大鼠慢性缺氧高二氧化碳肺动脉高压模型可溶性鸟苷酸环化酶的表达

本文通过观察大鼠慢性缺氧高CO2 肺动脉高压模型肺动脉可溶性鸟苷酸环化酶 (SGC)基因及其蛋白表达 ,分析SGV酶活性 ,探讨其与肺动脉高压的关系及进一步认识防治肺动脉高压的可能途径。作者选择了雄性SD大鼠 2 0只 ,随机分为 2组 ,每组 1 0只。A组 :慢性缺氧高CO2 肺动脉高压组 ,大鼠置于常压低氧高CO2 饲养舱 ,舱内氧浓度维持在 (1 0 .0± 0 .5 ) % ,CO2 浓度为 6 %～ 7% ,每天 8h。B组 :健康对照组 ,大鼠室温下常规饲养。免疫组化观察 2组大鼠肺中小动脉SGCα1 、β1 亚基蛋白的表达 ,原位杂交观察肺中小动脉SGCα1 亚基mRNA的…     

氟西汀对高原肺动脉高压大鼠重返平原肺动脉压力变化的影响

目的：观察氟西汀对高原肺动脉高压大鼠重返平原肺动脉压力及右室肥厚指数参数变化的影响.方法：采用随机数字表法将清洁级雄性Wistar大鼠分为氟西汀干预组（F组,91只）,蒸馏水对照组（C组,91只）,共低压低氧10天、20天、30天及重返平原10天、20天、30天、90天,合计7个时间段,共计14组,每组13只.各组大鼠全部置于模拟海拔5 000m低压低氧舱,每天22h,氟西汀组大鼠入舱当天开始给予3mg/（kg·d）氟西汀灌胃,C组大鼠按体重灌饲同等体积蒸馏水,持续灌饲30天,低压低氧30天后立即将F（4 ～7）组、C（4 ～7）组大鼠返回平原（陕西咸阳海拔386m）环境同等条件饲养.各组大鼠分别于上述7个时间段应用西门子6002有创血压监护系统,测定平均肺动脉压（MPAP）及右心室重/左心室＋室间隔重（RV/LV＋ S）比值.结果：①低压低氧时间段：低压低氧3个时间段两组大鼠MPAP及RV/LV ＋S缓慢升高,同时间段F组大鼠MPAP及RV/LV＋S均低于C组;②重返平原时间段：重返平原4个时间段两组大鼠MPAP及RV/LV ＋S均缓慢降低,同时间段F组大鼠MPAP及RV/LV ＋S均低于C组,但重返平原90天时间段,两组大鼠MPAP及RV/LV＋S无明显差别.结论：氟西汀在高原肺动脉高压形成过程中,具有降低肺动脉压力升高程度及右室肥厚指数增厚程度的作用;重返平原后高原肺动脉高压大鼠肺动脉压力及右室肥厚指数下降速度与低压低氧环境下升高程度成反比.     

慢性低氧性肺动脉高压大鼠肺内肺动脉中尾加压素Ⅱ的变化

为了研究尾加压素Ⅱ (ｕⅡ )在慢性低氧性肺动脉高压及肺血管结构重构形成中的变化 ,作者在大鼠慢性低氧性肺动脉高压模型上 ,采用免疫组化技术对慢性低氧性肺动脉高压大鼠不同节段肺内动脉ｕⅡ蛋白表达进行交位及半交量分析。结果显示 :低氧 1周和 2周组大鼠肺动脉平均压 (ｍＰＡＰ)、右心室肥厚指标Ｒ/(Ｌ +Ｓ)、肺动脉相对中膜面积 (ＲＭＡ)和相对中膜厚度 (ＲＭＴ)均明显高于对照组 (Ｐ <0 .0 0 1 )。低氧 2周组大鼠各节段肺内动脉内皮细胞中ｕⅡ表达较对照组分别下降 2 7.75 %、3 2 .5 0 %、3 9.63 % (Ｐ <0 .0 1 )。相关分析显示 :与…     

缺血预适应诱导PKCα、PKCε活化和失血性休克大鼠血管反应性和钙敏感性保护的机制

目的观察缺血预适应是否通过腺苷受体,诱导蛋白激酶Cα(protein kinase Cα,PKCα)、蛋白激酶Cε(protein kinase Cε,PKCε)活化和失血性休克大鼠血管反应性和钙敏感性保护。方法采用高效液相色谱法测定缺血预适应过程中腺苷浓度变化;采用western blot技术,观察A1、A2A、A2B、A3腺苷受体(A1、A2A、A2B、A3adenosine receptor,A1R、A2AR、A2BR、A3R)抑制剂对缺血预适应诱导PKCα和PKCε表达和转位的影响;采用离体微血管环张力测定技术,观察腺苷受体抑制剂对缺血预适应诱导失血性休克血管反应性和钙敏感性保护作用的影响。结果 (1)休克2小时后血浆腺苷浓度较正常对照组显著增高,5%失血量预适应可进一步增高休克后的血浆腺苷浓度,以在休克前30分钟缺血预适应组的腺苷浓度最高(P0.01);(2)5%失血量休克前30分钟预适应可促进PKCα和PKCε由胞浆向胞膜的转位(P0.01),A1R拮抗剂可显著抑制缺血预适应导致的PKCα和PKCε的转位,使PKCα的胞膜/胞浆部分比值分别由1.071回降至0.583,使PKCε的胞膜/胞浆部分比值由1.280回降至0.606(P0.01),A2AR、A2BR和A3R拮抗剂没有明显作用;(3)5%失血量休克前30分钟预适应可诱导血管反应性和钙敏感性的保护作用(P0.01),A1R拮抗剂可以显著抑制其保护作用,使去甲肾上腺素(norepinephrine,NE)和Ca2+的最大收缩力(Emax)分别降低59.3%和53.4%(P0.01),A2AR、A2BR、A3R拮抗剂均无显著抑制作用。结论缺血预适应通过A1R,诱导PKCα和PKCε活化和失血性休克大鼠血管反应性和钙敏感性的保护。     

二氯醋酸钠对模拟高原肺动脉高压大鼠肺动脉平滑肌细胞Kv1·5亚型的作用研究

本文通过研究电压门控性钾通道亚型（Kvl·5）在高原低压低氧性肺动脉高压中的作用并观察二氯醋酸钠（DCA）对高原低压低氧大鼠肺小动脉平滑肌细胞（PASMCs）Kvl·5基因表达的影响，旨在探讨DCA对高原性肺动脉高压的治疗作用。作者选取24只雄性SD大鼠随机分为正常对照组（N组，8只）、高原低压低氧组（HA组，8只）及DCA干预组（DCA组，8只）。     

阿斯匹林对大鼠在低O2高CO2下肺动脉高压的作用

阿斯匹林(ASA)为传统的抗血小板聚集药,它能高度特异性地阻断环氧化酶(COX)活性而抑制前列腺素的合成。血栓素A2 (TXA2 )与前列环素(PGI2 )平衡失调与肺动脉高压的形成有着密切的关系,本文采用慢性低氧高二氧化碳肺动脉高压大鼠模型,观察阿斯匹林对肺动脉高压肺血管重建的影响。作者将SD大鼠分为正常对照组、慢性低O2 高CO2 组、慢性低O2 高CO2 +阿斯匹林组。用光镜、放射免疫等方法观察各组大鼠肺动脉平均压(mPAP)、颈动脉平均压(mCAP)、肺细小动脉显微结构、血浆和肺匀浆TXB2 及6 -keto -PGFlα含量的变化。结果:①低O2 高C…     

氧化应激在低压缺氧性肺动脉高压形成中的作用

目的观察低氧对血清中活性氧(ROS)水平的影响,探讨氧化应激在低压缺氧性肺动脉高压形成中的作用。方法将24只Wistar大鼠随机分为平原对照组(C组),缺氧组(H组),N-乙酰半胱氨酸组(N组),缺氧+N-乙酰半胱氨酸组(H+N组)。建立低压缺氧模型21 d后,测定其右心室收缩压(RVSP)和平均肺动脉压(mPAP);HE染色观察各组大鼠的肺动脉壁厚度;比色法测定血清中ROS的含量。结果与C组相比,H组RVSP、mPAP明显升高(均P<0.05),HE染色示H组肺动脉壁增厚,且血清中ROS水平明显升高(P<0.05);给予ROS清除剂NAC后,RVSP及mPAP降低,肺血管重塑减弱。结论低氧时氧化应激参与了低压缺氧性肺动脉高压的形成。     

缺氧性肺动脉高压大鼠肺组织中肾上腺髓质的合成释放及其意义

为了研究缺氧性肺动脉高压 (ＨＰＨ)肺组织中肾上腺髓质素 (ＡＭ)的合成分泌及其在ＨＰＨ病理生理过程中的作用 ,作者模拟 5 0 0 0ｍ高原连续缺氧、复制大鼠ＨＰＨ动物模型。应用光镜、免疫组化、放射免疫测定等方法 ,观察、测定缺氧后 1 0天、2 0天、3 0天和对照组大鼠肺组织中ＡＭ蛋白表达及血浆、支气管肺泡灌洗液 (ＢＡＬＦ)ＡＭ含量的动态变化。结果显示 :各组大鼠肺血管内皮细胞 (ＥＣ)、血管及支气管平滑肌细胞 (ＳＭＣ)、支气管粘膜上皮、肺巨噬细胞(ＭΦ)、Ⅱ型肺泡上皮及支气管软骨细胞ＡＭ均呈阳性表达。缺氧各时相尤以 2 0天 ,…     

低氧时蛋白激酶C对内皮细胞表达血管内皮生长因子的调节作用

目的探讨低氧培养大鼠肺动脉血管内皮细胞生长因子 (VEGF)表达变化与蛋白激酶C(PKC)活性的关系。方法培养大鼠肺动脉血管内皮细胞 ,观察低氧 ( 1 %O2 )培养 0、1、3、6、1 2h大鼠肺动脉血管内皮细胞PKC活性和VEGFmRNA水平变化 ;同时对培养液中VEGF蛋白水平进行测定。培养基中加入PKC抑制剂 (staurosporine)后 ,立即进行低氧培养 ,测定低氧培养不同时间点上述指标的变化。 结果低氧培养 1hPKC活性首先明显升高 (P >0 .0 5 ) ,至 3hVEGFmRNA表达明显升高 (P <0 .0 1 ) ,6h培养液中VEGF蛋白水平显著升高 (P <0 .0 1 )。而加入PKC抑制剂后 ,低氧培养的内皮细胞PKC活性与 0h比较明显下降 (P <0 .0 1 ) ,相应各时间点的VEGFmRNA及蛋白水平与 0h比较无明显变化 (P >0 .0 5 )。结论低氧能够刺激大鼠肺动脉血管内皮细胞VEGF表达升高 ,低氧时PKC活性升高是调节VEGF表达升高的重要因素之一     

慢性缺氧性肺动脉高压大鼠右心室apelin-APJ基因表达降低

目的:研究慢性缺氧性肺动脉高压大鼠右心室组织apelin及其受体(APJ)基因表达的变化,探讨其在该病理过程中可能的作用及意义。方法:清洁级雄性SD大鼠20只,随机分为对照组和慢性缺氧组(10%O2,4w)。RT-PCR检测大鼠右心室apelin、APJ mRNA的表达变化。结果:①慢性缺氧组大鼠平均肺动脉压、右心室与左心室加室间隔重量比(RV/LV S)均显著高于对照组(P<0.01);②慢性缺氧组大鼠右心室apelin和APJ的mRNA表达均显著低于对照组(P<0.01)。结论:慢性缺氧性肺动脉高压大鼠右心室apelin-APJ系统表达降低,提示这一信号转导通路可能在慢性缺氧性肺动脉高压的发生发展中具有重要作用。     

Immunohistochemical investigation of a pulmonary surfactant in fatal mechanical asphyxia

We evaluated the usefulness of pulmonary surfactant protein A (SP-A) as a practical diagnostic marker of fatal mechanical asphyxia in forensic autopsy cases. A total of 27 cases of asphyxia were examined histologically and immunohistochemically and compared with a control group consisting of 16 cases of poisoning (n = 9) and peracute death (n = 7). Both groups showed histological findings of local atelectasis and local emphysema, congestion, intra-alveolar and interstitial edema in most cases and pulmonary hemorrhages in some cases. The mechanical asphyxia group showed a significantly increased intensity of SP-A staining in the intra-alveolar space accompanied by many massive aggregates in approximately 60% of cases, which was not found in the control group. These structures may be interpreted as aggregates of pulmonary surfactant released from the alveolar wall due to enhanced secretion caused by strong forced breathing or over-excitement of the autonomic nervous system by mechanical asphyxia. The results of our investigation suggest the practical usefulness of the immunohistochemical detection of SP-A in distinguishing mechanical asphyxia from other types of hypoxia.     

氡诱发小鼠肺损伤与P53和Bcl-2、Bax蛋白表达的研究

目的 建立氡染毒小鼠肺损伤模型,观察不同剂量组小鼠肺组织损伤情况,分析氡对P53、Bcl-2、Bax在肺组织中表达的影响。方法 建立氡染毒小鼠模型,使染毒累积剂量分别达到30工作水平月(WLM)和60WLM;采用TUNEL法检测小鼠肺组织细胞凋亡程度;采用免疫组化SP法及Westernblot法,检测各组肺组织P53、Bcl-2、Bax蛋白表达情况。结果 与正常对照组相比,氡染毒30和60WLM小鼠肺细胞凋亡指数均明显增加(t=18.11、-10.30,P<0.05);氡染毒30WLM组P53蛋白明显增加(t=-11.08,P<0.05);60WLM组P53蛋白和Bax蛋白表达明显增加(t=-7.00、-2.52,P<0.05),Bcl-2蛋白表达明显下降(t=4.36,P<0.05);氡染毒30和60WLM与对照组相比,Bcl-2、Bax比值均明显下降(t=2.78、4.07,P<0.05)。结论 氡染毒可使小鼠肺损伤,出现肺细胞凋亡,P53、Bcl-2、Bax途径可能参与了肺细胞的凋亡调节。     

血清淀粉样蛋白A水平在慢性阻塞性肺疾病急性加重期的变化及其意义

目的探讨血清淀粉样蛋白A在慢性阻塞性肺疾病急性加重期的变化及其意义,为临床诊疗提供参考。方法选取我院接诊的慢性阻塞性肺疾病急性加重期患者70例．将其分为A组（AECOPDI级）38例和B组（AECOPDⅡ／Ⅲ级）32例,选取同期在我院体检的健康人群30例为健康对照组。对比急性加重期患者、稳定期患者以及健康对照组受试者的血清淀粉样蛋白A以及C-反应蛋白（CRP）水平：对比A组和B组患者的血清淀粉样蛋白A和CRP两个指标的敏感度和特异度;分析痰培养结果和血清淀粉样蛋白A和CRP水平的关系。结果稳定期和急性加重期患者的血清淀粉样蛋白A以及CRP水平均显著高于健康对照组（均P〈0．05）;急性加重期的血清淀粉样蛋白A以及CRP水平均显著高于稳定期（均P〈0．05）;慢性阻塞性肺疾病患者血清淀粉样蛋白A水平显著高于CRP水平（P〈0．05）;B组的血清淀粉样蛋白A在区分急性加重期和稳定期的敏感度和特异度为84％、91％,AUC值=0．92,优于CRP的敏感度和特异度（69％、69％,AUC值=0．79）;有脓性痰或者痰培养结果阳性患者的血清淀粉样蛋白A水平为（79．36±15．72）mg/L,CRP水平为（24．97±6．52）mg／L,均显著高于没有脓性痰且痰培养结果阴性的患者（均P〈0．05）。结论检测血清淀粉样蛋白A对判断慢性阻塞性肺疾病患者病情严重程度有一定的指导意义,同时可以指导临床更有针对性地应用和停用抗生素,值得在临床上进一步推广应用。     

Tumor uptake of radioiodinated anti-human pulmonary surfactant-associated protein monoclonal antibody PE10 in nude mice bearing human pulmonary adenocarcinoma in combination with an unlabeled preload

This study assessed the potential use of radioimmunoscintigraphy of pulmonary alveolar Type II cells tumor with the radiolabeled anti-human surfactant-associated protein (SP) monoclonal antibody (MAb) PE 10 in combination with preloads of unlabeled MAb. The in vitro binding of iodine-125 (¹²⁵I)-labeled MAb PE 10 (1 μg), which had a specific radioactivity of 400 MBq/mg, on human pulmonary papillary adenocarcinoma NCI-H441 cells that produced SP was investigated. In NCI-H441 tumor-bearing nude mice, the tumor uptake of ¹²⁵I-MAb PE 10 (5 μg) was examined in combination with preloads of unlabeled MAb PE 10 (0, 5, 10, and 50 μg). An isotype-matched unassociated murine MAb was used as a control both in vitro and in vivo. ¹²⁵I-MAb PE 10 showed specific cell binding compared with ¹²⁵I-control MAb. Tumor uptake of ¹²⁵I-MAb PE 10 in vivo reached a peak of 4.97±0.33% injected dose per gram (%ID/g) at 48 h postinjection. Preloads of 5 and 10 μg unlabeled MAb PE 10 significantly enhanced tumor uptake at 48 h postinjection ( 5.94±0.29% ID/g and 5.72±0.29% ID/g, respectively), whereas preload of 50 μg unlabeled MAb PE 10 significantly decreased tumor uptake ( 2.75±0.32% ID/g) at 48 h. Preload of 5 μg unlabeled MAb PE 10 significantly increased the tumor-to-blood radioactivity ratio at 48 h ( 2.39±0.16). Preloads of unlabeled control MAb did not cause any significant change in tumor uptake. Immunohistochemistry showed the intracellular and pericellular patterns of SP expression in tumor cells. In conclusion, radioimmunoscintigraphy with MAb PE 10 labeled with a γ-emitting radioiodine such as ¹²³I might be a useful means of targeting pulmonary alveolar Type II tumor cells in combination with preloading with an optimal dose of the unlabeled MAb.     

Physical activity counteracts increased whole-body protein breakdown in chronic obstructive pulmonary disease patients

Chronic obstructive pulmonary disease (COPD) is associated with increased whole body protein breakdown and low-grade systemic inflammation. We aimed to determine if physical training of patients with COPD induces anti-inflammatory effects and decreases whole-body protein breakdown. Nineteen subjects with severe (FEV(1)=31+/-1) COPD were randomized into a training group (n=9) and a control group (n=10). Twenty healthy subjects were studied for baseline comparison. The "COPD training" group participated in an outpatient rehabilitation program consisting of endurance training (walking at 85% of VO(2max)) twice weekly for 7 weeks plus daily home-based training. Maximum walking distance increased by almost 70% in the training group after 7 weeks of training. At baseline, the concentrations of C-reactive protein (CRP) and IL-18 in plasma were increased in subjects with COPD compared with healthy subjects (P<0.05) and leucine rate of appearance (R(a)) was approximately 15% greater (P<0.05) in subjects with COPD. Training had no effect on the plasma concentration of inflammatory markers but decreased leucine R(a) in subjects with COPD by approximately 10% (P<0.05). In conclusion, 7 weeks of physical training markedly improved endurance in patients with COPD and accelerated whole-body protein breakdown in patients with COPD was attenuated by physical training independent of changes in inflammatory markers.     

MAPKs家族在中暑小鼠肺微血管内皮细胞凋亡中的作用及机制研究

目的 研究丝裂原活化蛋白激酶(MAPKs)活化对热打击致小鼠肺微血管内皮细胞(PMVECs)凋亡的影响.方法 建立重症中暑小鼠模型,采用TUNEL染色及免疫组化检测肺组织损伤情况.二次磁珠分选法分离乳鼠PMVECs,TUNEL染色检测PMVECs凋亡情况,Western blotting检测热打击恢复期(0、2、6h)MAPKs家族活化情况.通过检测单层内皮细胞跨膜电阻(TEER)及辣根过氧化物酶(HRP)值观察不同热打击温度对单层细胞通透性的影响,同时使用MAPKs家族抑制剂检测热打击对单层细胞通透性及凋亡的影响.结果 在重症中暑小鼠恢复期肺组织中可观察到PMVECs发生凋亡.TUNEL染色发现随着恢复期时间的延长,PMVECs凋亡数目增多,热打击可使PMVECs MAPKs家族活化且微血管通透性增加,给予p38活化抑制剂SB203580及ERK活化抑制剂PD98059预处理后细胞通透性增加,凋亡数目增多,而给予JNK抑制剂SP600125预处理后细胞则出现相反的变化.结论 重症中暑小鼠PMVECs可发生凋亡,p38及ERK起着抗凋亡的作用,JNK起着促凋亡的作用.     

Identification of radiation response genes and proteins from mouse pulmonary tissues after high-dose per fraction irradiation of limited lung volumes

Purpose: The molecular effects of focal exposure of limited lung volumes to high-dose per fraction irradiation (HDFR) such as stereotactic body radiotherapy (SBRT) have not been fully characterized. In this study, we used such an irradiation system and identified the genes and proteins after HDFR to mouse lung, similar to those associated with human therapy.

Methods and materials: High focal radiation (90?Gy) was applied to a 3-mm volume of the left lung of C57BL6 mice using a small-animal stereotactic irradiator. As well as histological examination for lungs, a cDNA micro array using irradiated lung tissues and a protein array of sera were performed until 4 weeks after irradiation, and radiation-responsive genes and proteins were identified. For comparison, the long-term effects (12 months) of 20?Gy radiation wide-field dose to the left lung were also investigated.

Results: The genes ermap, epb4.2, cd200r3 (up regulation) and krt15, hoxc4, gdf2, cst9, cidec, and bnc1 (down-regulation) and the proteins of AIF, laminin, bNOS, HSP27, β-amyloid (upregulation), and calponin (downregulation) were identified as being responsive to 90?Gy HDFR. The gdf2, cst9, and cidec genes also responded to 20?Gy, suggesting that they are universal responsive genes in irradiated lungs. No universal proteins were identified in both 90?Gy and 20?Gy. Calponin, which was downregulated in protein antibody array analysis, showed a similar pattern in microarray data, suggesting a possible HDFR responsive serum biomarker that reflects gene alteration of irradiated lung tissue. These genes and proteins also responded to the lower doses of 20?Gy and 50?Gy HDFR.

Conclusions: These results suggest that identified candidate genes and proteins are HDFR-specifically expressed in lung damage induced by HDFR relevant to SBRT in humans.     

肺表面活性蛋白A在皮质类固醇调节哮喘小鼠树突细胞共刺激分子表达中的作用

目的 研究皮质类固醇激素调节小鼠哮喘模型树突细胞表面共刺激分子表达的机制，以及肺表面活性蛋白A（SP-A）在其调节中的作用。方法 BALB/c小鼠30只，分为3组：哮喘组，采用卵蛋白（OVA）致敏和激发；对照组，以生理盐水代替OVA；治疗组，每次OVA激发后10min，腹腔注射地塞米松01mg。用免疫组化法检测SP-A在肺内的表达情况。采用Leica DM Snk软件进行图像采集，并用Qwin软件计算小气道内棕色区域面积，取平均值，进行统计分析。分离培养脾脏树突细胞，用流式细胞仪（FACS）检测树突细胞表面共刺激分子CD80的表达变化。结果 哮喘组肺组织表现为嗜酸性细胞及淋巴细胞浸润为主的炎症变化，治疗组和对照组无此变化。哮喘组的SP-A表达明显低于对照组和治疗组（P〈0．01），CD80的表达率明显高于治疗组（P〈0.01）；哮喘组小气道内SP-A表达与树突细胞CD80阳性率呈负相关（r=-0．907，P〈0．01）。结论 皮质类固醇对小鼠哮喘模型的肺表面活性蛋白有明显的保护作用，可通过激发肺表面活性蛋白抑制树突细胞表面共刺激分子CD80的表达。     

AECOPD患者hs-CRP水平与营养状况的关系研究

目的探讨慢性阻塞性肺疾病急性加重期（AECOPD）超敏c反应蛋白（hs-CRP）水平与营养状况的关系,为临床进行病情及营养状况预测及评估提供依据。方法选择177例AECOPD患者,进行hs-CRP水平与体重指数（BMI）、血清前血清蛋白（PA）、清蛋白（Alb）、血红蛋白（Hb）、淋巴细胞计数（LY）、总胆固醇（TC）等营养指标的相关性分析,研究营养状况与hs-CRP水平升高的关系,并比较不同营养状况间hs-CRP水平。结果AECOPD患者hs-CRP水平与PA、Alb、Hb以及TC等营养指标具有负相关性（r=-0．242,P=0．000;r=-0．193,P=0．000;r=-0．166,P=0．001;r=-0．289,P=0．002）。低蛋白血症（Alb〈35g／L）、低前清蛋白血症（PA〈180mg／L）和低胆固醇血症（TC〈3．1mmo/L）AECOPD患者hs-CRP显著升高,其发生率均显著高于正常水平患者（X^2=10．389,P=0．001;X^2=4．069,P=0．044;X^2=12．656,P=0．000）。其hs-CRP显著升高的几率比（OR）分别为2．931、1．851、11．172倍,低蛋白血症、低前清蛋白血症以及低胆固醇血症与hs-CRP显著升高有较强的关联度。低蛋白血症、低前清蛋白水平、贫血以及低胆固醇血症组hs-CRP水平显著高于正常水平组（z=-3．086,P=0．002;0=-3．284,P=0．001;z=-2．557,P：0．011;z=-3．942,P=0．000）。结论AECOPD患者hs-CRP水平与营养状况具有密切关系,可作为评价营养状况以及预后的指标之一。