机械通气相关性肺损伤大鼠肺组织水通道蛋白5表达的变化

目的 评价机械通气相关性肺损伤大鼠肺组织水通道蛋白5(AQP5)表达的变化.方法 健康雄性SPF级SD大鼠70只,周龄7周,体重200～250 g,随机分为7组(n=10),对照组(A组)仅切开气管保留自主呼吸;不同通气时间小潮气量组(B_1组和B_2组)V_T 7 ml/kg,分别通气2 h或4 h;不同通气时间中潮气量组(C_1组和C_2组)V_T20 ml/kg,分别通气2 h或4 h;不同通气时间大潮气量组(D_1组和D_2组)V_T 40 ml/kg,分别通气2 h或4 h.A组在气管切开即刻,其余各组在机械通气结束时处死大鼠,开胸取肺组织行病理损伤评分,测定AQP5蛋白及其mRNA表达,计算肺组织湿/干重比值(W/D比值),收集肺泡灌洗液,计数中性粒细胞(PMN).结果 与A组比较,C_1组、C_2组、D_1组、D_2组AQP5蛋白及其mRNA表达下调,W/D比值、PMN计数和病理损伤评分升高(P＜0.05).与B_1组比较,C_1组和D_1组AQP5蛋白及其mRNA表达下调,W/D比值、PMN计数和病理损伤评分升高(P＜0.05).与B_2组比较,C_2组和D_2组AQP5蛋白及其mRNA表达下调,W/D比值、PMN计数和病理损伤评分升高(P＜0.05).与C_1组比较,D_1组AQP5蛋白及其mRNA表达下调,W/D比值、PMN计数和病理损伤评分升高(P＜0.05).与C_2组比较,D_2组AQP5蛋白及其mRNA表达下调,W/D比值、PMN计数和病理损伤评分升高(P＜0.05).结论 AQP5表达下调参与了机械通气诱发大鼠肺水肿的发生.     

靶向小干扰RNA对小鼠肺缺血/再灌注损伤时细胞凋亡及CCAAT/增强子结合蛋白同源蛋白的作用

目的 观察靶向小干扰RNA (siRNA)对小鼠肺缺血/再灌注损伤(PIRI)时细胞凋亡及CCAAT/增强子结合蛋白同源蛋白(CHOP)的影响.方法 荧光标记法观察靶向siRNA在小鼠体内的分布并评估转染效率.C57BL/6J小鼠50只,随机分为5组(n=10):假手术组(Sham组)、缺血/再灌注组(I/R组)、I/R+载体组(VR+ Vehicle组)、I/R+阴性对照组(I/R+ Control-siRNA组)和I/R+ CHOP-siRNA组(I/R+ CHOP-siRNA组).取左肺,检测肺湿/干重比(W/D)、总肺水含量(TLW)和肺泡损伤定量评估(IQA),光镜和电镜观察肺组织结构改变,逆转录-聚合酶链反应(RT-PCR)、Western blot检测CHOP、葡萄糖调节蛋白78 (GRP78) mRNA和蛋白表达水平,原位末端转移酶标记(TUNEL)法检测细胞凋亡指数(AI).结果 靶向siRNA通过滴鼻法可有效分布于肺脏中.与Sham组比较,I/R组中CHOP、GRP78 mRNA和蛋白表达水平(0.80±0.03、0.80±0.02;0.80±0.04、0.84±0.02)均升高(P ＜0.05),W/D(5.24±0.49)、TLW(4.24 ±0.49)、IQA[(42.80 ±4.21)％]和AI[(34.50±1.51)％]均明显增加(P＜0.01)；肺组织形态结构发生明显损伤；与I/R+ Vehicle组和I/R+ Control-siRNA组比较,I/R+ CHOP-siRNA组中GRP78 mRNA和蛋白表达水平(0.84±0.04、0.85±0.04)无明显变化(P＞0.05),而CHOP mRNA和蛋白表达水平(0.40±0.03、0.44±0.04)均降低(P＜0.05),W/D(2.54±0.24)、TLW(1.54±0.24)、IQA[(16.71±2.33)％]和AI[(11.50±1.58)％]亦均降低(P＜0.01)；肺组织形态结构损伤减轻.结论 靶向siRNA对I/R损伤肺具有良好的保护作用,其机制可能与其对抗过度的未折叠蛋白反应(UPR)中CHOP介导的细胞凋亡有关.     

线粒体ATP敏感性钾通道阻断剂对在体大鼠肺缺血后处理的作用及其机制

目的 探讨缺血后处理(IPO)对大鼠在体肺缺血-再灌注损伤(I/R)的保护作用及线粒体ATP敏感性钾通道(mitoKATP)在缺血后处理效应中的作用.方法 将Wistar大鼠35只随机分为5组:假手术组(Sham组)、缺血再灌注损伤组(I/R组)、缺血后处理组(IPO组)、缺血再灌注损伤+5-羟基葵酸盐组(I/R+5-HD组)、缺血后处理+5-羟基葵酸盐组(IPO+5-HD组).观察各组肺组织中丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性、湿/干比值(W/D)以及病理形态学改变.结果 I/R组与Sham组比较MDA含量增加[(5.07±1.60)nmol/mg prot比(1.43±0.41)nmol/mgprot,P＜0.01],SOD活性减低[(12.38±2.24)U/mg prot比(45.51±5.42)U/mg prot,P＜0.01],W/D比值增高(5.45±0.82比3.05±0.47,P＜0.01),肺组织形态及超微结构明显受损;IPO+5-HD组与IPO组比较MDA含量增加[(3.74±0.71)nmol/mg prot比(2.60±0.43)nmol/mg prot,P＜0.01],SOD活性减低[(22.91±2.71)U/mg prot比(28.74±2.03)U/mg prot,P＜0.01],W/D比值增高(4.64±0.79比3.89±0.60,P＜0.01),肺组织形态及超微结构明显受损;IPO组与I/R组比较,肺组织MDA含量减少[(2.60±0.43)nmol/mg prot比(5.07±1.60)nmol/mg prot,P＜0.01],SOD活性增高[(28.74±2.03)U/mg prot比(12.38±2.24)U/mg prot,P＜0.01],W/D比值减低(3.89±0.60比5.45±0.82,P＜0.01),肺组织病理形态学改变轻于I/R组;I/R+5-HD组与I/R组比较,肺组织MDA含量[(5.14±1.30)mol/mg prot比(5.07±1.60)mol/mg prot,P＞0.05)、SOD活性[(11.65±1.82)U/mg prot比(12.38±2.24)U/mg prot,P＞0.05]、W/D比变化(5.54±0.61比5.45±0.82),差异无统计学意义(P＞0.05),肺组织病理形态学改变无明显差异.IPO+5-HD组的各项指标介于IPO组和I/R组之间.结论 缺血后处理能减轻大鼠在体肺缺血再灌注损伤,mitoKATP参与了肺缺血后处理效应.

Abstract：

Objective To investigate the protective effect of ischemic postconditioning (IPO) on lung ischemic reperfusion (L/R) in rats in vivo and the mechanism of mitochondrial ATP-sensitive potassium channel (mitoKATP) blocker in the ischemic postconditioning. Methods Thirty five Wistar rats were randomly divided into 5 groups: sham group, I/R group, ischemic postconditioning (IPO) group, I/R +5-hydroxydecanoate (I/R + 5-HD) group, IPO + 5-HD group. The concentration of malondialdehyde (MDA) and activity of superoide dismutase (SOD) were determined in the lung homogenate, wet to dry weight ratio (W/D) was measured and pathological changes were also observed. Results The levels of MDA[(5.07±1.60) vs (1.43 ±0.41) nmol/mg prot,P＜0. 01]and W/D (5.45 ±0.82 vs 3.05 ±0. 47,P ＜0. 01 ) were increased significantly in I/R group as compared with sham group, while the activity of SOD[( 12. 38 ±2. 24) vs (45.51 ±5.42) U/mg prot,P ＜0. 01]was decreased, and the injury of lung tissues was significantly aggravated in IPO + 5-HD group as compared with IPO group[MDA: (3.74 ±0. 71 ) nmol/mg prot vs (2. 60 ± 0. 43 ) nmol/mg prot , P ＜ 0. 01]; W/D: 4. 64 ± 0. 79 vs 3. 89 ± 0. 60,P＜0.01; SOD:[(22.91 ±2.71) U/mg prot vs (28.74±2.03) U/mg prot,P＜0. 01]. The levels of MDA[(2.60±0.43) vs (5.07 ±1.60) nmol/mg prot,P＜0. 01]and W/D (3.89 ±0.60 vs 5.45 ±0. 82,P ＜0. 01 ) were decreased significantly in IPO group as compared with I/R group, the activity of SOD[(28.74±2.03) vs (12.38 ±2.24) U/mg prot,P＜0. 01]increased and lung tissue histological damage attenuated. The difference in MDA[(5.14 ± 1.30) vs (5.07 ± 1.60) nmol/mg prot, P ＞ 0. 05],W/D (5.54±0.61 vs5.45 ±0.82,P＞0.05) and SOD[(11.65 ±1.82) vs (12.38 ±2.24) U/mgprot,P ＞ 0. 05]levels had no statistical significance between I/R + 5-HD group and I/R group, and the injury of lung tissues had no significant difference too. Each index in IPO + 5-HD group was between IPO and I/R groups. Conclusion Ischemic postconditioning can attenuate the lung I/R injury, and mitoKATP plays a vital role in the protective procession of ischemic postconditioning on lung ischemic reperfusion.     

缺血再灌注预处理对血浆MDA、SOD及脊髓AQP4 mRNA的表达影响

目的 探讨腹主动脉缺血预处理对再灌注不同时问血浆丙二醛(MDA)、超氧化物歧化酶(SOD)及脊髓组织中水通道蛋白4(AQP4) mRNA表达的影响.方法 将54只体质量189 ～ 207 g雌雄不拘的SD大鼠随机分为假手术组(Sham组)、缺血再灌注组(I/R组)和缺血预处理组(IPC组)3组.采用肾下腹主动脉阻断法,建立脊髓缺血再灌注模型;Sham组6只,手术开始步骤同其他两组,但不作肾下腹主动脉阻断即缝合伤口;I/R组24只,直视下采用动脉夹夹闭腹主动脉段左肾动脉分支起始处下方5 mm处(即肾动脉后型),仅阻断腹主动脉60 min后开放灌注;而IPC组24只,先阻断腹主动脉5min,开放5 min,再阻断60 min后开放灌注.再灌注后12h、1、2、5、10天分别进行神经功能评分,同时观察大鼠血浆MDA、SOD指标的水平,以及预处理对脊髓AQP4 mRNA表达的影响.结果 54只大鼠术后全部存活,I/R组行为学评分降低(P＜0.01),IPC组的神经功能评分在再灌注5天内均高于I/R组(P＜0.01),随着再灌注时间的延长行为学评分逐渐增加.I/R组血浆SOD水平仅在再灌注1天时较Sham组显著下降,随时间延长SOD水平逐渐升高与Sham组无差异,血浆各时间点MDA水平比Sham组低(P ＜0.05);IPC组SOD、MDA水平与Sham组比较没有差异.I/R组再灌注2天时AQP4mRNA表达显著增高(P＜0.01),之后降低至与Sham组无差异;IPC组在再灌注1天时即出现AQP4 mRNA表达明显升高(P＜0.05),之后表达逐渐降低,第5天时与Sham组无差异.IPC AQP4mRNA峰值明显低于I/R组(P＜0.01).结论 大鼠腹主动脉缺血再灌注的预处理IPC可能通过减轻由缺血再灌注造成的全身氧化应激反应和下调AQP4mRNA的表达,进而保护脊髓组织.     

雾化吸入利多卡因对哮喘大鼠肺组织水通道蛋白5含量及白细胞介素-13表达的影响

目的 观察雾化吸入利多卡因对大鼠支气管哮喘模型肺组织中水通道蛋白5(AQP5)表达及血清中白细胞介素-13(IL-13)浓度的影响.方法 Wistar大鼠32只,随机均分为四组:哮喘组(A组)、地塞米松组(D组)、利多卡因组(L组)和对照组(C组).A组用鸡卵清蛋白辅以氢氧化铝为佐剂注射致敏,2周后雾化吸入鸡卵清蛋白诱发哮喘.D组、L组大鼠用同样方法致敏,但在激发前分别雾化吸入0.02%地塞米松和0.04%利多卡因20 min.C组用生理盐水代替鸡卵清蛋白进行注射和吸入.末次雾化吸入后24 h内采集静脉血,测定血清中IL-13的浓度;取肺组织,计算湿干重比(W/D),观察AQP5表达及肺组织病理学结果.结果 与C组相比,A组肺组织AQP5表达降低,血清IL-13浓度及W/D增高(P＜0.05);与A组相比,D、L组肺组织AQP5表达增高,血清中IL-13的浓度及W/D降低(P＜0.05).A组肺组织呈支气管壁增厚、炎性细胞浸润表现,D、L组病理损伤程度减轻.结论 利多卡因雾化吸入可通过增加肺组织AQP5的表达,降低血清IL-13的浓度,减轻致敏原所激发的哮喘大鼠气道炎症.     

辛伐他汀预处理对肢体缺血再灌注诱发肺损伤大鼠肺组织血红素加氧酶-1表达的影响

目的 评价辛伐他汀预处理对肢体缺血再灌注诱发肺损伤大鼠肺组织血红素加氧酶-1(HO-1)表达的影响.方法 成年雄性SD大鼠48只,体重250～300 g,采用随机数字表法,将大鼠随机分为6组(n=8):假手术组(S组)、肢体缺血再灌注组(IR组)、辛伐他汀1、5、10 mg/kg组(S1组、S2组、S3组)和辛伐他汀对照组(SC组).采用夹闭股动脉2 h,再灌注3 h的方法制备肢体缺血再灌注模型.S组:仅分离股动脉和股静脉,不夹闭;IR组:制备肢体缺血再灌注模型;S1组、S2组、S3组:分别将辛伐他汀1、5、10 mg/kg溶于1 ml蒸馏水,于每13清晨灌胃1次,连续灌胃3 d后制备肢体缺血再灌注模型;SC组:辛伐他汀10 mg/kg溶于1 ml蒸馏水,于每日清晨灌胃1次,连续灌胃3 d.再灌注3 h时取颈动脉血样,行血气分析,记录PaO2和PaCO2,随后处死大鼠,取肺组织,观察病理学结果,计算湿重/干重比(W/D比),测定SOD活性,计数PMN,测定HO-1 mRNA及其蛋白的表达水平.结果 与S组比较,IR组PaO2及PaCO2降低,IR组、S1组和S2组肺组织W/D比和PMN计数升高,SOD活性降低(P＜0.05),S3组和SC组上述指标差异无统计学意义(P＞0.05),IR组、S1组、S2组、S3组和SC 组肺组织H0-1 mRNA及其蛋白表达上调(P＜0.01);与IR组比较,S1组、S2组和S3组PaO2、PaCO2及肺组织SOD活性升高,肺组织W/D比和PMN计数降低,肺组织HO-1 mRNA及其蛋白表达上调(P＜0.05或0.01);S1组、S2组和S3组肺组织WID比和PMN计数依次降低,SOD活性依次升高,HO-1 mRNA及其蛋白表达依次上调(P＜0.05或0.01).S1组、S2组和S3组肺组织病理性损伤较IR组减轻.结论 辛伐他汀预处理可上调肢体缺血再灌注大鼠肺组织HO-1的表达,从而产生肺保护作用,且呈剂量依赖性.

Abstract：

Objective To investigate the effects of simvastatin preconditioning on the pulmonary heme oxygenase-1 (HO-1) expression in rats with lung injury induced by ischemia-reperfusion (I/R) of hind limbs. Methods Forty-eight adult male SD rats weighing 250-300 g were randomly divided into 6 groups ( n = 8 each) : sham operation group (group S) ; I/R group; I/R + simvastatin 1,5, 10 mg/kg groups (S1 , S2, S3 groups) ; simvastatin control group (group SC) . I/R of hind limbs was produced by occlusion of bilateral femoral arteries for 2 h followed by 3 h reperfusion. Croups S1 , S2 , S3 received simvastatin 1, 5, 10 mg/kg respectively via an oro-gastric tube for 3 days before I/R. Group SC received simvastatin 10 mg/kg via an oro-gastric tube for 3 days. Arterial blood samples were taken at 3 h of reperfusion for blood gas analysis and PaO2 and PaCO2 were recorded. The animals were then sacrificed and the lungs removed immediately for pathologic examination and determination of the wet/dry lung weight ratio (W/D ratio), superoxide dismutase (SOD) activity and polymorphonuclear neutrophil (PMN) count . Hie expression of HO-1 mRNA and protein in lung tissues was detected using RT-PCR and Western blot analysis respectively.Results Alveolar edema, localized pulmonary atelectasis and large amount of PMN infiltration were found in I/R group and were ameliorated in S1, S2, S3 groups. Compared with group S, PaO2 and PaCO2 were significantly decreased in I/R group, W/D ratio and PMN count were increased and SOD activity was significantly decreased in I/R, S1 , S2 groups, and expression of HO-1 mRNA and protein was up-regulated in the other five groups ( P ＜ 0.05). PaO2, PaCO2 and SOD activity were significantly increased, W/D ratio and PMN count were significantly decreased, and HO-1 mRNA and protein expression was up-regulated in S1, S2 and S3 groups as compared with I/R group ( P ＜ 0.05 or 0.01). W/D ratio and PMN count were gradually decreased, SOD activity was gradually increased, and HO-1 mRNA and protein expression was gradually up-regulated in S1, S2 and S3 groups. Conclusion Simvastatin preconditioning has protective effect against lung injury induced by I/R of hind limbs in rats through up-regulation of HO-1 expression in the lung tissues and in a dose-dependent manner.     

急性胰腺炎肺损伤大鼠肺组织肿瘤坏死因子受体-1与窖蛋白-1的表达及清胰汤的治疗作用

目的 观察肿瘤坏死因子受体-1(TNFR-1)和窖蛋白-1(Cav-1)在急性胰腺炎肺损伤大鼠肺组织的表达及功能,探讨清胰汤的可能作用机制.方法 Wistar大鼠随机分为假手术组、模型组、地塞米松治疗组、清胰汤治疗组.经胰胆管逆行注射脱氧胆酸钠建立大鼠急性胰腺炎肺损伤模型.24 h后采血和肺组织,检测血清淀粉酶、肺湿/干重比值和肺组织病理切片判定损伤程度;放免法检测血清肿瘤坏死因子-α(TNF-α)水平;逆转录-聚合酶链反应(RT-PCR)和Western blot分别检测肺组织中TNFR-1和Cav-1的mRNA及蛋白表达.结果 模型组血清淀粉酶、肺湿/干重比值、血清TNF-α(4.82±0.14比2.96±0.30,P＜0.01)和肺组织病理损伤程度均明显升高;肺组织TNFR-1的mRNA表达上调(1.29±0.15比0.43±0.05,P＜0.01),而Cav-1的mRNA表达则下调(1.14±0.10比2.00±0.10,P＜0.01);脂筏内外表达的TNFR-1均升高,尤以脂筏内升高明显,而Cav-1则表达下降.与模型组比较,地塞米松和清胰汤组的血清淀粉酶、肺湿/干重比值、血清TNF-α(地塞米松组:3.79±0.11,清胰汤组:3.66±0.10,模型组:4.82±0.14,P＜0.01)和肺组织病理损伤程度均下降;肺组织TNFR-1的mRNA表达下降(地塞米松组:0.48±0.01,清胰汤组:0.49±0.02,模型组:1.29±0.15,P＜0.01),而Cav-1的mRNA则表达升高(地塞米松组:1.66±0.06,清胰汤组:1.52±0.04,模型组:1.14±0.10,P＜0.01);脂筏内外表达的TNFR-1均下降,而Cav-1则上升.结论 TNF-α/TNFR-1的表达增加和Cav-1表达的下降与急性胰腺炎肺损伤密切相关.地塞米松和清胰汤都能够明显降低TNFR-1的表达并上调Cav-1的表达,有效减轻肺损伤程度,这可能是清胰汤治疗急性胰腺炎肺损伤的作用机制之一.     

环腺苷酸-蛋白激酶A在大鼠内毒素性急性肺损伤时血红素加氧酶-1表达上调中的作用

目的 探讨环腺苷酸-蛋白激酶A(cAMP-PKA)在大鼠内毒素性急性肺损伤时血红素加氧酶-1(HO-1)表达上调中的作用.方法 健康清洁级雄性SD大鼠48只,体重180 ～ 220 g,2.5 ～ 3.0月龄,采用随机数字表法,将大鼠随机分为4组(n=12)∶正常对照组(C组)股静脉注射生理盐水(LPS溶媒)0.5 ml,2h后皮下注射生理盐水(H89溶媒)0.5 ml;内毒素性急性肺损伤组(ALI组)股静脉注射10 mg/kg LPS 0.5 ml,2h后皮下注射生理盐水0.5 ml; H89+内毒素性急性肺损伤组(H+ALI组),股静脉注射10 mg/kg LPS 0.5 ml,2h后皮下注射5 mg/kg H89 0.5 ml; H89组(H组)股静脉注射生理盐水0.5 ml,2h后皮下注射5 mg/kg H89 0.5 ml.静脉注射LPS后6h时处死大鼠,取肺组织,行病理学评分,测定肺组织含水量;采用Western blot法测定HO-1和PKA表达;采用荧光定量PCR法测定HO-1mRNA表达.结果 与C组比较,ALI组和H+ALI组肺组织含水量和病理学评分升高,肺组织PKA、HO-1和HO-1 mRNA表达上调(P＜0.05),H组上述各指标差异无统计学意义(P＞0.05);与ALI组比较,H+ALI组肺组织含水量和病理学评分升高,肺组织PKA、HO-1和HO-1 mRNA表达下调(P＜0.05).结论 大鼠内毒素性急性肺损伤时HO-1表达上调的机制与cAMP-PKA信号通路活化有一定关系.     

远隔肢体缺血预处理对兔单肺缺血-再灌注损伤细胞凋亡的影响

目的 从细胞凋亡的角度探讨远隔肢体缺血预处理影响兔肺缺血-再灌注(I-R)损伤的可能机制.方法 18只日本大耳白兔随机均分为三组:缺血-再灌注组(I-R组)、肢体缺血预处理组(R组)、假手术组(S组).建立兔在体左肺缺血-再灌注(I-R)损伤模型.通过采用脱氧核苷酸末端转移酶介导的DNA原位末端缺口标记技术(TUNEL)检测再灌注3 h时凋亡指数(AI)的变化,予Westernblotting检测肺组织中Bcl-2、Bax蛋白的表达情况.结果 与S组比较,I-R组肺组织细胞凋亡指数和Bax蛋白显著增高(P＜0.01),而Bcl-2蛋白含量显著降低(P＜0.01),Bcl-2/Bax比值降低(P＜0.05).R组细胞凋亡指数和Bcl-2蛋白表达明显高于I-R组(P＜0.01),而Bax蛋白的含量明显低于I-R组(P＜0.05),Bcl-2/Bax比值增高(P＜0.05).结论 远隔肢体缺血预处理可上调肺组织Bcl-2蛋白,下调Bax蛋白表达,增加Bcl-2/Bax比值,抑制肺组织细胞凋亡,从而对肺缺血-再灌注损伤起到保护作用.     

Enhancement of lung preservation by prevention of lung collapse

Previous investigations of important factors in lung preservation have stressed the importance of denervation and ischemia as deterimental factors. We believe that lung collapse below the level of functional residual capacity during preservation also decreases the ability of the transplanted lung to provide total pulmonary function.To validate this assumption, four groups of five dogs each were studied utilizing the in vivo isolated lung preparation. This preparation simulates autotransplantation but avoids the attendant time-consuming anastomoses which markedly increase collapse time. In Group I, the isolated ischemic lungs were ventilated for 3 hr with the chest open, thus allowing total collapse of the lung with each respiratory cycle. Subsequently, circulation was restored, the contralateral pulmonary artery was ligated, and the chest was closed for chronic survival. Groups II, III, and IV differed only in that the chest was closed during ischemic periods of 3, 4, and 5 hr, respectively, thus preventing lung collapse below FRC. No dogs survived in Group I. Chronic survivors in Groups II, III, and IV numbered three, two, and one, respectively, supporting the contention that prevention of lung collapse below FRC enhances the ability of lung grafts to assume total respiratory function after implantation.We believe that the prevention of collapse is a much more critical factor in lung preservation than is lung ischemia. So long as collapse time during harvesting, implantation, and the so-called preservation period is less than 30–60 min, one may be able consistently to preserve a lung, under conditions of normothermic ischemia with ventilation above FRC, for 3 hr, with occasional satisfactory preservation up to 5 hr.Failure to minimize lung collapse during the preservation period and during harvesting and implantation may mean the difference between survival and death in lung allograft recipients.     

正常肺组织和肺癌组织激光诱发自体荧光光谱

目的　分析正常肺组织和肺癌组织的激光诱发自体荧光光谱 ,特征 ,探讨激光诱发自体荧光光谱区分正常肺组织和肺癌组织的可行性。方法　收集肺癌手术标本 39例 ,使用三倍频YAG激光(波长 35 5nm)和光学多道分析仪 (OMA)测定肺癌组织和正常肺组织的激光诱发荧光光谱 ,寻找其自体荧光光谱特征并与病理结果比较。结果　 (1)正常肺组织和肺癌组织的主峰位置不同 [(471 6± 5 2 )nm对 (46 1 9± 4 3)nm],向右偏移 (P <0 0 0 1) ;(2 )肺癌组织的相对荧光强度大于正常肺组织 [(2 42 2 7± 434 9)对 (1485 4± 46 2 1) ](P <0 0 0 1) ;(3)正常肺组织在 5 6 0nm及 6 0 0nm处有 2个次峰 ,而肺癌组织平滑下降 ,正常肺组织在 5 80nm与 6 0 0nm的荧光强度比为 0 831± 0 178;肺癌为 1 2 6 9± 0 147(P <0 0 0 1)。结论　正常肺组织和肺癌组织的激光诱发自体荧光光谱有明显区别 ,可用于区分二者。     

Outcomes of extended donor lung recipients after lung transplantation

BACKGROUND: Lung transplantation is currently limited by the number of suitable donor organs. Many lung-transplant programs use lungs that do not meet the formal criteria for acceptability; however, the immediate and long-term consequences of this approach remain unclear. METHODS: We performed a retrospective cohort study of all patients who underwent lung transplantation at the Columbia University Medical Center from July 2001 to July 2003. We assessed the outcomes of recipients of extended donor lungs compared with those of recipients of optimal donor lungs after adjusting for confounding variables. RESULTS: Fifty-one patients underwent lung transplantation, of which 27 (53%) received extended donor lungs. Recipients of extended donor lungs had fewer intensive care unit-free days at 30 days (P=0.002) and a longer time to hospital discharge (P=0.007) than did recipients of optimal donor lungs. Extended donor recipients also had lower forced expiratory volume in 1 second % predicted at 1 year than did optimal donor recipients (P=0.03). There were no differences in the 30-day or longer-term survival of extended and optimal donor lung recipients. CONCLUSIONS: Recipients of extended donor lungs have a longer intensive care unit course, a prolonged hospital stay, and lower pulmonary function at 1 year than recipients of optimal lungs. Despite these differences, survival is similar between the two groups. The criteria for the optimal lung donor should be re-evaluated considering the current shortage of acceptable organs. Although some outcomes may differ with the use of extended donor lungs, the clinical impact of these differences should be assessed in future prospective multicenter studies.     

Technical evaluation of video-assisted lung resection for lung cancer

There are two major problems including indications and techniques in video-assisted lung resection for lung cancer. The current technique of video-assisted lung resection have various troublesome procedures as compared with conventional open thoracic surgery. We have designed a new thoracoscopic instrument as a ligation device. Between September 1997 and August 1999, 15 patients with early lung cancer underwent video-assisted lobectomy (VAL). In 5 patients, VAL was performed through skin incisions of 3 cm using this new device and at extraction of the resected lung the skin incision was elongated minimally (Group A). In 10 patients, a skin incision of 6-8 cm was made enough to perform VAL without the new device at the beginning of the operation (Group B). Total length of skin incisions (TLS) and total postoperative pleural discharge (TPD) were measured. TLS was 7.2 +/- 1.47 cm in group A, 11.9 +/- 4.50 cm in group B (p = 0.029). TPD was 492 +/- 256 ml in group A, 1.132 +/- 591 ml in group B (p = 0.032). TPD might be thought as an index of invasion of VAL and it was difficult to decrease TPD significantly. The new device made it possible to feel the ligature tension when the device was in touch with the chest wall. In a result, the device improved technical procedure of VAL and contributed toward less invasive surgery.     

Pressure-volume curve of the remaining lung after lung resection

In order to evaluate ventilatory function of the remaining lung after lobectomy, using dogs, we measured the pressure-volume curve of the right lower lobe separately from the other lobes. The right lower lobe bronchus was surgically separated from the other bronchi and the expiratory volume of the right lower lobe was measured independently. The dogs were put in an airtight box. Transpulmonary pressure and expiratory volume in the right lower lobe were measured before lobectomy, after the left upper lobectomy and subsequently after the right upper and middle lobectomy. As a result, the esophageal pressure at endoexpiratory state became more subatmospheric following the lobectomies and the pressure-volume curves of right lower lobe shifted down to the right. Though the right lower lobe was intact after surgery, the pressure-volume curve shifted. This might be caused by the imbalanced postoperative volume of the lung and thoracic cage, and it is one of the problems remaining after lobectomy.