烧伤后早期应用不同液体复苏血钠和红细胞变化的临床研究

目的　观察烧伤后早期应用不同液体复苏患者血钠和红细胞的变化。方法　将 15 0例烧伤患者分为 3组 ,A组为中、小面积烧伤患者 5 0例 ,给予平衡盐溶液 (钠离子 130mmol/L)复苏 ;B组为大面积烧伤患者 5 0例 ,液体复苏方法同A组 ;C组为大面积烧伤患者 5 0例 ,给予高渗乳酸钠溶液 (钠离子 174mmol/L)复苏。观察伤后 1～ 3d患者的补液总量、血钠、红细胞数量及红细胞平均体积 (MCV)的变化。对A、B组患者的烧伤指数 (BI)与其伤后 1d的血钠值作相关性分析。　 结果　伤后 3d内A组患者补液总量、补钠量均低于其他两组 (P <0.0 1);C组补液总量低于B组 ,而补钠量多于B组 (P <0.0 1)。伤后 3d内B组血钠值接近正常值下限 ,C组血钠值接近正常值上限 ,前者明显低于后者 (P <0.0 5或 0 .0 1)。伤后 3d内B、C组的红细胞数量相近 (P >0.0 5 )。伤后 1dB、C组患者的MCV分别为 (95 .5± 5 .5 )、(92 .1± 4 .5 )fl,伤后 2d各为 (93.2± 6 .4 )、(90 .9± 5 .4 )fl,组间比较差异无显著性意义 (P >0.0 5 )。A、B组患者伤后 1d的血钠值与自身BI呈负相关 (r=- 0 84,P<0.0 1)。　 结论　大面积烧伤患者伤后早期采用高渗盐溶液复苏 ,血钠值平稳且红细胞的肿胀程度较轻     

肠道双歧杆菌与烫伤大鼠肠源性细菌/内毒素移位

目的　观察肠道双歧杆菌在肠源性细菌 /内毒素移位中的变化和作用。　方法　制作严重烫伤大鼠模型 ,同时设假伤组。检测细菌和内毒素 (LPS)移位及盲肠膜菌群变化 ,ELISA法检测血浆白细胞介素 6(IL 6)浓度。　结果　大鼠严重烫伤后脏器细菌移位明显增多 (P <0 .0 1) ;血LPS水平在致伤 1、3、5d后分别为 (0 .2 3 6± 0 148)Eu/ml、(0 .197± 0 .15 6)Eu/ml、(0 10 4± 0 .0 90 )Eu/ml,显著高于假伤组的 (0 .0 72± 0 .0 49)Eu/ml(P <0 .0 5 ) ;盲肠膜菌群中双歧杆菌数剧减 2 0～2 5 0倍、真菌数剧增至 5～ 60倍、大肠杆菌数增加 0 .5～ 3 0倍 ,双歧杆菌与大肠杆菌比值由假伤组的2 5 0 0 0∶1降为伤后的 4～ 80 0∶1;血浆IL 6水平显著增高。经分层统计 ,与未发生肠道细菌移位大鼠相比 ,盲肠膜菌群移位大鼠的双歧杆菌量减少约 12 0倍 ,真菌数增加约 5 0倍 ,大肠杆菌数增加约 3 0倍。盲肠膜菌群中双歧杆菌数量与血浆中IL 6、LPS浓度呈负相关 (r1=- 0 .4817,r2 =- 0 .4912 ,P <0 .0 1) ,血IL 6和LPS浓度间存在显著正相关 (r =0 .82 5 8,P =0 .0 0 0 1)。　结论　严重烫伤可导致大鼠盲肠膜菌群紊乱 ,细菌和LPS移位增加 ;盲肠膜菌群中双歧杆菌的比例和数量的减少 ,可能促使了严重烫伤后肠源性细菌 /内毒素移位     

益生菌与核黄素联用对烫伤大鼠肠道屏障的保护作用

目的　观察益生菌与核黄素联合应用对烫伤大鼠细菌移位的防治效果 ,探讨其可能的作用机制。　方法　将Wistar大鼠随机分为烫伤对照组 (SC组 ,30只 )、烫伤治疗组 (ST组 ,30只 )、正常对照组 (NC组 ,10只 )。SC、ST组大鼠作 30 %ⅢTBSA度烫伤 ,ST组大鼠伤后立即向胃中灌注含双歧杆菌 5× 10 12 个集落形成单位 /L、蜡样芽孢杆菌 5× 10 10 个集落形成单位 /L和核黄素 5 0 0mg/L的等渗盐水混悬液 1.5ml,2次 /d。SC、NC组于相同时间灌注等量等渗盐水。观察细菌移位、肠道膜菌群、回肠分泌型免疫球蛋白A(SIgA)合成分泌及肠黏膜损伤修复等变化。　 结果　与SC组比较 ,ST组大鼠各脏器细菌移位率显著下降 (P =0.0 0 0～ 0.0 2 5),血浆内毒素水平在伤后 3d内降低显著 (P <0 0 5 ),回盲部膜菌群中双歧杆菌量升高 2 0～ 4 0倍 ,大肠杆菌和真菌量显著降低 ( P <0.0 1),致伤后 5d内黏膜损伤评分为 0～ 3(P <0.0 5),小肠黏液SIgA含量伤后 5d可恢复正常 ( P <0 0 1)。结论　益生菌与核黄素联合应用 ,可减轻烫伤大鼠细菌 /内毒素移位程度 ,有效保护肠道屏障     

大鼠烧伤休克延迟复苏肠道微血流量的改变及其与细菌移位的关系

目的　探讨烧伤休克期延迟复苏肠道局部微循环改变及其与肠道细菌移位的关系。方法　采用大鼠烧伤休克延迟复苏模型 ,动物分为烧伤休克不复苏组、伤后 8h延迟复苏组、立即复苏组和手术对照组 ,检测肠道细菌移位发生频率、回肠末端肠壁微血流量和体循环平均动脉压变化。　结果　伤后 8h复苏组细菌移位率高达 5 4.2 % ,明显高于立即复苏组 (P <0 .0 1) ,与不复苏组相差不显著 (P >0 .0 5 ) ;延迟复苏后 4h ,肠壁微血流量虽已得到改善 ,但远未达到立即复苏组同时相的微循环血流灌注量 ,而此时外周循环的平均动脉压已恢复至正常范围。　结论　烧伤休克延迟复苏后肠道细菌移位频率居高不下 ,可能与肠壁微血流量改善滞后有关     

前列腺素类药物改善烧伤后动物的细菌移位及其相关死亡率

本文评价了动物烧伤后细菌移位与生存率的关系,以及前列腺素(PGE)类药物预防肠道细菌移位改善生存率的作用。实验1;作者给27 只BALB/C小鼠管饲~(14)C大肠杆菌(10~(10)细菌/0.1mL)。采用Site-ritz和Holder技术造成20%全层皮肤烧伤4小时后,心脏穿刺取血测定~(14)C每分蜕变量(dpm)。处死动物。无菌制备肠系膜淋巴结(MLN)和肝标本,分     

天然蒙脱石防治烧伤后肠道细菌移位的实验研究

目的　探讨天然蒙脱石对烧伤大鼠肠道细菌移位的防治作用。　方法　SD大鼠54只,分为正常对照组6只、烧伤对照组与烧伤治疗组各24只。后两组大鼠预先喂服转染了质粒pUC19的示踪菌JM109,证实质粒已定植于其肠道后,制成30%TBSAⅢ度烫伤(以下称烧伤)模型。烧伤治疗组大鼠伤后立即喂服天然蒙脱石0. 6g d-1 kg-1,烧伤对照组大鼠不喂服药物。观察正常对照组大鼠以及烧伤对照组、烧伤治疗组大鼠伤后12h和1、3、5d血液、肠系膜淋巴结细菌移位情况,并行酶切鉴定;检测大鼠肠组织丙二醛(MDA)及超氧化物歧化酶(SOD)的含量;用病理学方法观察整段小肠的损伤情况,测量空肠黏膜绒毛高度并计算基底膜细胞核分裂相。　结果　血液细菌培养:伤后1、5d,烧伤对照组阳性鼠数多于正常对照组,烧伤治疗组阳性鼠数少于烧伤对照组(P<0 05).肠系膜淋巴结细菌定量:烧伤治疗组伤后1、5d为(38±16)、(68±20)集落形成单位(CFU) /g;烧伤对照组伤后1、5d为( 228±67 )、( 183±29 )CFU/g,明显高于前者(P<0. 01 ).MDA、SOD含量:烧伤治疗组与烧伤对照组伤后各时相点比较,差异有统计学意义(P<0. 05).烧伤治疗组大鼠伤后各时相点空肠绒毛高度及基底膜细胞核分裂相明显高于或多于烧伤对照组(P<0. 05或0. 01)。　结论　天然蒙脱石对严重烧伤大鼠肠     

小型猪火器伤时肠道细菌移位的检测

我们通过常规细菌培养、免疫组织化学和聚合酶链反应 (PCR )方法检测小型猪火器多发伤后血中及脏器中的细菌 ,对火器多发伤时检测肠道细菌移位的方法进行探讨。一、材料与方法1.实验动物及分组 :成年 (15± 5 )个月贵州Ⅲ系小型香猪 2 4只 ,体重 (2 5±5 )kg。动物随机分为 4组 (每组n =6) ,其中对照组 (C组 )模型制作术后不致伤 ;多发伤组 (M组 )模型制作术后 2d射击双侧大腿和颅顶骨 ,造成双侧股骨干骨折加颅骨切线伤 ;颅骨切线伤组 (H组 )射击致颅骨切线伤 ;骨折组 (L组 )射击致双侧股骨干骨折。2 .监测指标和方法 :(1)体循环血和门静…     

烫伤大鼠肠系膜淋巴结T淋巴细胞亚群及细胞凋亡变化

严重烧(创)伤后肠道细菌、内毒素可经淋巴、血液途径移位,肠集合淋巴结生发中心大量淋巴细胞凋亡[1],提示肠道免疫屏障受损.笔者拟观察细菌经淋巴途径移位最后一个环节--肠系膜淋巴结(MLN)T淋巴细胞亚群及细胞凋亡情况,以了解肠源性感染时淋巴途径免疫状态.     

烫伤大鼠肠系膜淋巴结T淋巴细胞亚群及细胞凋亡变化

严重烧(创)伤后肠道细菌、内毒素可经淋巴、血液途径移位,肠集合淋巴结生发中心大量淋巴细胞凋亡[1],提示肠道免疫屏障受损.笔者拟观察细菌经淋巴途径移位最后一个环节--肠系膜淋巴结(MLN)T淋巴细胞亚群及细胞凋亡情况,以了解肠源性感染时淋巴途径免疫状态.     

烫伤大鼠肠系膜淋巴结T淋巴细胞亚群及细胞凋亡变化

严重烧(创)伤后肠道细菌、内毒素可经淋巴、血液途径移位,肠集合淋巴结生发中心大量淋巴细胞凋亡[1],提示肠道免疫屏障受损.笔者拟观察细菌经淋巴途径移位最后一个环节--肠系膜淋巴结(MLN)T淋巴细胞亚群及细胞凋亡情况,以了解肠源性感染时淋巴途径免疫状态.     

Effects of endotoxin on regulation of intestinal smooth muscle nitric oxide synthase and intestinal transit

BACKGROUND: The disrupted intestinal transit during endotoxemia may be mediated by nitric oxide (NO). We hypothesized that the isoforms of nitric oxide synthase (NOS) are up-regulated in intestinal smooth muscle during endotoxemia and that the scavenging of NO will normalize transit. METHODS: Rats were given Escherichia coli lipopolysaccharide (LPS) 10 mg/kg intravenously and were killed 4 hours later. To determine the activity of NOS isoforms in the jejunum and ileum, the conversion of tritiated L-arginine to tritiated L-citrulline was measured. Western immunoblots were performed by incubating the extracted protein with specific polyclonal antibodies. To determine intestinal transit, rats were divided into 4 groups: 0.9% sodium chloride 1 mL/h intravenously for 5 hours, LPS 10 mg/kg intravenous bolus plus 1 mL/h 0.9% sodium chloride intravenously, LPS plus oxyhemoglobin 0.5 g/kg/h intravenously, and oxyhemoglobin 0.5 g/kg/h intravenously. RESULTS: LPS increased the constitutive and inducible NOS enzyme activities in the jejunum and ileum. Western blots demonstrated that LPS up-regulates both the NOS1 and NOS2 isoforms in jejunal and ileal smooth muscle. Oxyhemoglobin alone increased intestinal transit compared with controls, whereas endotoxemia increased intestinal transit, which was ameliorated with infusions of oxyhemoglobin. CONCLUSIONS: NO may play a major role in mediating the rapid intestinal transit induced by endotoxemia.     

Effects of diabetes,insulin and antioxidants on NO synthase abundance and NO interaction with reactive oxygen species

BACKGROUND: Earlier studies have provided evidence for increased production of reactive oxygen species (ROS) and altered nitric oxide (NO) metabolism in diabetes. This study was intended to explore the effect of type I diabetes and its treatment with insulin alone or insulin plus antioxidant-fortified diet on expression of NOS isoforms and ROS interactions with lipids, glucose and NO. METHODS: Rats with streptozotocin-induced diabetes were divided into once-daily insulin (ultralente)-treated, insulin plus antioxidant (vitamin E and vitamin C)-treated and untreated groups. After four weeks, plasma malondialdehyde (MDA) and tissue endothelial (eNOS), neuronal (nNOS) NO synthases, carboxymethyllysine (CML) and nitrotyrosine were determined. RESULTS: The untreated diabetic animals exhibited severe hyperglycemia, elevated blood pressure, increased plasma MDA, high tissue CML and reduced tissue nitrotyrosine denoting enhanced lipid, glucose and protein oxidation but reduced NO oxidation by ROS. This was coupled with significant reduction of eNOS and nNOS expression in renal cortex and eNOS in the left ventricle. Insulin therapy partially lowered blood pressure, tissue CML, plasma glucose and MDA, but significantly raised eNOS expression and nitrotyrosine abundance to supranormal levels. Combined insulin and antioxidant therapies resulted in normalization of blood pressure, plasma MDA, tissue CML and nitrotyrosine without affecting glucose level or NOS expression. CONCLUSION: Oxidative stress in untreated diabetes is associated with down-regulation of NOS isoforms and increased ROS-mediated oxidation of lipid and glucose, but not NO. Amelioration of hyperglycemia with once-daily insulin administration alone results in up-regulation of NOS isoforms, reduction of lipid and glucose oxidation and increased NO oxidation. However, insulin plus antioxidant supplementation can normalize all three parameters.     

比较局麻与全麻对病人血清NOS及NO浓度的影响

目的　比较局麻与全身麻醉对手术病人血清一氧化氮合酶 (NOS)和一氧化氮 (NO)的影响。方法　根据不同麻醉方法将 2 0例颌面外科手术病人分为局麻组 (A组 )和静吸复合全麻组 (B组 ) ,每组 10例 ,在麻醉诱导前、手术切皮和手术开始后 1h抽取静脉血 3ml,分别测定血清NOS和NO浓度。结果　A组血清NOS及NO含量在切皮和术中 1h与术前比较显著增高 (P <0 0 5 ) ,B组血清NOS及NO含量在切皮和术中 1h与术前比较无显著增高 (P >0 0 5 ) ;在切皮和术中 1hB组NOS及NO含量比A组显著降低 (P <0 0 5 )。结论　静吸复合麻醉能明显抑制NOS的活性 ,降低NO的生成     

饮食中亚硝酸盐对大鼠肝缺血再灌注损伤的保护作用

目的 探讨饮食中亚硝酸盐对大鼠肝脏缺血再灌沣(I/R)损伤的保护作用.方法 Wistar 大鼠随机分为I/R组(对照组)、亚硝酸钠预处理组(实验组)和假手术组.建立大鼠肝脏部分I/R模型,实验组的饮水中加入少量亚硝酸盐并喂养7 d后建模,检测血清谷丙转氨酶(ALT)和谷草转氨酶(AST)的水平,测定肝组织中超氧化物歧化酶(SOD),丙二醛(MDA),一氧化氮(NO),一氧化氮合酶(NOS)含量及活性.用Hoechst染色法检测细胞凋亡,并观察各组病理形态学的改变.结果 对照组AST,ALT,MDA水平和细胞凋亡的程度均明显异常.实验组上述指标的异常变化均明显减轻,NO明显高于对照组,差异有统计学意义(P＜0.01);但NOS并未增多,与对照组差异无统计学意义.结论 饮食中的亚硝酸盐对大鼠肝脏I/R损伤有明显的保护作用.     

Propofol attenuates intestinal mucosa injury induced by intestinal ischemia-reperfusion in the rat

PURPOSE: We investigated whether propofol at a sedative dose can prevent intestinal mucosa ischemia/reperfusion (I/R) injury, and if propofol can attenuate oxidative stress and increases in nitric oxide (NO) and endothelin-1 (ET-1) release that may occur during intestinal I/R injury. METHODS: Rats were randomly allocated into one of five groups (n=10 each): (i) sham control; (ii) injury (one hour superior mesenteric artery occlusion followed by three hours reperfusion); (iii) propofol pre-treatment, with propofol given 30 min before inducing intestinal ischemia; (iv) simultaneous propofol treatment, with propofol given 30 min before intestinal reperfusion was started; (v) propofol post-treatment, with propofol given 30 min after intestinal reperfusion was initiated. In the treatment groups, propofol 50 mg x kg(-1) was administrated intraperitoneally. Animals in the control and untreated injury groups received equal volumes of intralipid (the vehicle solution of propofol) intraperitoneally. Intestinal mucosa histology was analyzed by Chiu's scoring assessment. Levels of lactic acid (LD), NO, ET-1, lipid peroxidation product malondialdehyde (MDA) and superoxide dismutase (SOD) activity in intestinal mucosa were determined. RESULTS: Histological results showed severe damage in the intestinal mucosa of the injury group accompanied by increases in MDA, NO and ET-1 and a decrease in SOD activity. Propofol treatments, especially pre-treatment, significantly reduced Chiu's scores and levels of MDA, NO, ET-1 and LD, while restoring SOD activity. CONCLUSION: These findings indicate that propofol attenuates intestinal I/R-induced mucosal injury in an animal model. The response may be attributable to propofol's antioxidant properties, and the effects of inhibiting over-production of NO and in decreasing ET-1 levels.     

大鼠小肠组织中一氧化氮在肠道淤血过程中作用的探讨

目的　探讨肝门阻断后小肠淤血状态下一氧化氮 (NO)在小肠循环调节中所起的作用和氧自由基在肠道损伤过程中的作用。方法　分别阻断肝十二指肠韧带 (B组 )、肝右静脉及其伴行动脉、胆管 (C组 )、肝头静脉及其伴行动脉、胆管 (D组 ) ,制成肠淤血动物模型。观察小肠壁及其相连系膜的变化。取空肠起始端以下长 8cm小肠制成组织匀浆 ,检测其中 NO、SOD、MDA含量。结果　 A(对照组 )、B、C、D组 NO、MDA测定值相互之间无显著差异 ;A、C、D组 SOD测定值相互之间无显著差异 ,B组 SOD测定值较其它组降低 ,与 A、C、D组相比均有显著差异 (P<0 .0 1 )。结论　 NO可能不是肝门阻断后肠微循环调节的主要因素。氧自由基在肝门阻断后小肠粘膜损伤中所起的作用可能不大 ,小肠粘膜损伤的内在机制有待进一步探讨     

Effects of vitamins E, A and D on MDA, GSH, NO levels and SOD activities in 5/6 nephrectomized rats

BACKGROUND: Excessive generation of reactive oxygen species (ROS) contributes to the process of progressive renal injury in a variety of clinical and experimental renal diseases. The present study was designed to test the hypothesis that treatment with vitamins decreases renal injury in chronic renal failure (CRF). METHODS: Forty male Sprague-Dawley rats were divided into 5 groups: group 1, control; group 2, 5/6 nephrectomy (CRF); other groups 5/6 nephrectomy and injected vitamins (E, A, D). After 8 weeks, urea, creatinine and renal tissue malondialdehyde (MDA), glutathione (GSH), nitric oxide (NO) levels and superoxide dismutase (SOD) activities were determined. RESULTS: Renal tissue MDA levels were significantly lower in the control and Vit E groups compared to that of the CRF, Vit A and Vit D groups. GSH levels were significantly higher in the control group compared to that of other groups. However, GSH levels were significantly lower in the control group than those in the other groups. SOD activities of the control group were significantly higher than those in the other groups. SOD activities were significantly decreased in the Vit E group compared to the Vit A and Vit D groups. Tissue NO levels of control group were significantly increased compared to the other groups. CONCLUSION: According to this study, Vit E may at least in part prevent tissue injury by acting as a free radical scavenger.     

卡托普利对缺血-再灌注鼠心肌一氧化氮及其合酶活性的影响

目的　研究一氧化氮 (NO)和一氧化氮合酶 (NOS)在心肌再灌注损伤中的作用 ,探讨卡托普利(captopril)对缺血 -再灌注鼠心肌保护的机制。　方法　采用 L angendorff离体鼠心灌流模型 ,将 18只 SD大白鼠随机分为 3组 (每组 6只 ) ,对照组、缺血 -再灌注组、卡托普利组。观察心肌 NOS同工酶活性、过氧化物歧化酶活性、丙二醛含量、肌酸激酶含量和冠脉流出液 NO的变化。　结果　缺血 -再灌注组与对照组比较心肌诱导型 NOS(i NOS)活性增高 (P<0 .0 0 1) ,而心肌原生型 NOS(c NOS)活性及总 NOS活性显著降低 (P<0 .0 0 1,0 .0 5 ) ,冠脉流出液 NO含量下降(P<0 .0 1)。卡托普利组再灌注 30分钟 ,心肌 i NOS活性低于缺血 -再灌注组 (P<0 .0 1) ,c NOS活性和总 NOS活性高于缺血 -再灌注组 (P<0 .0 1,0 .0 5 ) ,再灌注期间冠脉流出液 NO水平高于缺血 -再灌注组 (P<0 .0 1) ,心肌损伤较缺血 -再灌注组减轻。　结论　心肌 NOS同工酶活性及 NO产生的失常是心肌再灌注损伤的重要机制之一 ,卡托普利可通过调节心肌 NOS同工酶活性 ,维持正常的 NO水平 ,起到心肌保护作用。     

自由基清除剂治疗实验性大鼠慢性细菌性前列腺炎的研究

目的: 探讨自由基清除剂在慢性细菌性前列腺炎 (CBP)中的治疗作用。　方法: ①将 58只健康雄性SD大鼠随机分为正常对照组(10只)与实验组(48只),后者通过利用微创技术开腹在直视下前列腺局部注射大肠埃希菌制备CBP动物模型;②将实验组动物随机分为A、B、C、D4组,A组不经任何药物处理,B、C、D组分别予维生素C、柳氮磺胺吡啶(SASP)、维生素C+SASP治疗;③检测前列腺组织超氧化物歧化酶(SOD)活力、丙二醛 (MDA)含量。　结果: 维生素C能明显提高SOD的水平和降低MDA的水平。实验组与对照组、治疗组与未治疗组差异有显著性(P>0. 05),但治疗组之间差异无显著性(P<0. 05)。　结论: 自由基清除剂可能成为治疗CBP的一种新方法。     

L-精氨酸和氨基胍在大鼠肺移植缺血再灌注损伤中的作用

目的 观察L-精氨酸(L-Arg)和氨基胍对大鼠肺移植后缺血再灌注的保护作用.方法 建立大鼠左单肺移植模型,术后随机分为A组(对照组,腹腔注射生理盐水),B组(腹腔注射L-Arg)、C组(腹腔注射氨基胍)和D组(腹腔注射L-Arg和氨基胍),每组6只.移植肺再灌注2 h后,检测肺组织髓过氧化物酶(MPO)、丙二醛(MDA)含量、超氧化物歧化酶(SOD)活力、内皮型一氧化氮合酶(eNOS)和诱导型一氧化氮合酶(iNOS)活性并测定移植肺干湿重比(W/D)及静脉血中一氧化氮(NO)含量,观察移植肺的病理学形态.结果 再灌注2 h后,B组移植肺的W/D(5.10±0.21)、MPO(1.74±0.26)U/g和MDA(20.87±2.90)μmol/g均低于A组W/D(5.74 ±0.14)、MPO(2.36±0.32)U/g和MDA(31.33 ±3.46)μmol/g;SOD活性(424.29±27.86)U/mgprot、NO含量(175.12 ±17.40)μmol/L、iNOS活性(3.62 ±0.26)U/mgprot和eNOS活性(5.36±0.28)U/mgprot均较A组SOD活性(268.01±26.06)U/mgpro、NO含量(98.29±6.95)μmol/L、iNOS活性(2.53 ±0.22)U/mgprot和eNOS活性(3.57 ±0.40)U/mgprot高(P＜0.05).C组的NO含量(84.13±5.18)μmol/L、iNOS活性(1.81 ±0.09)U/mgprot均较A组低(P＜0.05).D组的W/D(4.79 ±0.19)、MPO(1.24±0.13)U/g、MDA(14.60±4.14)μmol/g、iNOS活性(1.99±0.17)U/mgprot低于A组,SOD活性(493.75±24.95)、NO含量(149.61±10.70)μmol/L、eNOS活性(5.50±0.27)U/mgprot高于A组(P＜0.05).与B组比较,D组的W/D、MPO、MDA、NO含量、iNOS活性降低,SOD升高(P＜0.05).病理形态学检查显示D组炎细胞浸润及渗出最轻,B组次之,A组和C组最差.结论 移植后再灌注早期应用L-Arg可减轻缺血再灌注损伤,应用氨基胍并不能减轻移植肺的损伤,但联合应用L-Arg和氨基胍优于单纯应用L-Arg.

Abstract：

Objective To investigate the effects of L-arginine (L-Arg) and aminoguanidine on ischemia-reperfusion injury following rat lung transplantation. Methods The models of rats lung transplantation were established and 4 groups ( n = 6 each) were randomly set up: group A ( normal control group)and treated groups B, C and D. In these groups, different medicines (NS, group A; L-Arg, group B;aminoguanidine, group C; L-Arg and aminoguanidine, group D) were intraperitoneally administered to the recipient rats before reperfusion. After reperfusion for 2 h, the lung graft was harvested for measurements of lung wet/dry ratio ( W/D ) , myeloperoxidase ( MPO ) , malondialdehyde ( MDA ) , superoxide dismutase (SOD) , endothelial nitric oxide synthase (eNOS) , inducible nitric oxide synthase (iNOS). The contents of plasma nitric oxide (NO) were determined. The pathological changes in the lung grafts were observed.Results After reperfusion for 2 h, W/D (5. 10 ±0.21), MPO (1.74 ±0.26) U/g, MDA (20.87 ±2. 90) μmol/g in group B were significantly lower [W/D (5. 74 ± 0. 14), MPO (2. 36 ± 0. 32) U/g,MDA (31. 33 ±3.46) μmol/g] (P ＜ 0. 05), and the levels of SOD (424. 29 ± 27. 86) U/mg protein,NO (175. 12 ± 17. 40) μmol/L, iNOS (3. 62 ±0. 26) U/mg protein and eNOS (5. 36 ±0. 28) U/mg protein were significantly higher than in group A [SOD (268.01 ±26.06) U/mg protein, NO (98.29 ±6.95) μmol/L, iNOS (2.53 ±0.22) U/mg protein and eNOS (3. 57 ±0.40) U/mg protein] (P＜0. 05). The contents of NO (84. 13 ±5. 18) μmol/L and iNOS (1. 81 ±0. 09) U/mg protein in group C were significantly lower than in group A (P ＜ 0. 05). W/D (4. 79 ± 0. 19) , MPO (1. 24 ± 0. 13 ) U/g,MDA (14. 60 ±4. 14) μmol/g, iNOS (1. 99 ±0. 17) U/mg protein were significantly lower than in group A (P ＜0. 05) , and SOD (493. 75 ±24. 95) , NO (149. 61 ± 10. 70) μmol/L and eNOS (5. 50 ±0. 27)U/mg protein in group D were significantly higher than in group A (P＜0. 05). W/D, MPO, MDA, NO and iNOS in group D were significantly reduced as compared with group B (P ＜ 0. 05 ) , and SOD was significantly increased in group B ( P ＜ 0. 05 ) . The pathological examination revealed that the inflammatory cell infiltration in group D was the mildest, followed by groups B, A and C. Conclusion The L-Arg could alleviate the lung ischemia-reperfusion injury after transplantation, the combined used of L-Arg and aminoguanidine could obtain better effects than L-Arg used alone. The aminoguanidine used alone could not alleviate ischemia-reperfusion injury after transplantation.