内源性硫化氢在慢性阻塞性肺疾病患者中的变化及意义

目的研究内源性硫化氢(H2S)在慢性阻塞性肺疾病(COPD)发病中的作用。方法COPD急性加重组(AECOPD组)27例、稳定期COPD组37例和健康对照组13名,在入选时测定血清H2S和一氧化氮(NO)水平、肺功能、诱导痰细胞分类计数,对AECOPD患者行超声心动图和血气分析。结果(1)血清H2S水平稳定期COPD组[(50·8±2·5)μmol/L]比健康对照组[(39·8±1·6)μmol/L]、AECOPD组[(33·5±2·2)μmol/L]均显著增加(P均<0·01)。(2)AECOPD组吸烟者血清H2S[(28·1±1·3)μmol/L]比非吸烟者[(39·4±3·9)μmol/L,P<0·05]和健康非吸烟者显著降低[(39·8±1·6)μmol/L,P<0·01]。(3)稳定期COPD组不同程度气流阻塞患者血清H2S水平呈线性下降趋势(P<0·05),COPD全球创议(GOLD)Ⅲ期[(45·1±4·1)μmol/L]较Ⅰ期患者[(70·2±6·2)μmol/L]血清H2S水平显著下降(P<0·05)。(4)AECOPD组伴有肺动脉高压患者血清H2S水平显著降低[(26·3±2·2)、(36·2±2·5)μmol/L,P<0·05]。(5)血清H2S与NO、第一秒用力呼气容积占预计值百分比(FEV1占预计值%)、诱导痰淋巴细胞计数、诱导痰巨噬细胞计数均呈正相关(r=0·278~0·533,P均<0·05或0·01),与肺动脉收缩压(PASP)、诱导痰中性粒细胞计数均呈负相关(r=-0·561、-0·422,P=0·011、0·001)。结论内源性H2S可能参与COPD气流阻塞的发病,作为一种无创指标监测疾病严重程度和活动度具有一定意义。     

哮喘患者白细胞介素(IL)-12和IL-13的变化及糖皮质激素对其的影响

目的　观察哮喘患者血清中白细胞介素 (IL) 12和IL 13水平的变化及糖皮质激素对其的影响。方法　采用ELISA法分别检测中度哮喘急性发作期患者 (2 5例 )口服泼尼松治疗 1周前后、缓解期患者 (2 0例 )和健康对照组者 (15例 )血清中IL 12和IL 13水平 ,并同时测 1秒钟用力呼气容积(FEV1)占预计值的百分比和气道阻力 (R5)占预计值的百分比。结果　IL 12水平急性发作期治疗前[(5 8 5± 14 2 )ng/L]较缓解期 [(71 3± 16 2 )ng/L]为低 (P <0 0 5 ) ,与健康对照组 [(85 5± 13 1)ng/L]、急性发作期治疗后 [(79 3± 19 1)ng/L]比较 ,差异均有显著性 (P <0 0 1)。IL 13水平急性发作期治疗前 [(131 3± 2 8 4 )ng/L]较缓解期 [(113 1± 2 6 5 )ng/L]为高 (P <0 0 5 ) ,与健康对照组 [(92 3± 14 4 )ng/L]、急性发作期治疗后 [(84 1± 19 8)ng/L]比较 ,差异均有显著性 (P <0 0 1)。FEV1占预计值的百分比下降和R5占预计值的百分比升高 (P <0 0 1)。直线相关分析表明 ,血清中IL 12与FEV1占预计值的百分比呈正相关 (r=0 4 85 ,P <0 0 5 ) ,与R5占预计值的百分比呈负相关 (r =- 0 5 16 ,P<0 0 5 ) ,与IL 13呈负相关 (r =- 0 5 4 9,P <0 0 1) ;IL 13与FEV1占预计值的百分比呈负相关 (r =- 0 4 93,P <     

一氧化碳体系对慢性肺心病大鼠肺血管结构重建的抑制作用

目的　研究内源性一氧化碳体系对慢性肺心病肺血管结构重建的调控作用。方法　将36只SD大鼠随机分为正常对照组 (A组 )、4周低O2 高CO2 组 (B组 ) ,4周低O2 高CO+ 2 血晶素组 (C组 ) ,每组 12只。测定各组大鼠肺动脉平均压 (mPAP)、右心室 / (左心室 +室间隔 )重量比 [RV/ (LV +S) ]、肺细小动脉显微和超微结构、血CO浓度、血清及肺组织匀浆上清液血红素氧合酶 1(HO 1)活性和肺细小动脉HO 1及其基因表达的变化。结果　 (1)B组mPAP为 (2 0 1± 0 8)mmHg(1mmHg =0 .133kPa)、RV/ (LV +S)为 (35 5± 1 7) %、与A组 [(15 3± 1 4 )mmHg、(2 6 7± 1 7) % ]及C组[(16 5± 3 7)mmHg、(30 2± 1 6 ) % ]比较差异有显著性 (P均 <0 0 1)。 (2 )B组肺细小动脉血管结构重建的显微形态测定指标与A、C组比较差异也有显著性 (P <0 0 1)。 (3)B组全血CO含量、血清及肺组织匀浆HO 1活性、肺细小动脉HO 1及其mRNA分别为 (2 1± 0 9) %、(73± 18)nmol·L-1·h-1、(175 1± 311)pmol·mg-1·h-1、0 191± 0 0 12和 0 30 1± 0 0 17,与A组 [(0 5± 0 3) %、(2 5± 8)nmol·L-1·h-1、(385± 4 6 )pmol·mg-1·h-1、0 0 5 9± 0 0 0 5、0 131± 0 0 11]和C组 [(4 9± 2 1) %、(132±39)nmol·L-1·h-1     

妊娠对乙型肝炎肝郁脾虚型患者血清细胞因子浓度的影响及临床意义

目的 :探讨妊娠对慢性乙型肝炎 (乙肝 )肝郁脾虚型患者血清白细胞介素 - 10、12 (IL - 10、IL - 12 )、γ-干扰素 (IFN-γ)浓度的影响及临床意义。方法 :用酶联免疫法 (EL ISA)检测孕期和非孕期患者 IL - 10、IL - 12及 IFN -γ血清浓度 ,并作同期肝功能指标检查。患者分为早孕期 (2 6例 )、晚孕期 (32例 )、非孕期 (31例 ) 3组。 2 0例非孕期健康者为对照组。结果 :早孕期组 IL - 10水平 [(2 6 .0± 9.8) ng/ L ]较非孕期组 [(18.0± 1.3) ng/ L ]升高 (P <0 .0 5 ) ,而与对照组 [(2 9.4± 5 .1) ng/ L ]相近 (P >0 .0 5 )。IL - 12、IFN -γ分别为 (5 4 .1± 2 6 .0 ) ng/ L和 (45 .5± 17.3) ng/ L ,较对照组 [(8.2± 2 .1) ng/ L、(2 4 .5± 6 .1) ng/ L ]和非孕期组 [(8.0± 2 .7) ng/ L、(16 .7± 3.7) ng/ L ]均明显升高 (均P <0 .0 1)。晚孕期组与其他各组比较 ,IL - 10 [(9.4± 1.9) ng/ L ]明显下降 (P <0 .0 1) ,但 IL - 12 [(16 6 8.0± 318.2 )ng/ L ]、IFN -γ[(46 1.0± 10 3.3) ng/ L ]显著升高。结论 :妊娠可使慢性乙肝肝郁脾虚型患者血清 IL - 12、IFN-γ浓度升高 ,在晚孕期表现更为明显。     

体位改变对急性肺损伤兔肺功能与CT及病理的影响

目的　通过观察不同体位下急性肺损伤 (ALI)肺的氧合功能、呼吸力学、肺CT以及病理等的变化 ,来探讨不同体位的效应和可能机制。方法　采用油酸型ALI兔模型 ,分为正常对照组(Ⅰ组 )、仰卧位油酸组 (Ⅱ组 )、俯卧位油酸组 (Ⅲ组 )、旋转体位油酸组 (Ⅳ组 ) ,观察各组兔实验过程中动脉血氧分压 (PaO2 )、呼吸力学的变化。并进行肺CT扫描加以分析 ,最后作病理切片检查。结果Ⅲ、Ⅳ组的PaO2 [(15 8± 5 1)、(16 6± 37)mmHg]、肺的顺应性 [(2 8± 0 9)、(2 6± 0 7)ml/cmH2 O]显著高于Ⅱ组 [PaO2 (87± 2 4 )mmHg、肺的顺应性 (1 6± 0 5 )ml/cmH2 O ,P均 <0 0 5 ];Ⅲ、Ⅳ组肺内分流 [(2 1± 5 ) %、(18± 5 ) % ]显著低于Ⅱ组 [(2 9± 8) % ,P <0 0 5 ];Ⅳ组的气道峰压 [(2 0± 2 )cmH2 O]显著高于Ⅲ组 [(16± 2 )cmH2 O ,P <0 0 5 ];3个实验组的PaO2 与肺的顺应性呈显著正相关 ,与肺内分流呈显著负相关。ALI兔肺CT呈明显的重力依赖效应 ,体位的变化对肺CT的影响非常迅速。肺水肿在重力依赖区重 ,旋转后 ,重力依赖现象减轻。结论　俯卧位和旋转体位都能改善兔油酸型ALI肺的氧合 ;ALI肺出现重力压迫性肺不张 ,旋转体位能减轻肺不张的程度和使肺水肿趋于均匀。     

肺移植对5例慢性阻塞性肺疾病患者肺功能的影响

目的研究单肺移植手术治疗慢性阻塞性肺疾病(COPD)对呼吸生理及肺功能的影响。方法5例患者均为Ⅳ级COPD男性患者,年龄51～63岁。术前2周测定患者用力肺活量(FVC)、第一秒用力呼气容积(FEV1)、FEV1/FVC、最大通气量(MVV)、残气容积(RV)、肺总量(TLC)、残总比(RV/TLC)、深吸气量(IC)、胸腔气体容积(TGV)、呼气峰流量(PEF)、总气道阻力(Rawtotal)、肺一氧化碳弥散量(DLCO)、每升肺泡容积肺一氧化碳弥散量(DLCO/V·A)、6分钟行走距离(6MWD)、动脉血氧分压(PaO2)、肺泡气动脉血氧分压差[P(Aa)O2]、动脉血氧饱和度(SaO2)、动脉血二氧化碳分压(PaCO2)及平均肺动脉压(mPAP)等参数。术后2个月再行上述测定。结果5例患者术前2周、术后2个月检测的参数为MVV(23.6±5.8)、(71.6±21.8)L,FEV1(0.68±0.21)、(1.85±0.46)L,FEV1/FVC(37.4±8.3)、(75.6±13.9)%,PaO2(60.0±9.1)、(86.2±2.9)mmHg(1mmHg=0.133kPa),SaO2(90.0±4.6)%、(96.8±0.5)%及mPAP(31.2±5.5)、(16.6±1.8)mmHg,均有显著改善(P均<0.05);3例患者IC[(1.16±0.26)、(1.83±0.35)L]、TGV[(6.52±0.27)、(4.52±0.29)L]、RV[(5.12±0.39)、(3.20±0.32)L]、RV/TLC[(71.0±5.6)、(51.3±2.5)%]及Rawtotal[(6.62±0.99)、(2.48±0.87)cmH2O·L-1·s-1]改善显著(P均<0.05);4例患者PEF[(1.65±0.40)、(3.92±1.63)L/s]、DLCO[(8.5±3.0)、(21.0±6.2)ml·min-1·mmHg-1]及6MWD[(46.8±14.7)、(246.8±51.9)m]也显著增加(P均<0.05);FVC[(1.85±0.40)、(2.45±0.49)L]、TLC[(7.19±0.15)、(6.26±0.73)L]、DLCO/V·A[(2.90±1.50)、(5.41±0.87)L·min-1·mmHg-1]、P(Aa)O2[(37.6±16.3)、(17.8±6.3)mmHg]及PaCO2[(44.6±7.7)、(37.4±3.4)mmHg]有所改善,但差异无统计学意义(P均>0.05)。结论COPD患者肺移植术后肺通气、气道阻力、残气、弥散、运动耐力及气体交换功能均明显改善。     

高血压病患者血清Ⅰ型和Ⅲ型前胶原浓度变化及其临床意义探讨

目的　探讨高血压病 (EH)患者心肌纤维化的无创性检测指标。方法　采用放免法测定 30例正常人和 6 0例EH患者 (伴心肌肥厚者 35例和不伴心肌肥厚者 2 5例 )血清Ⅰ型前胶原 (PCⅠ )和Ⅲ型前胶原 (PCⅢ )的浓度 ,用M型超声测算左室重量指数 (LVMI) ,用多普勒超声测定二尖瓣口舒张早期和晚期最大血流速度 (VE 和VA)。结果　①EH患者血清PCⅠ和PCⅢ均明显高于正常对照组 [(4 6 6 5± 11 0 1)μg/Lvs (34 31± 5 91) μg/L ,P <0 0 5和 (146 0 0± 2 9 35 ) μg/Lvs (96 2 4± 2 1 18) μg/L ,P <0 0 1]。②EH非左室肥厚组血清PCⅢ浓度明显高于正常对照组 [(12 0 6 2± 16 2 3) μg/Lvs(96 2 4± 2 1 18) μg/L ,P <0 0 1],而血清PCⅠ与正常对照组无差别 [(33 73± 6 83) μg/Lvs (34 31± 5 91) μg/L ,P >0 5 ];EH左室肥厚组血清PCⅢ高于非肥厚组 [(16 4 14±2 2 2 8) μg/Lvs (12 0 6 2± 16 2 3) μg/L ,P <0 0 1]和正常对照组 [(16 4 14± 2 2 2 8) μg/Lvs (96 2 4± 2 1 18) μg/L ,P <0 0 1];血清PCⅠ亦高于非肥厚组 [(5 5 88± 12 86 ) μg/Lvs(33 73± 6 83) μg/L ,P <0 0 1]和正常对照组 [(5 5 88±12 86 ) μg/Lvs (34 31± 5 91) μg/L ,P <0 0 1]。③血清PCⅢ与V     

缬沙坦和尼群地平对原发性高血压患者血清可溶性粘附分子影响的对比研究

目的　对比研究缬沙坦和尼群地平对原发性高血压 (EH )患者血压及血清可溶性粘附分子sICAM 1,sVCAM 1水平的影响。方法　随机对照方法设计 ,将 6 4例轻中度原发性高血压患者分为两组 ,分别予缬沙坦 (80mg/d)和尼群地平 (10～ 30mg/d)治疗 6周 ,治疗前后抽血 ,用酶联免疫方法 (ELISA)测定外周血清中可溶性粘附分子sICAM 1,sVCAM 1水平。另选择 2 5例健康人作为对照组。结果　治疗前与对照组比较 ,高血压患者血清中可溶性粘附分子sICAM 1,sVCAM 1水平升高 ,分别为 [(318 2± 2 7 5 ) μg/Lvs (2 71 5± 2 6 8) μg/L ,P <0 0 5 ]和 [(5 90 6± 4 0 1) μg/Lvs (4 17 9± 38 7) μg/L ,P <0 0 1]。治疗后两组的血压均明显下降 (P <0 0 5 ) ,两组间无差异。缬沙坦组可溶性粘附分子sICAM 1,sVCAM 1水平均较治疗前明显下降 ,分别为[(32 0 5± 2 3 6 ) μg/Lvs (2 80 2± 2 5 4 ) μg/L ,P <0 0 5 ]和[(5 86 2± 4 2 5 ) μg/Lvs (4 5 1 2± 38 9) μg/L ,P <0 0 1]。而尼群地平组可溶性粘附分子sICAM 1,sVCAM 1水平较治疗前无明显下降 (P >0 0 5 )。结论　与尼群地平比较 ,缬沙坦不仅能有效降低血压 ,还能抑制血管壁的炎症反应 ,有利于预防和延缓动脉粥样硬化的发生和发展。     

一氧化氮合酶2抑制剂改善大鼠心肌梗死后心功能的作用

目的 :探讨一氧化氮合酶 2 (NOS2 )改善心肌梗死 (MI)后心功能障碍的作用。方法 :选用选择性NOS2抑制剂S 甲基硫脲 (SMT)抑制NOS2。于MI后 4周观察SMT对心功能的影响。结果 :MI组MI后 4周 ,心肌NOS2表达及血浆一氧化氮 (NO)水平均较假手术组升高 [(0 .2 6 1± 0 .0 2 5 )∶(0 .0 92± 0 .0 11)A·μm-2 ,P<0 .0 5 ];(4 6 .6± 4 .2 )∶(30 .6± 2 .1) μmol/L ,P <0 .0 5 ]。SMT干预 4周可使MI后血浆NO水平降低 [(2 6 .6±2 .2 )∶(4 6 .6± 4 .2 ) μmol/L ,P <0 .0 5 ],心室肥厚减轻 ,MI范围缩小 ,心功能改善 [左室舒张末压 (6 .1± 0 .7)∶(11.0± 1.2 )mmHg(1mmHg =0 .133kPa) ,P <0 .0 5 ];中心静脉压 (0 .8± 0 .1)∶(1.6± 0 .2 )mmHg ,P <0 .0 5 ]。结论 :抑制NOS2可以改善MI后心功能。NOS2及其产物NO在MI后心功能障碍的发生发展过程中起促进作用     

催乳素对Graves 病甲状腺细胞与自体外周血单个核细胞体外相互作用的影响

目的　研究催乳素对Graves病 (GD)甲状腺细胞与自体外周血单个核细胞 (PBMC)在体外共同培养时相互作用的影响。方法　利用免疫荧光染色和流式细胞仪等 ,测定在不同羊催乳素(oPRL)水平进行共同培养时PBMC的活化、增殖反应和甲状腺细胞对人类白细胞抗原基因复合体(HLA) DR及CD4 0 的表达。结果　oPRL浓度为 2 0 0 μg/L时与GD甲状腺细胞共同培养的PBMC中CD4 CD2 5 细胞百分率 [(13 0 8± 2 5 4) % ,P <0 0 1]和增殖指数 [(17 82± 3 0 2 ) % ,P <0 0 1]及 10 0 0μg/L时的增殖指数 [(16 5 7± 2 5 6 ) % ,P <0 0 5 ]均较 0 [分别 (10 15± 2 6 0 ) %和 (14 38± 2 6 4) % ]、12 5及 5 0 μg/L时有显著增加。在 2 0 0和 10 0 0 μg/L时相应甲状腺细胞中CD4 0 细胞百分率 [(4 8 2 5± 6 6 3) % ,(5 2 2 8± 6 94) % ]和平均荧光强度 (dMF ;42 94± 10 2 4,49 5 1± 12 34)明显低于 0 [(5 8 38± 6 6 2 ) %和 6 7 30± 2 0 2 0 ]、12 5及 5 0 μg/L剂量组。而在 5 0 μg/L时其HLA DR 细胞百分率[(4 6 79± 7 5 1) % ,P <0 0 1]和dMF(2 1 0 2± 5 43 ,P <0 0 1)显著高于 0 [(33 5 1± 8 5 8) %和 13 91±3 88]、12 5、2 0 0及 10 0 0 μg/L剂量组。除此以外 ,oPRL各剂量组间差异均     

慢性阻塞性肺疾病患者运动能力与其呼吸驱动及呼吸肌功能关系的研究

目的探究慢性阻塞性肺疾病（COPD）患者运动能力与呼吸驱动及呼吸肌功能之间的关系。方法对28例COPD患者和26名正常对照者分别检测静息常规肺功能、肺弥散功能（DLCO）、口腔阻断压（P0.1）、最大吸气压（PImax）及最大呼气压（PEmax）,并进行运动负荷试验观测氧耗量（VO2）、二氧化碳产生量（VCO2）、分钟通气量（E）、潮气量（T）等气体代谢指标,同时记录受试者运动中的呼吸困难指数（BorgScale）。运动负荷前、后检测动脉血气分析。结果（1）COPD组患者PImax（40±15）mmHg明显低于正常人组（53±19）mmHg（P<0.05）,PEmax在两组中差异无显著性（P>0.05）,COPD组患者P0.1（2.8±0.9）mmHg明显高于正常人组（2.0±0.7）mmHg（P<0.05）,P0.1/PImax（0.069±0.021）也明显高于正常人组（0.037±0.009）（P<0.01）。（2）COPD组患者VO2max与P0.1及PImax未发现明显的相关关系（P>0.05）,但与P0.1/PImax明显正相关（r=0.66,P<0.01）,BorgScale与P0.1/PImax明显正相关（r=0.49,P<0.05）。结论COPD患者运动能力下降除与气道阻塞程度及气体交换障碍等有关外,呼吸驱动相对增高及呼吸肌功能障碍也是其运动能力的限制因素。     

Sleep quality, carbon dioxide responsiveness and hypoxaemic patterns in nocturnal hypoxaemia due to chronic obstructive pulmonary disease (COPD) without daytime hypoxaemia.

In order to clarify whether nocturnal hypoxaemia (arterial oxygen saturation, SaO2 < 90%) may exist in the long-term before daytime hypoxaemia (PaO2 < 8.0 kPa) occurs in chronic obstructive pulmonary disease (COPD), 21 patients with stable severe COPD without daytime hypoxaemia (PaO2 > or = 8.0 kPa) were studied prospectively. Subjects were monitored twice by polysomnography (PSG) 12 months apart. Spirometry was performed, and diffusion capacity (DLCO) and hypercapnic respiratory drive response delta PI0.1 delta PCO2(-1)) were measured during the daytime in conjunction with polysomnography. At the start of the study our subjects had FEV1 %P (FEV1 as a percentage of predicted value) of 26.1 +/- 7.2%, a mean nocturnal nadir SaO2 of 83 +/- 5%, and a mean SaO2 during nocturnal hypoxaemic episodes of 88.0 +/- 0.7%. The patients' delta PI0.1 delta PCO2(-1) was 1.8 +/- 1.4 cm H2O kPa-1 (within the normal range). For the entire study group, no significant change in any lung function or blood gas parameter was noted during the year of observation, and nocturnal SaO2 remained unaltered. Stage I sleep decreased (P < 0.05) after 12 months. Prolonged stage I sleep was associated with nocturnal hypoxaemia at the second PSG. Five subjects developed daytime hypoxaemia and they showed poorer lung function but similar nocturnal hypoxaemia and delta PI0.1 delta PCO2(-1) level compared to the rest of the patients. Patients with sudden SaO2 dips had more pronounced nocturnal hypoxaemia and prolonged wakefulness than 'non-dippers'. In conclusion, the mean level of nocturnal hypoxaemia may persist unaltered for at least 1 yr. COPD patients with exclusively nocturnal hypoxaemia have a hypercapnic drive response within the normal range. Prolonged nocturnal hypoxaemia and reduced whole night oxygenation are associated with increased superficial sleep. Sleep fragmentation and high carbon dioxide sensitivity may be important defence mechanisms against sleep-related hypoxaemia. The appearance of daytime hypoxaemia is preceded by a substantial deterioration in lung function, but by only a minor deterioration of nocturnal hypoxaemia.     

Energy balance in chronic obstructive pulmonary disease

A substantial number of patients with chronic obstructive pulmonary disease (COPD) suffer from gradual and significant weight loss during the natural course of their illness. The aim of this study was to determine the contribution of resting energy expenditure (REE) and energy intake (E-Intake) to weight loss in 80 patients with stable COPD: age (mean +/- SEM) 65 +/- 3 yr and FEV1 1.0 +/- 0.1 L. A total of 39 patients exhibited a continued weight loss in the previous year. REE measured with a ventilated hood system was significantly (p less than 0.005) higher in weight-losing compared to weight-stable patients when values were normalized for predicted metabolic rate (117 +/- 3 and 108 +/- 2%, respectively) or kg fat-free mass using bioelectrical impedance (FFM-BI): 35.0 +/- 0.8 and 31.8 +/- 0.6 kcal/kg, respectively). Normalized values of E-Intake were not significantly different between weight-losing and weight-stable patients. REE/FFM-BI correlated significantly with FEV1 (r = 0.22, p less than 0.05), maximal inspiratory mouth pressure (Plmax; r = 0.35, p less than 0.001), and E-Intake/FFM-BI (r = 0.48, p less than 0.001). Classification in three subgroups by severity of disease, (1) FEV1 greater than 35%, (2) FEV1 less than or equal to 35%, and (3) PaO2 less than 7.3 kPa, revealed a higher prevalence of weight loss in the more compromised groups and a significantly decreased (p less than 0.05) E-Intake in the hypoxemic patients.(ABSTRACT TRUNCATED AT 250 WORDS)     

Elevated O2 cost of ventilation contributes to tissue wasting in COPD

BACKGROUND AND OBJECTIVES: Thirty to 50% of all COPD patients experience tissue wasting that may be caused by hypermetabolism, but the cause of the perturbed metabolic state is unclear. We hypothesized that the elevated O2 cost of ventilation (O2 COV) may be a contributing factor. All of the data are presented as means (+/-SEM). Ten hypoxemic (a PaO2 of 54+/-3 mm Hg) stable COPD patients (an FEV1/FVC ratio of 42+/-4%) and five healthy control subjects were studied. The patients were divided into two groups based on nutritional status. Group 1 (n = 6) was malnourished (a body mass index [BMI] of 17.6+/-0.7 kg/m2), and group 2 (n = 4) was normally nourished (a BMI of 26.0+/-3 kg/m2). The O2 COV was determined by measuring the change in the oxygen consumption (VO2) and the minute ventilation (VE) caused by CO2-induced hyperventilation. RESULTS AND CONCLUSIONS: Group 1 had an elevated O2 COV when compared to group 2 and the control group, respectively: 16.4+/-1.0 vs 9.7+/-1.0 and 2.4+/-0.2 mL O2/L of VE (p < 0.05). The VO2 at rest was higher for group 1 than for group 2 and the control group, respectively: 4.5+/-0.3 vs 3.1+/-0.5 and 3.4+/-0.2 mL/kg/min (p < 0.05). The resting energy expenditure (REE) % predicted for group 1 was also higher than group 2 and the control group, respectively: 125+/-3% vs 87+/-7% and 97+/-2% (p < 0.05). Significant correlations were observed that implicate the increased O2 COV as a cause of tissue wasting: O2 COV vs BMI (r = -0.79; p = 0.007), O2 COV vs REE % predicted (r = 0.66; p = 0.039), and REE % predicted vs BMI (r = -0.83; p = 0.003). The O2 COV was also correlated with lung function: FEV1/FVC vs O2 COV (r = -0.84; p = 0.002). We conclude that in these COPD patients the O2 COV is associated with an increased metabolic rate which, in turn adversely affects the nutritional status.     

死腔负荷对慢性阻塞性肺疾病患者肺功能及呼吸肌功能和运动耐力的影响

目的评价死腔负荷对肺通气功能和呼吸肌的影响,测试呼吸肌氧耗的检测方法,探讨呼吸肌氧耗在慢性阻塞性肺疾病(COPD)运动耐力下降中的作用.方法 26例中度COPD患者和29名年龄相近健康对照者在300 ml呼吸管路死腔(长46 cm)负荷下,完成30 W或55 W功率恒定运动试验,并在死腔负荷下检测运动前、后肺功能和运动中分钟通气量((V·)E)和摄氧量((V·)O2).结果无论COPD或健康对照组,在静息状态或运动后,增加死腔对用力肺活量(FVC)、一秒钟用力呼气容积(FEV1)和FEV1/FVC无显著影响.COPD组静息死腔负荷下FVC、FEV1和FEV1/FVC分别为(3.03±0.15)L、(1.95±0.09)L和(64.9±2.5)%;55 W运动后上述指标分别为(3.03±0.18)L、(2.00±0.13)L和(66.3±3.2)%(P均＞0.05).每例受试个体,无论静息或运动中,附加死腔均导致(V·)E和(V·)O2在原有基础上显著增加,卸除死腔后(V·)E和(V·)O2回落.死腔负荷下(V·)O2的增加量(Δ(V·)O2)在静息和30 W运动时,COPD组和健康对照组之间差异无显著性.在55 W运动时,COPD组Δ(V·)O2显著高于健康对照组[(272±24)ml/min与(194±19)ml/min,P<0.05].结论本组患者呼吸管路加长46 cm(300 ml死腔),伴随中等强度运动未导致COPD患者气流阻塞的进一步加重,也未出现明显呼吸肌疲劳征象.COPD患者呼吸肌具有氧耗优势,呼吸肌与肢体运动肌摄氧比例不平衡,可能是导致COPD患者运动耐力下降的因素之一.     

Normocapnia during nIPPV in chronic hypercapnic COPD reduces subsequent spontaneous PaCO2

Hypercapnia has been accepted during nasal intermittent positive pressure ventilation (nIPPV) and during subsequent spontaneous breathing in patients with chronic hypercapnic respiratory failure (HRF) due to COPD. We tested the hypothesis that nIPPV aimed at normalizing PaCO2 will reduce PaCO2 during subsequent spontaneous breathing. For that purpose 14 consecutive inpatients (age 61.4 +/- 9.9 years) with chronic HRF due to COPD were established on passive pressure-controlled nIPPV in a stepwise approach. Assisted ventilation with supplemental oxygen to reach normoxemia was started followed by passive ventilation with a stepwise increment in the inspiratory pressure and finally by a stepwise increase in the respiratory rate to establish normocapnia. Baseline pulmonary function parameters were: FEV1 0.97 +/- 0.43 l, PaCO2 59.5 +/- 8.4 mmHg, PaO2 49.9 +/- 7.8 mmHg, HCO3- 35.6 +/- 5.2 mmol/l, pH 7.39 +/- 0.04. Normoxemia as well as normocapnia was thus established by decreasing PaCO2 by 19.5 +/- 7.0 mmHg during nIPPV within 8.8 +/- 3.8 days (P < 0.001) (inspiratory pressure 29.8 +/- 3.8 mmHg, respiratory rate 22.9 +/- 1.9 BPM). Spontaneous PaCO2 measured 4 h after cessation of nIPPV decreased to 46.0 +/- 5.5 mmHg (P < 0.001), and HCO3- decreased to 27.2 +/- 3.0 mmol/l (P < 0.001). At 6 months of follow-up, II patients continued nIPPV with stable blood gases and with a decrease of P0.1/Plmax from 9.4 +/- 4.3% to 5.9 +/- 2.0% (P < 0.005). In conclusion, normalization of PaCO2 by passive nIPPV in patients with HRF due to COPD is possible and leads to a significant reduction of PaCO2 during subsequent spontaneous breathing and is associated with improved parameters of respiratory muscle function.     

肥胖通气低下综合征呼吸中枢反应性的改变与二氧化碳潴留相关作用

目的 观察肥胖通气低下综合征患者呼吸中枢反应性的改变与二氧化碳（ＣＯ２）潴留的相关作用。方法 测定了５例白天动脉血二氧化碳分压（ＰａＣＯ２）〉４５ｍｍＨｇ的睡眠呼吸暂停综合征（ＳＡＳ）患者呼吸中枢柢氧反应性（△Ｐ０．１／△ＳａＯ２ｗ、△Ｖｅ／△ＳａＯ２）及高ＣＯ２反应性（△Ｐ０．１／△ＰａＣＯ２、△Ｖｅ／△ＰａＣＯ２）,并选择５例年龄、性别、身高、体重、呼吸暂停病程及睡眠呼吸率乱指数（ＡＨＩ）相近     

The energy expenditure of the mechanically ventilated critically ill patient. An analysis

This study characterizes the pattern of caloric expenditure of a group of 19 mechanically ventilated critically ill patients after surgery. Continuous measurements of metabolic rate were used to examine the total energy expended over an eight-hour period (10 AM to 6 PM) on 21 occassions. This allowed for determination of the energy expended during activity, rest, and sleep. The patients were observed to be resting, defined as lying motionless with eyes open and responsive to surrounding events, for 44 +/- 4 percent (SE) of the studied period. Sleeping, a state where the patient was not aroused by surrounding events, was observed for 17 +/- 3 percent of the studied period. Total energy expenditure was 4.8 +/- 1.8 percent greater than resting energy expenditure (REE). The REE was 13.1 +/- 2.3 percent above sleeping energy expenditure (awakeness factor), while activity energy expenditure was 17.1 +/- 2.9 percent above REE (activity factor). The respiratory quotient (RQ) during activity in the 15 patients receiving infusions of physiologic saline solution or 5 percent dextrose solution was significantly less (p less than 0.02) than the RQ during rest. This appears to be due to increased fat oxidation during activity.     

Incidence of nocturnal desaturation while breathing oxygen in COPD patients undergoing long-term oxygen therapy

STUDY OBJECTIVE: It is suggested that oxygen flow be increased by 1 L/min during sleep in COPD patients undergoing long-term oxygen therapy (LTOT) in order to avoid nocturnal desaturations. The purpose of this study was to investigate the occurrence of nocturnal desaturations while breathing oxygen in COPD patients receiving LTOT. SETTING: Inpatient/university hospital. PATIENTS: We studied 82 consecutive COPD patients. Their functional characteristics were as follows (mean +/- SD): FVC, 2.15 +/- 0.69 L; FEV(1), 0.87 +/- 0.33 L; PaO(2), 51.6 +/- 5 mm Hg; and PaCO(2), 47 +/- 8 mm Hg. MEASUREMENTS: Overnight pulse oximetry (PO) was performed twice: (1) while breathing air and (2) while breathing supplemental oxygen assuring satisfactory diurnal resting oxygenation (mean PaO(2) during oxygen breathing, 67 +/- 6 mm Hg; mean arterial oxygen saturation [SaO(2)] during oxygen breathing, 93%). RESULTS: PO performed while patients were breathing air showed a mean overnight SaO(2) of 82.7 +/- 6.7%. Patients spent 90% of the recording time with an SaO(2) of < 90%. While breathing oxygen, 43 patients (52.4%) remained well oxygenated. Their mean overnight SaO(2) while breathing oxygen was 94.4 +/- 2.1%, and time spent with saturation < 90% was 6.9 +/- 8.6%. Thirty-nine patients (47.6%) spent > 30% of the night with an SaO(2) of < 90% while breathing supplemental oxygen. Their mean overnight SaO(2) while breathing oxygen was 87.1 +/- 4.5%, and time spent with an SaO(2) of < 90% was 66.1 +/- 24.7% of the recording time. Comparison of ventilatory variables and daytime blood gases between both groups revealed statistically significantly higher PaCO(2) on air (p < 0.001) and on oxygen (p < 0. 05), and lower PaO(2) on oxygen (p < 0.05) in the group of patients demonstrating significant nocturnal desaturation. CONCLUSIONS: We conclude that about half of COPD patients undergoing LTOT need increased oxygen flow during sleep. Patients with both hypercapnia (PaCO(2) > or = 45 mm Hg) and PaO(2) < 65 mm Hg while breathing oxygen are most likely to desaturate during sleep.