼠小肠黏膜组织病理学损害,保护肠黏膜完整性,降低肠壁通透性,防止内毒素血症发生.     

乌司他丁对失血性休克大鼠回肠黏膜细胞凋亡的影响

目的 探讨乌司他丁对失血性休克大鼠回肠黏膜细胞凋亡的影响。方法 采用前瞻对照动物研究，用改良Chaudry方法制备大鼠失血性休克模型，60min后回输血液和生理盐水进行复苏，部分加用乌司他丁治疗。检测不同时间点血清肿瘤坏死因子-α（TNF-α）、丙二醛（MDA）含量和回肠黏膜细胞Bax、Bcl-2、caspase3蛋白的表达水平。结果 大鼠失血性休克及复苏后血清TNF-α、MDA含量以及回肠黏膜细胞Bax、caspase3蛋白的表达较正常对照组均明显升高，Bcl-2明显降低。复苏后血清TNF-α含量下降，MDA含量升高；回肠黏膜细胞Bax、caspase3蛋白的表达均明显下降，Bcl-2蛋白明显升高；乌司他丁复苏组上述指标的恢复程度较生理盐水复苏组为好。结论 乌司他丁可抑制失血性休克大鼠回肠黏膜细胞的凋亡，对失血性休克大鼠起保护作用。     

不同的复苏压力对非控制失血性休克大鼠肺功能的影响

目的 比较不同的液体复苏压力对非控制失血性休克大鼠肺功能的影响.方法 制备大鼠创伤非控制失血性休克模型.将60只远交群大鼠随机分为6组各10只:NC组为对照组;NF组为休克不复苏组;NS40、NS60(限制性液体复苏组)、NS80、NS100(大量液体复苏组).各液体复苏组在大鼠的平均动脉压(MAP)降至35～40 mm Hg(1 mm Hg=0.133 kPa)时分别给予生理盐水输注,使血压维持在各相应水平.输液1 h后,各液体复苏组均给予手术止血、回输血液及给予足量的液体输注,保持大鼠的MAP≥90 mm Hg.结果 在出血未控制的情况下,限制性液体复苏组的出血量明显低于大量液体复苏组,肺组织病理学损害、酸中毒程度较大量液体复苏组明显减轻.NS60组有9只大鼠存活超过72 h,NS40组3只存活超过72 h,而NF组与NS80、NS100组无一只存活超过72 h.结论 创伤非控制失血性休克及不同的液体复苏压力均可造成不同程度的肺损伤,限制性液体复苏对肺功能具有保护作用.     

Resuscitation with hydroxyethyl starch solution prevents nuclear factor kappaB activation and oxidative stress after hemorrhagic shock and resuscitation in rats

Fluid resuscitation is vital for treating traumatic hemorrhagic shock (HS), but reperfusion is believed to have the adverse consequences of generating reactive oxygen species and inflammatory cytokines, both of which cause multiple organ dysfunctions. We investigated the effects of various resuscitation fluids on the changes of redox-sensitive molecules after HS and fluid resuscitation (HS/R). We induced HS by bleeding male Sprague-Dawley rats to a blood pressure of 30 to 40 mmHg for 60 minutes. Thirty minutes later, the rats were killed (HS group) or immediately resuscitated with shed blood (HS + BL group), L-isomer lactated Ringer's solution (HS + LR group), or hydroxyethyl starch (HS + HES group). After HS, we found a significant increase in nuclear factor kappaB DNA binding activity, which was effectively inhibited using HES solution or blood resuscitation. Moreover, resuscitation with blood or LR solution, but not HES solution, induced significant oxidative stress, manifested by a high ratio of oxidized glutathione to reduced glutathione in the lungs, liver, and spleen. HS alone, however, did not increase the ratio of the oxidized glutathione to reduced glutathione in all organs. Although the protein expression of anti-apoptotic Bcl-2 and pro-apoptotic Bax varied in different organs, we found that resuscitation using HES solution prevented the HS-induced reduction of the Bcl-2/Bax ratio in the heart. HES solution was an appropriate resuscitation fluid in reversing nuclear factor kappaB activation, maintaining the Bcl-2/Bax ratio, and preventing oxidative stress after acute HS.     

早期复苏中高渗盐胶体对小肠黏膜形态学的影响

目的 观察高渗盐复合胶体液在失血性休克早期复苏中对小肠黏膜形态学特征的影响.方法 36只SD大鼠随机分为三组,通过控制性颈动脉放血制成失血性休克模型,分别应用相同容量的乳酸钠林格氏液、7.5%高渗盐水和琥珀酸明胶的混合液、ATP-MgCl2-乳酸钠林格氏液进行液体复苏,复苏结束后2 h处死动物,取末端回肠,常规固定切片染色,以光学图像分析法观察比较复苏后回肠黏膜的黏膜厚度和绒毛长度以及回肠黏膜上皮损伤指数等.结果 三组复苏方案之间的回肠黏膜损伤指数比较有显著性差异（P＜0.05）,高渗盐明胶组的回肠黏膜损伤指数最小.三组复苏方案之间的回肠黏膜厚度和绒毛长度比较均无显著性差异.结论 高渗盐复合胶体溶液在控制性失血性休克的早期复苏中对回肠黏膜的形态学损伤较小,能相对较好地保护肠黏膜物理屏障.     

高渗氯化钠溶液复苏抑制失血性休克大鼠肺细胞凋亡的初步研究

目的 探讨高渗氯化钠溶液(HS)复苏对失血性休克大鼠肺细胞凋亡的影响及其意义. 方法 将23只SD大鼠制作成重度失血性休克模型,随机分为假手术组(Sham组,8只)、高渗氯化钠溶液复苏组(HS组,9只)和等渗盐水复苏组(NS组,6只),采用流式细胞仪FITC-AnnexinV/PI荧光染色法定量测定休克/复苏后各组大鼠肺组织细胞的凋亡情况,并加以比较和分析. 结果 在失血性休克/复苏后的早期阶段,HS组和NS组大鼠的肺组织细胞即有大量凋亡发生,其肺细胞凋亡率均明显高于Sham组,差异有统计学意义(P＜0.01).同时,NS组大鼠的肺细胞凋亡率则显著高于HS组,差异有统计学意义(P＜0.01). 结论 在重度失血性休克大鼠模型中,与等渗盐水复苏相比较,高渗氯化钠溶液复苏能显著抑制失血/复苏后肺细胞的凋亡,有助于减轻休克后急性肺损伤,这可能也是高渗氯化钠溶液复苏肺保护作用的重要机制之一.     

Survival in a rat model of lethal hemorrhagic shock is prolonged following resuscitation with a small volume of a solution containing a drag-reducing polymer derived from aloe vera

Drag-reducing polymers (DRP) increase tissue perfusion at constant driving pressure. We sought to evaluate the effects of small-volume resuscitation with a solution containing a DRP in a rat model of hemorrhage. Anesthetized rats were hemorrhaged at a constant rate over 25 min. In protocol A, total blood loss was 2.45 mL/100 g, whereas in protocol B, total blood loss was 3.15 mL/100 g. Five minutes after hemorrhage, the animals were resuscitated with 7 mL/kg of either normal saline (NS) or NS containing 50 microg/mL of an aloe vera-derived DRP. In protocol B, a third group (CON) was not resuscitated. Whole-body O2 consumption (Vo2) and CO2 production (Vco2) were measured using indirect calorimetry. In protocol A, 5/10 rats in the NS group and 8/10 rats in the DRP group survived for 4 h (P = 0.14). Mean arterial pressure was higher in the DRP-treated group than in the NS-treated group 45 min after resuscitation (89 +/- 8 vs. 68 +/- 5 mmHg, respectively; P < 0.05). In protocol B, survival rates over 2 h in the DRP, NS, and CON groups were 5/15, 1/14, and 0/7, respectively (P < 0.05). Compared with NS-treated rats, those resuscitated with DRP achieved a higher peak Vo2 (9.0 +/- 1.0 vs. 6,3+/- 1.0 mL/kg/min) and Vco2 (9.0 +/- 1.1 vs. 6.0 +/- 1.0 mL/kg/min) after resuscitation. We conclude that resuscitation with a small volume of DRP prolongs survival in rats with lethal hemorrhagic shock.     

异丙酚对失血性休克复苏大鼠应激激素和免疫平衡的影响

目的 观察异丙酚对失血性休克复苏后大鼠应激激素、细胞因子的影响及对重要脏器的保护作用.方法 雄性Wistar大鼠66只被随机分为对照组、失血性休克复苏组和异丙酚治疗组.制备失血性休克复苏动物模型后,异丙酚组经股静脉输注异丙酚10 mg-1·kg-1.h-1,休克复苏组输注等量生理盐水.休克复苏组和异丙酚组分别于术后30、60、120、180和240 min取6只大鼠,采集腹主动脉血及肺和小肠组织标本,用酶联免疫吸附法(ELISA)检测血浆皮质醇、γ-干扰素(IFN-γ)和白细胞介素-4(IL-4)水平,光镜下观察肺和小肠组织病理学改变,并行组织病理学评分.结果 与对照组比较,休克复苏组大鼠血浆皮质醇水平明显降低(P均<0.01);IFN-γ和IL-4呈进行性升高,IFN-γ/IL-4比值随病程进展逐渐下降(P均<0.01);肺和小肠组织损伤明显,病理学评分显著增加[肺:(3.09±0.56)分比(0.31±0.25)分,小肠:(7.6l±1.20)分比(0.86±0.72)分,P均<0.013).异丙酚组低皮质醇血症程度降轻,IFN-7和IL-4升高程度降低,IFN-γ/IL-4比值下降趋于减缓(P<0.05或P<0.01);肺和小肠组织损伤明显减轻,病理学评分显著降低[肺:(1.27±0.40)分,小肠:(3.69±1.28)分,P均<0.013.结论 异丙酚可减轻失血性休克复苏大鼠的低皮质醇血症,调节炎症反应,保护重要脏器.     

延迟液体复苏对失血性休克大鼠炎性反应的影响

目的:探讨延迟液体复苏对失血性休克大鼠炎性反应的影响。方法:将40只大鼠随机分为休克后即刻复苏组、休克后延迟30 min复苏组、休克后延迟60 min复苏组、未复苏组。采用Wiggers方法制备可控性失血性休克模型。记录复苏开始即刻(0 min),30、90、150、210、270、330 min平均动脉压水平,并采血测定IL-6、TNF-α和IL-10浓度。结果:液体复苏组复苏开始后各时点平均动脉压水平无明显差异。与未复苏组相比,休克后延迟30、60 min复苏组IL-6、TNF-α浓度明显增加,休克后延迟60 min复苏组IL-10浓度显著降低(P<0.01)。结论:在控制性失血性休克动物模型,延迟液体复苏可使促炎细胞因子生成增加,其增加的程度与延迟复苏时间密切相关。     

两种液体复苏对失血性休克大鼠细菌移位及肠道炎症反应的影响

目的探讨复方氯化钠溶液（林格液，RS）和质量分数为6％的中分子羟乙基淀粉溶液（HES）对失血性休克大鼠细菌移位及肠道炎症反应的影响。方法50只健康雄性SD大鼠按随机数字表法分为假手术组（SHA组，n=10）、RS组n=20）、HES组（n=20），RS组和HES组制备可控性失血性休克模型。分别于液体复苏后1h和24h处死大鼠，检测和比较各组大鼠细菌移位、肠组织肿瘤坏死因子-α（TNF—α）及髓过氧化物酶（MPO）活性的变化，并进行病理学检查。结果HES组和RS组在死亡率、放血量、病理学检查方面没有明显差别。与SHA组比较，HES组和RS组在菌落计数和TNF—α方面明显升高，其中HES1h组比RS1h组明显升高，HES 24h组比RS24h组明显下降。与SHA组比较，HES1h组和RS1h组的MPO活性明显升高，HES24h组和RS24h组MP0活性没有明显差别。结论RS能明显改善复苏后1h的肠道功能，HES能明显改善复苏后24h的肠道功能。     

Effect of initial fluid resuscitation on subsequent treatment in uncontrolled hemorrhagic shock in rats

SUMMARY: Using a modified uncontrolled hemorrhage shock model with massive splenic and vascular injury, we evaluated outcome and tissue oxidation injury with different resuscitation interventions during prehospital and hospital phases. The aim of our study was to explore the effect of initial fluid resuscitation on subsequent treatment of uncontrolled hemorrhagic shock in rats. Uncontrolled hemorrhagic shock was produced in 114 Wistar rat by sharp transection both of the splenic parenchyma at one location between the major branches of the splenic artery into the spleen and of one of the major branches of the splenic artery. Experimental design consisted of three phases: a "prehospital phase" (resuscitation with balanced saline to a mean arterial pressure (MAP) of 40, 50, 60, 80, and 100 mmHg, respectively, when MAP reached 30 mmHg), followed by a "hospital phase" (120 min, including control of hemorrhage and resuscitation with balanced saline and whole blood (2:1) or balanced saline alone to a MAP >80 mmHg), and a 240-min observation phase. Blood loss, infused volume, hematocrit, and survival rate were recorded. At the end of the experiment, survivors were sacrificed, and the lung, kidney, and distal ileum were harvested for determination of malondialdehyde (MDA) content and total antioxidative capacity (T-AOC). All rats that were resuscitated to a MAP >80 mmHg in the prehospital phase and received balanced saline alone in the hospital phase died, whereas those that had been resuscitated to a MAP of 40 or 50 mmHg during the prehospital phase and then resuscitated with balanced saline and whole blood in the hospital phase survived throughout the experiment. The animals whose MAP was kept higher than 80 mmHg had significantly higher MDA content and lower T-AOC than those whose MAP was maintained 40, 50, or 60 mmHg during the prehospital phase. In the hospital phase, resuscitation with balanced saline and whole blood not only relieved tissue damage but also improved the survival, as indicated by 44.4% survival rate in the rats that resuscitated to a MAP of 80 or 100 mmHg in the prehospital phase. These results suggested that in our uncontrolled hemorrhagic shock model, limited resuscitation in the prehospital phase had benefit for subsequent treatment in the hospital phase in terms of alleviated tissue damage and improved survivorship.     

Adverse effects of resuscitation with lactated ringer compared with ringer solution after severe hemorrhagic shock in rats

Lactated Ringer (LR) is a widely used resuscitation fluid that is known to mediate beneficial effects on acid-base balance when compared with normal saline. We here compared LR with the more physiological Ringer solution (RS) regarding acid-base status, hemodynamics, survival, and organ injury following fluid resuscitation subsequent to severe hemorrhagic shock. Anesthetized rats were hemorrhaged to a mean arterial blood pressure of 25 to 30 mmHg within 30 min. After 60 min, they were resuscitated with either RS or LR (three times the shed blood volume) or with RS or LR plus blood (shed blood plus twice its volume) within 30 min. Subsequently, the animals were observed for further 150 min. When the rats were resuscitated with pure LR or RS, all animals of the shock/LR group, but only three of eight shock/RS group rats were dead 100 min later (median survival, 50 ± 13.1 vs. 120 ± 14.1 min; P < 0.05). Coadministration of the shed blood with RS or LR increased the survival rates to 100%. In these blood-resuscitated groups, organ injury, especially of the kidney, was diminished by the use of RS compared with LR. Time-matched acid-base parameters were not different in all shock groups until death of the animals or euthanasia at the end of experimental time. We conclude that, in severe hemorrhagic shock, resuscitation with RS leads to an improved outcome compared with resuscitation with LR, regardless whether blood is coadministered or not.     

不同的复苏压力对非控制失血性休克大鼠肺功能的影响

目的比较不同的液体复苏压力对非控制失血性休克大鼠肺功能的影响。方法制备大鼠创伤非控制失血性休克模型。将60只远交群大鼠随机分为6组各10只：NC组为对照组;NF组为休克不复苏组;NS40、NS60（限制性液体复苏组）、NS80、NS100（大量液体复苏组）。各液体复苏组在大鼠的平均动脉压（MAP）降至35-40mmHg（1mm Hg=0．133kPa）时分别给予生理盐水输注,使血压维持在各相应水平。输液1h后,各液体复苏组均给予手术止血、回输血液及给予足量的液体输注,保持大鼠的MAP≥90mmHg。结果在出血未控制的情况下,限制性液体复苏组的出血量明显低于大量液体复苏组,肺组织病理学损害、酸中毒程度较大量液体复苏组明显减轻。NS60组有9只大鼠存活超过72h,NS40组3只存活超过72h,而NF组与NS80、NS100组无一只存活超过72h。结论创伤非控制失血性休克及不同的液体复苏压力均可造成不同程度的肺损伤,限制性液体复苏对肺功能具有保护作用。     

高渗氯化钠溶液复苏对失血性休克大鼠T淋巴细胞亚群的早期影响

目的 探讨高渗氯化钠溶液(HS)复苏对失血性休克大鼠T淋巴细胞亚群的早期影响及其意义.方法 将18只SD大鼠制作成重度失血性休克模型,随机分为假手术组(Sham组)、高渗氯化钠溶液复苏组(HS组)和等渗盐水复苏组(NS组),每组6只,采用双抗体标记流式细胞分析技术测定休克前及复苏/急救后各组大鼠的外周血CD4+、CD8+的百分率及二者比值CD4+/CD8+.结果 在失血性休克/复苏/急救后的早期阶段,HS组和NS组大鼠的外周血CD4+细胞亚群表达均显著升高(P＜0.05),HS组大鼠的外周血CD8+细胞亚群表达也有所升高,而NS组大鼠的外周血CD8+细胞亚群表达则无明显改变,从而导致NS组大鼠的外周血CD4+/CD8+比值较Sham组和HS组明显增高,差异具有统计学意义(P＜0.05).结论 在重度失血性休克大鼠模型中,与NS复苏相比较,HS复苏能明显减轻复苏后早期的免疫炎症调节功能紊乱,有助于维持T细胞的辅助-抑制免疫炎症调节网络的平衡.     

Prolonged Blood Storage Does Not Effect Survival in an Animal Model of Hemorrhagic Shock

SUMMARY: BACKGROUND: Red blood cell (RBC) transfusion in hemorrhagic shock is life saving. However, several clinical trials have shown that blood transfusion in the critically ill patient might be associated with adverse outcomes. Furthermore, an association between prolonged blood storage and adverse effects of RBC transfusion has been postulated. The aim of this study is to examine the effect of blood storage time on resuscitation outcome, in an animal model of hemorrhagic shock. METHODS: 20 Wistar rats were phlebotomized in order to induce reversible hemorrhagic shock. Half of them were resuscitated with blood stored for a short period of time (4 days), and the other ones were resuscitated with blood stored for a prolonged time (14 days). Blood samples for hemoglobin, pH, lactate, bicarbonate and creatinine were drawn prior to the induction of shock and 24 h after resuscitation. Five days after resuscitation the animals were sacrificed, and liver, lung and kidney histology was examined. RESULTS: At 24 h after bleeding, the hemoglobin levels decreased by 3.2 and 1.7 g/dl, the pH decreased by 0.008 and 0.001, while the lactate levels increased by 1.6 and 2.7 mg/dl in the fresh and old blood resuscitation groups, respectively, with no significant difference between the groups. A trend toward more severe renal damage occurred in the old compared to the fresh blood resuscitation group (p = 0.089). CONCLUSION: The results of the present study show that in this animal model of hemorrhagic shock the duration of storage of RBCs used for transfusion did not affect the outcome of resuscitation.     

Organ-specific extravasation of albumin-bound Evans blue during nonresuscitated hemorrhagic shock in rats

Shock-induced enhanced capillary permeability is associated with alterations in the interstitial matrix composition and contributes to organ damage. This study was designed to evaluate albumin extravasation in various organ tissues during severe, hemorrhagic shock without fluid resuscitation and reperfusion. Target value of hemorrhagic shock was a reduction of cardiac output (CO) by 50% induced by removal of blood. Twelve anesthetized Sprague-Dawley rats (260-325 g) kept under continuous hemodynamic monitoring were randomly assigned to a group of hemorrhagic shock (n = 6) and a control group of normovolemic animals (n = 6). After 30 min of shock 50 mg/kg b.w. Evans blue (EB) was injected intravenously followed by an incubation period of 20 min. Exsanguination and wash out of the intravascular space was performed by a pressure-controlled perfusion with heparinized saline before harvesting organs to quantify albumin-bound EB extravasation. We found that withdrawal of 4.7 +/- 0.4 mL (mean, +/-SEM) blood, which accounts for 21.1% of the calculated total blood volume, resulted in a reduction of CO from 36.1 +/- 3.1 to 19.4 +/- 2.7 mL/min. Simultaneously, MAP decreased from 98 +/- 6 to 40 +/- 1 mmHg. In hemorrhaged rats, the interstitial concentration of EB in lung and kidney was significantly higher than observed in intact animals, whereas heart, spleen, liver, ileum, skeletal muscle, and skin showed no significant microvascular damage. We conclude that despite the absence of fluid resuscitation and reperfusion, microvascular damage in lung and kidney is evident within the first thirty minutes of hemorrhagic shock.