杀菌／通透性增加蛋白对休克大鼠组织细胞因子mRNA表达的影响

作者在大鼠失血性休克模型上,观察了重组杀菌／通透性增加蛋白（ＢＰＩ）对肺组织肿瘤坏死因子（ＴＮＦ）、白人素－６（ＩＬ－６）ｍＲＮＡ表达及急性肺损伤的影响,并对肠源性内毒素血症与炎症细胞因子诱发的关系进行了探讨。结果显示：失血性休克可导致血浆内毒素含量显著升高,肺组织ＴＮＦ,ＩＬ－６ｍＲＮＡ表达分别在复苏后２、８小时明显增多（Ｐ〈０．０５－０．０１）;给予ＢＰＩ治疗则完全中和休克所致内毒素血症,并不     

不同剂量6%HES 130/0.4容量治疗对失血性休克大鼠肺损伤的影响

目的 评价不同剂量6%羟乙基淀粉130/0.4(6%HES 130/0.4)容量治疗对失血性休克大鼠肺损伤的影响.方法 健康雄性SD大鼠24只,随机分为4组(n=6),假手术组(S组)、乳酸钠林格氏液组(RS组)和6%HES130/0.4 33ml/kg组(H1组)、6%HES130/0.4 50ml,kg组(H2组).除S组外,RS组、H1组和H2组均经右颈总动脉放血,制备失血性休克模型.于模型制备成功后RS组静脉输注3倍最大放血量的乳酸钠林格氏液;H1组和H2组分别静脉输注33、50ml/kg 6%HES 130/0.4和乳酸钠林格氏液(总量均为3倍最大放血量),容量治疗时间45 min.于放血前(T0,基础状态)、容量治疗结束后2 h(T1)、3 h(T2)时采集动脉血样,进行血气分析,计算PaO2/FiO2;最后一次采集血样后,进行支气管肺泡灌洗,测定支气管肺泡灌洗液(BALF)蛋白浓度,取肺组织测定湿,干重比(W/D比值)、TNF-α、m-1β和IL-10的含量,光镜下观察肺组织病理学结果.结果 与S组比较,RS组、H1组和H2组肺组织TNF-α、IL-1β、IL-10含量、BALF蛋白浓度和W/D比值升高,RS组T1.2时PaO2/FiO2降低,H2组T2时PaO2/FiO2降低(P<0.05),H1组T1.2时PaO2/FiO2差异无统计学意义(P>0.05);与RS组比较,H1组和H2组肺组织TNF-α、IL-1β含量、BALF蛋白浓度和W/D比值降低,H1组T1.2时,H2组T1时PaO2/FiO2升高(P<0.05).与H1组比较,H2组T2时PaO2/FiO2降低,肺组织IL-10含量降低(P<0.05).H1组和H2组肺组织病理损伤程度轻于RS组,其中H1组病理学损伤程度最轻.结论 6%HES 130/0.4 33和50 ml/kg容量治疗均可减轻失血性休克大鼠肺损伤,33 ml/kg效果更好.     

杀菌/通透性增加蛋白对内毒素休克大鼠微循环灌注的保护作用

目的 探讨杀菌／通透性增加蛋白（ＢＰＩ）对内毒素休克时血液动力学和内脏微徨灌注的保护作用及其机制。方法 采用大鼠内毒素休克模型,动态观察血液动力学、内脏微循环灌注量和血浆生物喋吟、一氧化氮（ＮＯ）水平的变化。结果 休克早期给予重组ＢＰＩ,可显著提高平均支流压、心脏指数及每搏输出量,明显改善肝、肾、小肠抽徨灌注量及动物预后（Ｐ〈０．０５～０．０１）,循环ＮＯ产生亦不同程度受到抑制。结论 早期应用ＢＰ     

不同剂量6%HES 130/0.4容量治疗对失血性休克大鼠肺损伤的影响

Objective To evaluate the effects of volume therapy with different doses of 6% hydroxyethyl starch 130/0.4 (6% HES 130/0.4) on lung injury in a rat model of hemonhagic shock.Methods Twenty-four male SD rats weighing 220-300 g were randomly divided into 4 groups ( n = 6 each) : group I sham operation (group S); group II Ringer's solution (group RS); group HI and IV 2 HES groups (group H1, H2 ). The animals were anesthetized with intraperitoneal 1% sodium pentobarbital 45 ing/kg. Right common carotid artery (CCA) and left femoral vein were cannulated for blood letting, MAP monitoring, fluid administration and blood sampling. Hemonhagic shock was induced by withdrawing blood from right CCA in group II , III and IV . MAP was reduced to 35-45 mmHg which was maintained for 90 min. In group RS, hemorrhagic shock was resuscitated with Ringer's solution 3 times of the volume of blood withdrawn, while group H1 and H2 received HES 33 and 50 ml/kg respectively and Ringer' s solution (the total volume was equal to 3 times of the volume of blood removed) . Arterial blood samples were taken before blood letting (T0 , baseline), and at 2, 3 h after volume therapy (T1,2) for blood gas analysis and PaO2/FiO2 was calculated. The animals were then sacrificed by exsanguination and the lungs were immediately removed for microscopic examination and determination of protein concentration in broncho-alveolar lavage fuid (BALF), W/D lung weight ratio and TNF-α, IL-1 β and IL-10 contents in the lung.Results TNF-α, IL-1β and IL-10 content in the lung, protein concentration in BALF and W/D ratio were significantly higher in group RS, H1 and H2, while PaO2/FiO2 was significantly lower at T,2 in group RS and at T2 in group H2 than in group S (P < 0.05). TNF-α and IL-1β contents in the lung, protein concentration in BALF and W/D ratio were significantly lower in group H1 and H2 , while PaO2/FiO2 was significantly higher at T,i2 in group H1 and at T1 in group H2 than in group RS (P <0.05) . PaO2/FiO2 at T2 and IL-10 content in the lung were significantly lower in group H2 than in group H, ( P < 0.05) . The lung damage was significantly ameliorated in group H1 and H2 especially in group H, as compared with group RS. Conclusion Volume therapy with 6% HES 130/0.4 33 or 50 ml/kg can attenuate lung injury in a rat model of hemorrhagic shock and the efficacy of 33 ml/kg is better.     

不同剂量6%HES 130/0.4容量治疗对失血性休克大鼠肺损伤的影响

Objective To evaluate the effects of volume therapy with different doses of 6% hydroxyethyl starch 130/0.4 (6% HES 130/0.4) on lung injury in a rat model of hemonhagic shock.Methods Twenty-four male SD rats weighing 220-300 g were randomly divided into 4 groups ( n = 6 each) : group I sham operation (group S); group II Ringer's solution (group RS); group HI and IV 2 HES groups (group H1, H2 ). The animals were anesthetized with intraperitoneal 1% sodium pentobarbital 45 ing/kg. Right common carotid artery (CCA) and left femoral vein were cannulated for blood letting, MAP monitoring, fluid administration and blood sampling. Hemonhagic shock was induced by withdrawing blood from right CCA in group II , III and IV . MAP was reduced to 35-45 mmHg which was maintained for 90 min. In group RS, hemorrhagic shock was resuscitated with Ringer's solution 3 times of the volume of blood withdrawn, while group H1 and H2 received HES 33 and 50 ml/kg respectively and Ringer' s solution (the total volume was equal to 3 times of the volume of blood removed) . Arterial blood samples were taken before blood letting (T0 , baseline), and at 2, 3 h after volume therapy (T1,2) for blood gas analysis and PaO2/FiO2 was calculated. The animals were then sacrificed by exsanguination and the lungs were immediately removed for microscopic examination and determination of protein concentration in broncho-alveolar lavage fuid (BALF), W/D lung weight ratio and TNF-α, IL-1 β and IL-10 contents in the lung.Results TNF-α, IL-1β and IL-10 content in the lung, protein concentration in BALF and W/D ratio were significantly higher in group RS, H1 and H2, while PaO2/FiO2 was significantly lower at T,2 in group RS and at T2 in group H2 than in group S (P < 0.05). TNF-α and IL-1β contents in the lung, protein concentration in BALF and W/D ratio were significantly lower in group H1 and H2 , while PaO2/FiO2 was significantly higher at T,i2 in group H1 and at T1 in group H2 than in group RS (P <0.05) . PaO2/FiO2 at T2 and IL-10 content in the lung were significantly lower in group H2 than in group H, ( P < 0.05) . The lung damage was significantly ameliorated in group H1 and H2 especially in group H, as compared with group RS. Conclusion Volume therapy with 6% HES 130/0.4 33 or 50 ml/kg can attenuate lung injury in a rat model of hemorrhagic shock and the efficacy of 33 ml/kg is better.     

α-黑色素细胞刺激素对急性呼吸窘迫综合征大鼠血清细胞因子水平的影响

目的 研究α-黑色素细胞刺激素(α-MSH)对急性失血性休克合并肺内毒素损伤两次打击致急性呼吸窘迫综合征大鼠血清细胞因子水平的影响。方法 30只雄性SD大鼠随机分成生理对照组(A组)、急性呼吸窘迫综合征组(B组)和给药组(C～F组,在不同时间点静脉注射α-MSH 1.7 mg·kg-1)。观察各组血清细胞因子(TNF-α、IL-1、IL-6、IL-10)水平的变化。结果 生理对照组(A组)大鼠血清细胞因子水平各时间点间差异无显著性(P>0.05);急性呼吸窘迫综合征组(B组)大鼠随打击因素和病程进展,血清细胞因子TNF-α、IL-1、IL-6、IL-10水平均显著增高(P<0.01),促/抗炎细胞因子平衡失衡;给药组(C、D、F组)与B组相比能显著降低血清TNF-α、IL-1水平(P<0.01),增加IL-6、IL-10浓度(P<0.01);其中多次给药组(F组)作用最明显,而内毒素致伤后1 h给药组(E组)各细胞因子水平与B组各时间点相比差异无显著性(P>0.05)。结论 α-MSH可降低急性呼吸窘迫综合征大鼠血清促炎细胞因子水平促进抗炎细胞因子产生。α-MSH可能通过调节促/抗炎细胞因子平衡而发挥其保护作用。     

重组杀菌/通透性增加蛋白对内毒素休克中肝脏一氧化氮合酶的影响

目的：探讨重组杀菌／通透性增加蛋白（ｒＢＰＩ_(２１)）对内毒素休克中肝组织一氧化氮合酶（ＮＯＳ）的影响及其意义。方 法：大鼠腹腔注射大肠杆菌内毒素（１５．０ｍｇ／ｋｇ）复制内毒素休克模型,动物随机分成正常对照组、内毒素休克组和 ｒＢＰＩ_(２１)治疗组。检测肝组织ＮＯＳ活性、三磷酸鸟苷环水解酶１（ＧＴＰ－ＣＨＩ）活性及生物喋呤含量,同时还观察肝脏微循环 血流灌注量的改变。结果：内毒素攻击后肝组织诱生型ＮＯＳ（ｉＮＯＳ）活性急剧升高（Ｐ＜０．０１）,但原生型ＮＯＳ（ｃＮＯＳ）活 性变化不明显（Ｐ＞０．０５）。 ｒＢＰＩ_(２１)治疗可显著抑制ｉＮＯＳ活性,明显提高肝脏微循环灌注量（Ｐ＜０.０１）;同时局部组织的 ＧＴＰ－ＣＨＩ活性降低（Ｐ＜０．０１）,生物喋呤含量也显著Ｆ降（Ｐ＜０.０５）。结论：内毒素休克早期给予ｒＢＰＩ_(２１)能选择性抑制肝 组织ｉＮＯＳ活性并改善局部微循环,其作用机理可能与降低组织ＧＴＰ－ＣＨＩ活性及其介导生物喋呤诱生有关。     

盐酸戊乙奎醚预先给药对失血性休克大鼠急性肺损伤时TLR4 mRNA表达的影响

目的 探讨盐酸戊乙奎醚预先给药对失血性休克大鼠急性肺损伤时Toll样受体4(TLR4)mRNA表达的影响.方法 健康SD大鼠40只,体重200～250 g,随机分为5组(n=8):假手术组(S组)、失血性休克致急性肺损伤组(ALI组)和低、中、高剂量盐酸戊乙奎醚预先给药组(P1～3组).S组仅行动静脉穿刺,不放血,ALI组股动脉放血至35～45 mm Hg制备急性肺损伤模型,P1～3组分别于放血前30 min股静脉注射盐酸戊乙奎醚0.3、1.0、3.0 mg/kg,随后制备急性肺损伤模型.各组复苏后4 h时处死大鼠取肺,称重后计算肺湿干重比,检测TLR4 mRNA和NF-κB p65蛋白的表达水平,观察病理学结果.结果 与S组比较,ALI组和P1组TLR4 mRNA、NF-κB p65蛋白表达水平及肺湿干重比升高(P＜0.05或0.01),P2.3组差异无统计学意义(P＞0.05);与ALI组比较,P2,3组TLR4 mRNA、NF-κB p65蛋白表达水平及肺湿干重比降低(P＜0.05或0.01);P2组和P3组上述指标比较差异无统计学意义(P＞0.05).P2,3组肺组织病理学损伤程度较ALI组明显减轻.结论 盐酸戊乙奎醚预先给药可通过抑制肺组织TLR4 mRNA表达上调,进而降低NF-κB活性,从而减轻失血性休克诱发大鼠的急性肺损伤.     

ω-3多不饱和脂肪酸对创伤性休克大鼠急性肺损伤的影响

目的 探讨ω-3多不饱和脂肪酸(ω-3 PUFA)对创伤性休克大鼠急性肺损伤的影响.方法 雄性Wistar大鼠36只,体重240～260 g,月龄3月,采用随机数字表法,将大鼠随机分为3组(n=12):对照组(C组);创伤性休克组(TS组)采用骨折复合失血致创伤性休克;ω-3 PUFA组于造模前12 h及2 h经尾静脉注射ω-3 PUFA 2 ml/kg,C组和TS组注射生理盐水2 ml/kg.模型制备成功后120 min时采集颈动脉血样,处死取肺组织.用ELISA法检测血清TNF-α、8-异前列腺素F2α(8-iso-PGF2α)、IL-1β及IL-10的浓度;计算肺组织湿/干重比(W/D比);光镜下观察肺组织病理变化,行病理学评分.结果 与C组比较,TS组和ω-3 PUFA组血清TNF-α、8-iso-PGF2α、IL-1β及IL-10的浓度、肺组织W/D比及病理学评分明显升高(P＜0.01).与TS组比较,ω-3 PUFA组血清TNF-β、8-iso-PGf2α及IL-1β的浓度、肺组织W/D比及病理学评分明显降低,血清IL-10浓度升高(P＜0.05或0.01).结论 ω-3 PUFA可有效地抑制创伤性休克大鼠全身炎性反应,减轻急性肺损伤.

Abstract：

Objective To investigate the effects of ω-3 polyunsaturated fatty acid (ω-3 PUFA) on acute lung injury (ALI) in a rat model of traumatic shock. Methods Thirty-six male Wistar rats aged 3 months were randomly assigned into 3 groups ( n = 12 each): control group (group C) ; traumatic shock group (group TS) and ω-3 PUFA + TS group (group to-3 PUFA) . Traumatic shock was induced by fracture of femur and hemorrhage according to the method described by Feeney in groups TS and ω-3 PUFA. In group ω-3 PUFA, ω-3 PUFA 2 ml/kg was injected via the caudal vein at 12 and 2 h before induction of traumatic shock. Arterial blood samples were taken at 120 min after traumatic shock was successfully induced for determination of serum concentrations of TNF-α, IL-1β, IL-10 and 8-iso-PGF2α by ELISA. The animals were then sacrificed and lungs were removed for-determination of W/D lung weight ratio and microscopic examination. Results Traumatic shock significantly increased serum concentrations of TNF-α, IL-1β, IL-10 and 8-iso-PGF2α, W/D ratio and pathologic scores of lung tissues in groups TS and ω-3 PUFA as compared with group C.ω-3 PUFA significantly attenuated traumatic shuck-induced increase in serum concentrations of TNF-α, IL-1β and 8-iso-PGF2α , W/D ratio and pathologic scores of lung tissues but further increased the serum IL-10 concentration in group ω-3 PUFA as compared with group TS. Conclusion ω-3 PUFA can significantly inhibit the svstemic inflammatory response and ameliorate traumatic shock-induced ALI.     

利多卡因对失血性休克大鼠肺损伤的保护作用

目的 探讨利多卡因对失血性休克大鼠肺损伤的保护作用。方法 80只雄性Wistar大鼠建立失血性休克模型后,随机分为四组,假手术组(Ⅰ组,n=8)、休克组(Ⅱ组,n=8)、生理盐水组(Ⅲ组,n=32)、利多卡因组(Ⅳ组,n=32)。Ⅰ组于假手术后,Ⅱ组于休克60 min,Ⅲ、Ⅳ组分别于复苏开始后2、4、8、12 h,测定中性粒细胞(PMNs)表面粘附分子CD11b/CD18表达、肺组织中髓过氧化物酶(MPO)活性,并采用光镜和透射电镜观察肺组织的病理学改变。结果 与Ⅰ组比较,Ⅲ组、Ⅳ组复苏后各时点PMNs表面CD11b/CD18表达均升高(P<0.01),Ⅱ组差异无显著性(P>0.01),Ⅱ组、Ⅲ组、Ⅳ组复苏后各时点肺组织中MPO活性升高(P<0.05或0.01)。与Ⅲ组比较,Ⅳ组复苏后同一时点、Ⅰ组、Ⅱ组PMNs表面CD11b/CD18表达及肺组织中MPO活性降低(P<0.01)。结论 小剂量利多卡因可以抑制失血性休克大鼠PMNs表面CD11b/CD18的表达,减少PMNs在肺组织中的浸润,从而减轻肺损伤。     

Toll样受体4在失血性休克复苏致小鼠急性肺损伤中的作用

目的 探讨Toll样受体4(TLR4)在失血性休克复苏致小鼠急性肺损伤中的作用.方法 TLR4基因突变型C3H/HeJ小鼠和野生型C3H/HeN小鼠各24只,两种品系小鼠各随机分为2组:假手术组(S组,n=6)、失血性休克复苏组(HSR组,n=18)制备失血性休克复苏模型,并于复苏后6、24、48 h时各取6只小鼠颈动脉放血处死后开胸取肺组织,免疫组织化学法检测p38 MAPK表达水平,酶联免疫吸附法测定白细胞介素(IL)-10和IL-6含量,透射电镜下观察肺组织超微结构.结果 与C3H/HeN小鼠比较,C3H/HeJ小鼠复苏后肺组织p38 MAPK表达下调,IL-6和IL-10含量降低(P<0.05或0.01),病理损伤程度减轻.两种品系小鼠中,与S组比较,HSR组复苏后24 h时肺组织IL-6和IL-10含量增加,复苏后48 h时肺组织IL-6含量增加(P<0.05或0.01);C3H/HeN小鼠中,与S组比较,HSR组复苏后6 h和24 h时肺组织p38 MAPK蛋白表达上调,复苏后48 h时肺组织IL-10含量增加(P<0.01).结论 TLR4参与小鼠失血性休克复苏致急性肺损伤的发生,其机制与激活p38 MAPK信号转导通路有关.     

严重烫伤后高迁移率族蛋白-1基因表达的改变及意义

目的　观察烫伤后肝、肺组织高迁移率族蛋白-1（HMG-1）mRNA表达的变化规律及其与器官功能损害的关系。　方法　采用大鼠35%Ⅲ度烫伤模型,动物随机分为正常对照组、烫伤组和重组杀菌/通透性增加蛋白(rBPI21)治疗组,留取组织和血标本分别检测组织内毒素含量、HMG-1mRNA表达及器官功能指标。　结果　严重烫伤后早期肝、肺组织HMG-1基因表达改变不明显（正常对照组肝组织0.202±0.097;肺组织0.263±0.091）,伤后24h则明显增多(肝组织0.487±0.189;肺组织0.513±0.069,P＜0.05,0.01),且一直持续至伤后72h(肝组织0.687±0.142;肺组织0.520±0.076,P＜0.01)。给予rBPI21治疗可有效抑制肝和肺中内毒素水平的升高,并显著抑制肝、肺组织HMG-1mRNA水平(P＜0.01)。相关分析结果显示,肝组织HMG-1mRNA表达与血清谷丙转氨酶、谷草转氨酶水平、肺组织HMG-1mRNA表达与髓过氧化物酶活性呈显著正相关（P＜0.05,0.01）。　结论　严重烫伤后肝、肺组织HMG-1表达显著增多,且持续时间较长,局部组织HMG-1诱生与烧伤后内毒素介导的重要器官功能损害关系密切。     

缝隙连接在兔失血性休克复苏诱发肺损伤中的作用

目的 评价缝隙连接在兔失血性休克复苏诱发肺损伤中的作用.方法 健康家兔24只,体重1.5～2.2 kg,经股动脉放血制备失血性休克模型.随机分为2组(n=12),传统治疗组(A组)静脉输注乳酸钠林格氏液1.5 ml·kg-1·min-1 30 min(T3);辛醇组(B组)静脉输注乳酸钠林格氏液1.5 ml·kg-1·min-1 30 min(T3),同时腹腔注射99.5%辛醇5 mmol/kg.然后两组回输全部放血及等放血量的乳酸钠林格氏液后静脉输注乳酸钠林格氏液2.5 ml·kg-·h-1 150 min(T4).于放血前(T1)、模型制备成功即刻(T2)、T3、T4时记录左心室收缩压(LVSP)和HR,记录复苏期间兔的病死情况.于T时处死,测定肺组织Na+-K+-ATP酶和Ca2+-ATP酶的活性,计算肺通透性指数和肺湿重/干重(W/D)比,光镜下观察肺组织病理学结果.结果 与A组比较,B组T3时HR和LVSP降低,T4时LVSP升高,HR降低,Na+-K+-ATP酶和Ca2+-ATP酶活性升高,肺通透性指数降低,肺组织W/D比和病死率降低(P＜0.05或0.01).B组肺组织病理学损伤程度较A组明显减轻.结论 缝隙连接参与了兔失血性休克复苏诱发肺损伤.     

Toll样受体4在内毒素和“两次打击”致小鼠急性肺损伤中作用的比较

目的 比较Toll样受体4(TLR-4)在内毒素(LPS)和“两次打击”致小鼠急性肺损伤(ALI)中的作用.方法 雄性野生型小鼠C3H/HeN和TLR-4基因突变型小鼠C3H/HeJ各36只,采用随机数字表法,将2种小鼠各随机分为2组(n＝18),假手术/LPS组(S/LPS组)只进行手术操作而不实施放血诱导休克,失血性休克复苏/LPS组(HSR/LPS组)制备失血性休克复苏模型.复苏后24h时2组气管内滴注LPS 30μg/kg.分别于给予LPS后即刻(T1)、3 h(T2)和6 h(T3)时取6只小鼠,采集动脉血样,测定Pa02,然后处死小鼠,取肺组织,计算肺组织湿/干重比,并测定髓过氧化物酶(MPO)活性、IL-10和IL-6的含量.以T1时均数作为基础值,计算T2.3时各指标的变化率.结果 与S/LPS组比较,C3H/HeN小鼠的HSP/LPS组T2.3时Pa02变化率降低,肺组织W/D比、MPO、IL-6和IL-10的变化率升高(P< 0.05或0.01),C3H/HeJ小鼠的HSR/LPS组T2时Pa02变化率降低,肺组织W/D比、MPO、IL-6和IL-10的变化率升高(P<0.05或0.01),T3时上述指标差异无统计学意义(P＞0.05).结论 与LPS致小鼠ALI中的作用比较,TLR-4在“两次打击”致ALI中的作用明显增强.     

L-精氨酸对内毒素诱导急性肺损伤大鼠肺表面活性物质的影响

目的 评价L-精氨酸对内毒素(LPS)诱导急性肺损伤大鼠肺表面活性物质的影响.方法 健康雄性SD大鼠48只,随机分为4组:正常对照组(C组,n=16)、LPS组(n=16)、LPS 3 h+L-精氨酸治疗组(L1组,n=8)和LPS 6 h+L-精氨酸治疗组(L2组,n=8).LPS组、L1组和L2组静脉注射LPS 5mg/kg,C组给予等容量生理盐水.L1组和L2组分别于给予LPS后3 h或6 h腹腔注射L-精氮酸500 mg/kg.L1组和L2组于给予L-精氨酸后3 h(C组和LPS组分别于给予生理盐水或LPS后6、9 h)取8只大鼠,取肺组织,测定表面活性物质结合蛋白A(SP-A)mRNA的表达水平、肺泡灌洗液(BALF)中总磷脂(TPL)和总蛋白(TP)浓度,光镜下观察肺组织病理学结果.结果 与C组比较,LPS组SP-A mRNA表达下调,BALF中TPL浓度降低,TP浓度升高(P＜0.01).与LPS组比较,L1组SP-A mRNA表达上调,BALF中TPL浓度升高,TP浓度降低(P＜0.05或0.01);L2组上述指标差异无统计学意义(P＞0.05).L1组肺损伤程度轻于LPS组和L2组.结论 L-精氨酸可促进肺表面活性物质合成,从而对大鼠内毒素诱导急性肺损伤具有治疗作用.