肺心病患者血清hs-CRP与心肌酶的临床观察

目的探讨血清hs-CRP(超敏C反应蛋白)、CK-MB(磷酸肌酸激酶同工酶MB)、CK(磷酸肌酸激酶)、LDH(乳酸脱氢酶)、AST(天门冬酸氨基转移酶)在慢性肺心病患者急性发作期及治疗缓解期的变化情况。方法测定95例确诊为肺心病急性发作期患者治疗前后、60例肺心病治疗缓解期患者及30例正常人血清hs-CRP、心肌酶水平。结果肺心病患者血清hs-CRP、心肌酶明显高于健康人群,且急性发作期明显高于临床缓解期(P<0.05);急性发作期患者治疗前后血清hs-CRP、心肌酶差异显著(P<0.05);死亡组血清hs-CRP、心肌酶明显高于存活组(P<0.05)。结论血清hs-CRP与心肌酶的变化可作为肺心病患者的预后及疗效判断的有效指标。     

慢性肺心病缺氧程度与血清酶的关系

目的探讨慢性肺源性心脏病（肺心病）病情、预后与缺氧程度的关系。方法84例肺心病患者分为临床缓解期、急性加重期两组，以正常健康人为对照，同时测定血清中的5种酶即磷酸肌酸激酶（CPK）、乳酸脱氢酶（LDH）、天冬氨酸转移酶（AST）、丙氨酸氨基转移酶（Au）、γ-羟丁酸脱氢酶（HBD）及PaO2、SaO2。结果发现肺心患者HBD、LDH活力显著增高；重度缺氧的肺心病急性加重期患者AST、ALT活力也增高明显，与正常人比较差异有显著性。急性加重期轻、中、重度缺氧3组经方差分析，血清酶HBD、LDH与PaO2、SaO2存在线性负相关。结论慢性肺心病患者血清酶变化以HBD、LDH最敏感，它们增高在肺心病患者可作为心肌损伤、病程变化的一种标志物。血清酶活力与缺氧程度密切相关，缺氧愈严重，酶活力增高愈明显。血清酶中的HBD、LDH、AST、ALT等活力显著增高是病情危重信号，是估计预后的有效指标。     

肺心病患者血清肿瘤坏死因子α测定及其意义

目的：探讨血清肿病坏死因子α在COPD合并肺心病的作用。方法：COPD（慢性阻塞性肺疾病）缓解期患者16例，急性发作期20例；肺心病缓解期14例，急性发作期46例；正常对照组50例，肺心病急性发作期患者又依NYHA心功能分级分为4组，用放射免疫法测定血清的TNFα水平。结果：COPD缓解期组，肺心病缓解期组TNFα明显高于正常对照组。COPD急性发作期组，肺心病急性发作期组TNFα又分别明显高于其缓解期。肺心病急性发作期组随着心功能不全的加重TNFα又逐级显著升高。结论：TNFα可作为衡量COPD、肺心病及心功能严重程度及判断预后的辅助指标。     

肺心病患者血清肿瘤坏死因子a测定及其意义

目的：探讨血清肿病坏死因子a在COPD合并啼心病的作用。方法：COPD(慢性阻塞性肺疾病)缓解期患16例，急性发作期20例；肺心病缓解期14例，急性发作期46例；正常对照组50例．肺心病急性发作期患又依NYHA心功能分级分为4组．用放射免疫法测定血清的TNF0水平。结果：COPD缓解期组，肺心病缓解期组TNFa明显高于正常对照组。COPD急性发作期组，肺心病急性发作期组TNFa分别明显高于其缓解期。肺心病急性发作期组随着心功能不全的加重TNFa又逐级显升高。结论，TNFQ可作为衡量COPD、肺心病及心功能严重程度及判断预后的辅助指标。     

急性发作期COPD患者血清XOD、MDA水平变化及盐酸氨溴索治疗观察

目的观察急性发作期慢性阻塞性肺疾病(COPD)患者血清黄嘌呤氧化酶(XOD)、丙二醛(MDA)水平变化,以及盐酸氨溴索对其的影响。方法 62例急性发作期COPD患者,随机分为盐酸氨溴索治疗组32例和常规治疗组30例。另取32例缓解期COPD患者为缓解期组,32例健康老年人为正常对照组。采用MTS/PMS比色法和硫代巴比妥酸(TBA)法测定盐酸氨溴索治疗组和常规治疗组治疗前后、缓解期组、正常对照组受检者血清XOD和MDA。所有患者均测定1秒钟用力肺活量实测值/预计值百分比(FEV1.0%)和第一秒用力呼气量占用力肺活量百分率(FEV1.0/FVC)。结果急性发作期COPD患者血清XOD、MDA与缓解期组、正常对照组受检者相比均明显升高(P均<0.01)。急性发作期COPD患者经治疗后病情缓解,XOD、MDA水平均比治疗前明显降低(P均<0.05)。采用盐酸氨溴索治疗的急性发作期COPD患者治疗后XOD、MDA与未采用盐酸氨溴索治疗者相比明显降低(P均<0.05)。结论急性发作期COPD患者血清XOD、MDA增高。盐酸氨溴索可降低急性发作期COPD患者血清XOD、MDA水平。     

COPD患者血清中LTB4和TNF-α的检测及其临床意义

目的 研究COPD患者血清中白三烯B4(LTB4)和肿瘤坏死因子(TNF-α)浓度的改变及其临床意义.方法 收集COPD患者急性发作期(30例)和缓解期(30例)以及正常对照组(30例)的血清,检测血清中LTB4和TNF-α.结果 ①30例COPD患者急性发作期LTB4为14.9±6.3.μg/L,30例缓解期为5.7±4.1 μg/L,30例正常对照组为1.5±0.7 μg/L,三组差异有显著性,P ＜0.05;②COPD患者急性发作期TNF-α为1154.5±107.6 ng/L,缓解期为776.3±82.5 ng/L,正常对照组为440.0±78.7 ng/L,三组差异有显著性,P＜0.05.结论 COPD的急性发作期,LTB4和TNF-α水平的升高反映了氧化应激增强.     

IL-4、IL-8和IL-10在支气管哮喘和慢性阻塞性肺疾病中的对比研究

目的 比较支气管哮喘和慢性阻塞性肺疾病(COPD)患者外周血IL4、IL-8和IL10的水平.方法 采用双抗体夹心法检测急性加重期和稳定期COPD患者各50例、急性发作期和缓解期哮喘患者各50例及50例健康志愿者血清中IL-4、IL-8、IL-10的水平.结果 两种疾病的急性发作期患者血清IL-4、IL-8水平均显著高于缓解期患者及对照组(P均＜0.05),血清IL-10水平显著低于缓解期患者和对照组(P均＜0.05).哮喘急性发作期患者血清IL-4水平显著高于COPD急性加重期患者(P＜0.05);IL-8和IL-10水平低于COPD急性加重期患者(P＜0.05).哮喘缓解期患者血清IL-10水平低于COPD缓解期患者(P＜0.05).结论 IL-4、IL-8和IL10参与了哮喘和COPD的气道炎症反应,IL4在哮喘的气道炎症形成中起重要的作用,而IL-8和IL-10为COPD的主要炎症因子.     

COPD急性加重期的炎性指标临床研究

目的研究慢性阻塞性肺疾病急性发作期患者血清C反应蛋白(CRP)、趋化因子配体18(CCL18)含量变化及临床意义。方法检测30例COPD急性加重期、第7天和缓解期及30例体检者血清CRP、CCL18浓度,同时测定1 s用力呼气容积占预计值百分数(FEV1%pred)和动脉血氧分压(PaO2)。结果COPD急性加重期患者及缓解期血清CRP和CCL18水平较对照组均明显升高,有显著差异性(P0.05);而治疗组缓解期血清CRP和CCL18水平均较急性发作期明显降低,具有统计学意义(P0.01)。COPD患者CRP和CCL18水平与FEV1%pred、PaO2均呈直线负相关关系(P0.05)。结论检测血清CRP和CCL18对COPD发生发展及疾病严重程度的判断,指导抗生素的使用有一定意义。     

慢性阻塞性肺疾病患者淋巴细胞颗粒溶素的表达及其与血清γ干扰素、白介素2相关性研究

目的 探讨慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患者不同病期颗粒溶素表达特点以及和γ干扰素(interferon-γ,IFN-γ)、白介素2(interleukin-2,IL-2)之间的关系.方法 采用免疫细胞化学技术检测108例COPD患者及46名健康对照组外周血淋巴细胞的表达水平,采用双抗体夹心ABC-ELISA法同步测定血清IFN-γ、IL-2浓度.结果 颗粒溶素在COPD患者和健康对照组外周血淋巴细胞中的阳性表达率比较差异有统计学意义(P<0.01).颗粒溶素在健康对照组、临床缓解期、急性发作期的外周血淋巴细胞中表达比较差异有统计学意义(P<0.01).COPD患者急性发作期血清IFN-γ、IL-2浓度较临床缓解期和健康对照组显著增高(P<0.01).COPD患者急性发作期和临床缓解期颗粒溶素表达与血清IFN-γ、IL-2浓度变化均呈正相关,并随着病情变化存在明显消长关系.结论 颗粒溶素参与了COPD炎症过程,起着清除病原体的积极作用.IFN-γ、IL-2与颗粒溶素在消除病原体方面可能起着相互协同的作用,可能影响颗粒溶素的释放.     

COPD患者血清中8-异前列腺素的检测及其意义

目的研究慢性阻塞性肺疾病（COPD）患者血清中8-异前列腺素（8-isoPG）浓度的改变及临床意义。方法收集COPD患者（40例）急性发作期和缓解期以及正常对照组（30例）的血清,用酶标记法检测血清中8-isoPG,同时检测AECOPD患者的第一秒呼气容量（FEV1）、最大呼气流速（PEF）、pH值、PaCO2、PaO2及血白细胞总数。结果①COPD患者急性发作期8-isoPG为35.43±7.29ng/L,高于缓解期（24.71±8.25ng/L）及正常对照组（13.31±6.19ng/L）,P〈0.05;②COPD患者8-isoPG浓度与痰量呈正相关,r=0.217,P〈0.05。结论 COPD的急性发作期,8-isoPG升高反映了氧化应激增强。     

慢性阻塞性肺病急性加重期心肌酶谱的变化

目的:探讨慢性阻塞性肺疾病(COPD)患者急性加重期低氧血症对心肌酶水平的影响。方法:68例COPD急性加重期患者按动脉血氧分压的水平分成3组。测定各组患者动脉血氧分压(PaO2)及血清天冬氨酸转氨酶(AST)、肌酸激酶(CK)、肌酸激酶同工酶(CK-MB)、乳酸脱氢酶(LDH)、α-羟丁酸脱氢酶(HBDH),并分析其PaO2与血清心肌酶水平的相关性。结果:重度低氧血症组患者血清心肌酶水平明显高于中度低氧血症组和轻度低氧血症组(P<0.01)。COPD急性加重期患者PaO2水平与对应的血清心肌酶呈直线负相关(r=-0.67～-0.87,P<0.01)。结论:低氧血症可导致COPD患者血清心肌酶水平增高,且动脉血氧分压与相应的心肌酶呈直线负相关。     

血清TNF-α、hs-CRP和PA检测在老年慢性阻塞性肺疾病中的临床价值

目的探讨血清肿瘤坏死因子α(TNF-α),高敏C反应蛋白(hs-CRP)和前白蛋白(PA)在老年慢性阻塞性肺疾病(COPD)诊疗中的临床意义。方法分别检测58例COPD急性加重期患者和24例缓解期患者血清TNF-α、hs-CRP和PA水平,并与同期50例体检健康者比较。结果 TNF-α和hs-CRP水平在COPD急性加重期较缓解期明显增高,急性加重期和缓解期TNF-α和hs-CRP水平较对照组明显增高(P<0.01)。而PA水平急性加重期和缓解期低于对照组,急性加重期水平低于缓解期(P<0.01)。随着肺功能下降,TNF-α和hs-CRP水平也逐渐增高(P<0.01);而相反,PA水平则逐渐降低(P<0.01)。结论 TNF-α、hs-CRP和PA表达水平与疾病严重程度相关,可能参与了COPD气道炎症反应,检测三者可作为判断COPD临床分期、气流受限程度的指标。     

Serum CPK isoenzymes after cardiac catheterization.

Exclusion of acute myocardial infarction preoperatively, particularly in patients undergoing cardiac catheterization, is an important requirement for optimal results following coronary revascularization. Unfortunately, activity of conventionally measured serum enzymes (AST, LDH, total CPK) is frequently raised because of enzyme released from non-cardiac sources during the catheterization procedure. however, serum activity of the MB CPK isoenzyme, an isoenzyme found primarily in heart muscle, appears to be more specific. Accordingly, in the present study, total CPK and MB CPK activities were determined in serum samples from 53 patients undergoing diagnostic catheterization, immediately before study and serially for 24 hours afterwards. A comprehensive range of catheterization procedures included selective coronary arteriography in 39 patients by brachial (17) or femoral (22) artery approaches. Myocardial infarction was excluded by clinical and electrocardiographic criteria in all patients before and after the procedure. MB CPK isoenzyme activity was also measured in serum samples from 50 patients with actue myocardial infarction documented electrocardiographically, and in 20 controls admitted to hospital but without cardiovascular disease. In patients with acute myocardial infarction, both total CPK and MB CPK isoenzyme levels were significantly raised (0.78 +/- 0.087 and 0.086 +/- 0.037 IU/ml, respectively), exceeding the upper limit of normal in all cases. MB CPK activity remained within normal limits (less than 0.004 IU/ml) in all 20 subjects without cardiovascular disease. Peak total serum CPK activity exceeded control levels in all patients undergoing catheterization (0.260 +/- 0.033). However, in each case, MB CPK isoenzyme activity remained within normal limits (less than .004). Thus, in contrast to an increase of activity of conventionally used serum enzymes, increased MB CPK isoenzyme activity is a reliable indicator of myocardial infarction, even in patients undergoing cardiac catheterization.     

Serum CPK isoenzymes after cardiac catheterization.

Exclusion of acute myocardial infarction preoperatively, particularly in patients undergoing cardiac catheterization, is an important requirement for optimal results following coronary revascularization. Unfortunately, activity of conventionally measured serum enzymes (AST, LDH, total CPK) is frequently raised because of enzyme released from non-cardiac sources during the catheterization procedure. however, serum activity of the MB CPK isoenzyme, an isoenzyme found primarily in heart muscle, appears to be more specific. Accordingly, in the present study, total CPK and MB CPK activities were determined in serum samples from 53 patients undergoing diagnostic catheterization, immediately before study and serially for 24 hours afterwards. A comprehensive range of catheterization procedures included selective coronary arteriography in 39 patients by brachial (17) or femoral (22) artery approaches. Myocardial infarction was excluded by clinical and electrocardiographic criteria in all patients before and after the procedure. MB CPK isoenzyme activity was also measured in serum samples from 50 patients with actue myocardial infarction documented electrocardiographically, and in 20 controls admitted to hospital but without cardiovascular disease. In patients with acute myocardial infarction, both total CPK and MB CPK isoenzyme levels were significantly raised (0.78 +/- 0.087 and 0.086 +/- 0.037 IU/ml, respectively), exceeding the upper limit of normal in all cases. MB CPK activity remained within normal limits (less than 0.004 IU/ml) in all 20 subjects without cardiovascular disease. Peak total serum CPK activity exceeded control levels in all patients undergoing catheterization (0.260 +/- 0.033). However, in each case, MB CPK isoenzyme activity remained within normal limits (less than .004). Thus, in contrast to an increase of activity of conventionally used serum enzymes, increased MB CPK isoenzyme activity is a reliable indicator of myocardial infarction, even in patients undergoing cardiac catheterization.     

急性肺血栓栓塞患者血清酶学及肌钙蛋白I的变化

目的观察急性肺血栓栓塞（PTE）患者血清酶学及肌钙蛋白Ⅰ（TnI）的变化，了解其与估测肺动脉收缩压、右心运动功能及预后的关系。方法519例PTE患者来自北京24家医院参与的国家“十五”科技攻关课题——肺栓塞规范化诊治方法的研究。根据2001年5月中华医学会呼吸病学分会制定的《肺血栓栓塞症的诊断与治疗指南（草案）》的诊断标准确定大面积、次大面积、非大面积肺栓塞患者。大面积、次大面积肺栓塞患者采用溶栓治疗，非大面积肺栓塞患者采用抗凝治疗。按中心随机方法将患者分组，应用尿激酶和重组组织型纤溶酶原激活剂及普通肝素和低分子肝素。结果（1）大面积肺栓塞患者治疗前血清丙氨酸转氨酶（ALT）、天冬氨酸转氨酶（AST）、肌酸激酶（CPK）、乳酸脱氢酶（LDH）水平[（74±33）、（88±40）、（157±75）、（419±264）U／L]明显高于次大面积肺栓塞患者[（52±21）、（43±18）、（75±30）、（284±176）U／L]和非大面积肺栓塞患者[（38±13）、（35±11）、（78±24）、（239±178）U／L]；（2）非大面积肺栓塞患者应用普通肝素治疗7d后血清ALT[（84±39）U／L]明显高于应用低分子肝素患者[（67±26）U／L]；（3）519例患者中45例肺动脉收缩压≥80mmHg（1mmHg=0．133kPa），治疗前存在右心运动功能减弱169例，预后不良48例。大面积肺栓塞患者中17例（41．5％）AIJT升高，次大面积中76例（45．5％），非大面积中26例（54．5％）。大面积肺栓塞患者中24例（54．4％）LDH升高，次大面积中68例（40．2％），非大面积中15例（30．8％）；（4）39例血清TnI≥0．07μg／L的患者中右心功能减弱24例（63．3％），预后不良者8例（24．2％）。结论（1）急性PTE患者可出现血清ALT、ASF、CPK、LDH水平升高；（2）非大面积肺栓塞患者应用抗凝治疗，普通肝素较低分子肝素更易引起血清ALT升高；（3）血清ALT、LDH以及TnI的升高与PTE患者的肺动脉收缩压、右心运动功能及预后密切相关，其变化可能有助于对急性肺栓塞患者进行危险分层。     

心肌酶谱对血停跳液心肌保护作用的评价

在５２例复杂先心病心内矫正术中，应用血停跳液（ＢＣＰ）加强心肌保护，与晶体停跳液（ＣＣＰ）进行比较。记录术前、术后６、１２、２４、４８、７２小时内ＣＰＫ、ＣＫ－ＭＢ、ＡＳＴ、ＬＤＨ的变化。结果显示５：术后７２小时内，ＢＣＰ组ＣＫ－ＭＢ值均低于ＣＣＰ组，其峰值只是ＣＣＰ组的５９．８％（Ｐ＜０．０５），酶的释出量大为减少，并于７２小时降至正常，恢复比ＣＣＰ组早；ＣＰＫ、ＡＳＴ、ＬＤＨ值均显示较ＣＣＰ组低。血停跳液能增加心肌能量储备，提高心肌抗缺血的能力，减轻心肌损伤的程度，在加强复杂先心病的心肌保护中，显示出显著的效果。ＢＣＰ心肌保护的效果优于ＣＣＰ。     

COPD患者血清和诱导痰中前列腺素-E2水平的变化及意义

目的 检测慢性阻塞性肺疾病急性加重期(AECOPD)和稳定期血清和诱导痰中前列腺素-E2(Prostagland E2 PGE2)的水平,探讨PGE2在COPD发病机制中的作用.方法 选择AECOPD患者30例,稳定期患者30例,健康对照组30例.对诱导痰进行炎症细胞分类计数,测定血清和诱导痰上清液中PGE2水平,并分析PGE2与中性粒细胞、气流阻塞之间的相关性.结果 AECOPD患者血清及诱导痰中PGE2水平明显高于COPD缓解期,比较差异有统计学意义(P＜0.05),AECOPD组和COPD缓解期组痰中PGE2水平高于健康对照组,比较差异有统计学意义(P＜0.05).AECOPD患者诱导痰中PGE2水平与中性粒细胞数呈正相关(P＜0.05),与第一秒用力呼气容积占预计值的百分比(FEV1占预计值％)呈负相关(P＜0.05).结论 PGE2参与COPD的炎症过程;诱导痰中PGE2水平可以作为COPD严重程度的指标.     

Effect of physical loading on serum enzyme activity in post-myocardial infarct patients

The study of patterns of serum AST, ALT, CPK, LDH, and glycogen phosphorylase (GP) activity following bicycle ergometry in 26 male patients 1 to 1.5 months after myocardial infarction demonstrated no increase in AST, ALT and CPK activity, whereas total LDH activity was increased, with a tendency to elevated LDH-1 and LDH-2 fractions, as compared to the baseline, in those cases where exercise was discontinued because of ST depression. Patients with favorable response to bicycle ergometry that continued until the submaximum heart rate for a given age was achieved showed a tendency to elevated LDH-5 that may be a physiological response to exercise. The demonstrated increase in total GP activity, both in patients with exercise-induced ST depression and in those with elevated ST from the leads corresponding to the site of myocardial infarction, may reflect stress-induced reversible ischemia.