肺心病患者血浆内源性一氧化碳水平及其临床意义

目的　探讨慢性肺源性心脏病患者血浆内源性一氧化碳 (CO)的水平及其临床意义。方法　肺心病组 30例 ,正常对照组 30例。血浆CO测定采用分光光度法 ,同时测定血浆内皮素 1(ET 1)水平、动脉血氧分压 (PaO2 )及反映肺动脉压的超声指标—右室射血前期时间 (RVPEP)与肺动脉血流加速时间 (AT)的比值。结果　肺心病组急性加重期血浆CO水平 (1.78± 0 .79)ng/L和缓解期血浆CO水平 (1.2 1± 0 .38)ng/L ,均高于正常对照组 (0 .87± 0 .2 3)ng/L(均P <0 .0 0 1) ,且血浆CO水平与ET I、RVPEP/AT呈正相关 ,与PaO2 呈负相关。结论　内源性CO参与了肺心病的病理生理过程 ,肺心病患者血浆CO水平升高对于延缓肺动脉高压的发展具有一定的保护意义     

肺心病患者血浆内源性一氧化碳水平及临床意义

目的:探讨慢性肺原性心脏病患者血浆内源性一氧化碳(CO)的水平及其临床意义。方法:肺心病组30例,正常对照组30例。血浆CO测定采用分光光度法,同时测定血浆内皮素—1(ET-1)水平、动脉血氧分压(PaO_2)及反映肺动脉压的超声指标—右室射血前期时间(RVPEP)与肺动脉血流加速时间(AT)的比值。结果:肺心病组急性加重期血浆CO水平(1.78±0.79)和缓解期血浆CO水平(1.21±0.38)均高于正常对照组(0.87±0.23)(P<0.001,P<0.001);且血浆CO水平与ET—1、RVPEP/AT呈正相关;与PaO_2呈负相关。结论:内源性CO参与了肺心病的病理生理过程,肺心病患者血浆CO水平升高对于延缓肺动脉高压的发展具有一定的保护意义。     

哮喘患者血浆内源性一氧化碳的水平及意义

目的 :探讨一氧化碳 (carbon monoxide,CO)在哮喘发病中的作用和意义。方法 :应用 Chalmers血红蛋白结合及联二亚硫酸盐还原法测定支气管哮喘急性发作期、缓解期 2 6例及正常对照组 2 8例的血浆一氧化碳水平 ,同时测定了一氧化氮 (NO2 :/ NO3:)的水平及 Pa O2 、FEV1 .0 %。结果 :支气管哮喘患者急性发作期血浆 CO水平及 NO2 :/ NO3:水平均高于缓解期及正常对照组 ,且与 Pa O2 、FEV1 .0 %呈负相关 ,与 NO2 :/ NO3:水平呈正相关 (P<0 .0 1)。结论 :内源性 CO参与了哮喘的病理生理过程。     

二重滤过血浆置换治疗难治性高脂血症的近期和远期疗效

目的 :了解单次二重滤过血浆置换治疗非家族性、难治性高脂血症的短期疗效及对靶器官的长期保护效果。方法 :2 8例非家族性高脂血症患者接受二重滤过血浆置换疗法 ,取治疗前和治疗结束时的血样 ,分别测量血浆TC、TG、LDL、Apo(A)、Apo(B)、Lp(a)、HDL和纤维蛋白原水平。结果 :2 0例患者具有完整的记录 ,平均年龄 5 1.73± 6 .5 8(2 6～ 6 2 )岁 ;平均病程 6 .8年。单次治疗的总置换量为 4 183± 6 6 7(30 0 0～ 5 0 0 0 )ml,治疗前后TC、TG、LDL、Apo(A)、Apo(B)、Lp(a)、HDL和纤维蛋白原水平分别为 6 .86± 1.17mmol/Lvs 3.4 2± 0 .6 3mmol/L、3.92± 2 .13mmol/Lvs 3.5 7± 1.82mmol/L、4 .0 3± 0 .86mmol/Lvs 1.13± 0 .6 6mmol/L、1.34± 0 .37g/Lvs 0 .85± 0 .30g/L、1.34± 0 .5 7g/Lvs 0 .70± 0 .34g/L、176 .14± 75 .5 3mg/Lvs 98.4 3± 4 4 .0 8mg/L、1.0 3± 0 .2 8mmol/Lvs 0 .6 8± 0 .2 2mmol/L、2 6 3.6± 86 .5mg/dlvs 15 4 .9± 4 4 .1mg/dl。TC平均下降 5 1% ;LDL下降约 72 % ;Apo(a)和Apo(b)分别下降 32 %和 4 4 %左右。Lp(a)平均降低 4 0 % ,纤维蛋白原平均下降 4 3%。配对t检验提示单次置换后血浆TC、LDL、Apo(A)、Apo(B)、Lp(a)和纤维蛋白原水平有明显下降 (P <0 .0 5或P <0     

氨氯地平抗家兔动脉粥样硬化的作用机制

目的　探讨氨氯地平抗动脉粥样硬化的作用机制。方法　建立兔动脉粥样硬化模型 ,分为实验 1、2、3组、实验对照组 (AS组 )、空白对照组 ,检测各组不同时期血清中一氧化氮 (NO)、血浆中内皮素 (ET)水平。结果　血清中NO平均值 ,实验 1、2、3组、AS、空白对照组分别为 :4 .71± 0 .35 ,4 .6 2± 0 .4 8,3.71± 0 .5 6 ,2 .12± 0 .34,6 .72± 0 .37mmol/l。实验组与实验对照组比较 ,NO值明显升高 ,差异显著 (P <0 .0 1)。血浆中ET平均值 ,上述各组分别为 :30 2 .11±4 6 .2 1,2 84 .32± 37.2 5 ,35 7.79± 34.18,1835 .83± 2 6 .6 5 ,10 7.2 4± 2 4 .8Pg/ml。实验组与实验对照组比较 ,ET值明显降低 ,差异显著 (P <0 .0 1)。结论 :　氨氯地平抗动脉粥样硬化的作用机制可能与升高血清中NO、降低血浆中ET有关。     

慢性支气管炎患者内源性一氧化碳的变化

目的　探讨内源性一氧化碳 (CO)在慢性支气管炎 (简称慢支 )急性发作期和缓解期的变化及临床意义。方法　采用分光光度法测定 36例慢支患者急性发作期和缓解期的碳氧血红蛋白 (HbCO)百分含量和血红素氧合酶 (HO 1)活性 ,并以 36例健康不吸烟者和 36例健康吸烟者作为对照。结果　健康不吸烟者 (1.0 5±0 .4 8) % ,健康吸烟者 (3.6 2± 2 .70 ) % ,慢支急性发作期 (5 .18± 2 .2 6 ) % ,缓解期 (4.86± 2 .0 4 ) % ,慢支急性发作期HbCO与对照组比较差异有显著性 (P <0 .0 0 1)。健康不吸烟者HO 1活性 (以吸光度表示 )为 0 .0 4 6± 0 .0 10 ,健康吸烟者为 0 .0 5 0± 0 .0 14 ,慢支急性发作期为 0 .10 7± 0 .0 2 8,慢支缓解期为 0 .0 6 0± 0 .0 2 2。慢支急性发作期HO 1活性明显高于对照组和缓解期 (P <0 .0 0 1) ,与HbCO含量呈正相关 (r =0 .89)。结论　慢支急性发作期HO 1活性增高 ,引起内源性CO含量增加     

老年糖尿病患者血浆一氧化氮、内皮素水平变化及意义

目的 :探讨老年糖尿病患者血浆 ET- 1、NO水平变化及其临床意义。方法 :采用放免分析法、硝酸还原酶法分别测定 38例老年糖尿病患者和 30例正常老年人的血浆 ET- 1、NO水平。结果 :无血管并发症老年糖尿病患者的血浆ET- 1水平 (5 7.2 1± 2 9.5 4) ng/ L较正常老年人 (4 1.71± 11.33) ng/ L显著升高 ,有血管并发症 (137.70± 5 3.72 ) ng/ L 较无并发症者显著升高 (P均 <0 .0 0 1)。无血管并发症的老年糖尿病患者血浆 NO水平 (12 4.18± 5 1.15 ) μmol/ L较正常老年人 (6 9.36± 2 5 .44 ) μmol/ L 显著升高 ,有血管并发症的老年糖尿病患者血浆 NO水平 (4 7.19± 16 .93) μmol/ L较无并发症者和正常人显著降低 (P<0 .0 0 1)。结论 :ET与 NO在老年糖尿病血管并发症的发生、发展中起了重要作用     

脓毒性休克患者血中一氧化碳含量的变化与APACHEⅡ评分的关系

目的观察脓毒性休克患者血中一氧化碳含量的变化及其与APACHE Ⅱ评分的关系及意义.方法选择ICU脓毒性休克患者62例,在入ICU 24 h 内对每个患者进行APACHE Ⅱ评分,同时测动脉血中Hb和碳氧血红蛋白(COHb)含量,按照预后分为死亡组24例,存活组38例.另选同期无感染行择期手术的患者为对照组20例,测患者术前动脉血中Hb和COHb含量.结果对照组血中Hb含量为(135.1±9.3) g/L,脓毒性休克患者血中Hb含量较对照组略低,为(126.3±15.4) g/L,但差异无显著性.脓毒性休克患者血中COHb含量明显高于对照组,两组分别为(2.19±0.76)%和(0.64±0.31)%,P＜0.05.脓毒性休克患者APACHE Ⅱ各分段血中COHb含量与病死率随APACHE Ⅱ评分的增加而增加,COHb含量与APACHE Ⅱ评分呈显著正相关关系(r＝0.78,P＜0.05).死亡组血中COHb含量及APACHE Ⅱ评分高于存活组.结论内源性一氧化碳与脓毒性休克的病理机制密切相关,且与APACHE Ⅱ评分呈正相关关系,动态监测血中COHb含量的变化可能为预测病情提供参考.     

内皮功能异常在X综合征发病中的作用

目的　探讨内皮功能异常与 X综合征病因上的联系及其临床意义。方法　测定了 16例 X综合征患者的血浆一氧化氮 (NO)、内皮素 (ET- 1)水平 ,并采用高分辨超声技术检测其血管内皮功能 ,与 18例正常人 (对照组 )作比较。结果　 X综合征组血浆 ET- 1含量明显高于对照组 (85 .2± 2 1.2比 6 2 .6± 2 0 .0 ,P<0 .0 1) ;NO差异无显著性 (85 .0±2 0 .1比 90 .5± 2 5 .3,P>0 .0 5 ) ;X综合征组肱动脉血流介导性内皮舒张功能较对照组明显减退 [(4 .5± 1.5 ) %比 (13.1± 3.6 ) % ,P<0 .0 1],而两组对硝酸甘油的反应差异无显著性 [(2 2 .3± 7.7) %比 (2 1.2± 7.0 ) % ,P>0 .0 5 ];肱动脉血管内皮依赖性舒张功能与 ET- 1含量呈明显负相关 (r=- 0 .80 5 ,P<0 .0 1) ,与 NO/ET- 1呈正相关 (r=0 .6 92 ,P<0 .0 1) ,与NO基本无相关性 (r=0 .2 6 2 ,P<0 .0 1)。结论　冠脉微血管内皮功能异常导致其扩张储备功能降低在 X综合征发病中起着重要作用。     

慢性肺心病血浆一氧化氮水平和影响因素关系的研究

目的 :研究慢性肺心病不同状态血浆NO产物 (NO-2 /NO-3 )及其他相关指标 (L Arg、TNF、Ca2 )的水平变化以及它们之间的相互关系。方法 :采用高效液相色谱分析法 (HPLC)、放射免疫测定法 (RIA ) ,检测了 68例慢性肺心病患者、2 0例健康对照者血浆NO产物 (NO-2 /NO-3 )及其他相关指标。结果 :慢性肺心病患者不同状态血浆NO产物水平变化不同 ,与对照组 ( 2 72 2 .5 3± 80 4.40 )ng/ml比较 ,急性发作期PaO2 <60mmHg( 8kPa)时 ,血浆NO产物 ( 2 2 46.2 3±670 .5 4)ng/ml,明显降低 ( P <0 .0 1) ,当PaO2 >60mmHg时 ,其水平明显升高 ( 3 877.47± 93 0 .10 )ng/ml( P <0 .0 1) ,缓解期为 ( 2 82 8.96± 73 7.11)ng/ml,与对照组比无变化 ( P >0 .0 5 ) ,血浆NO产物变化与PaO2 呈正相关。慢性肺心病急性发作期PaO2 >60mmHg组血浆L Arg( 0 .3 5± 0 .19)mmol/L明显降低 (P <0 .0 1) ,而PaO2 <60mmHg组及缓解期组与对照组之间无差异 (P >0 .0 5 ) ,且NO与L Arg呈线性负相关。急性发作期TNF高于缓解期 ( P <0 .0 5 )。结论 :慢性肺心病急性发作期NO的水平变化与PaO2 呈正相关 ,与L Arg呈线性负相关。     

Measurement of critical lower limb tissue hypoxia by coupling chemical and optical techniques

It has been a long-term goal to develop non-invasive methods that can detect critical levels of tissue hypoxia to help in the management of chronic lower limb ischaemia. In the present study, skeletal muscle oxygenation was measured using a new Clark-type TCPO2 [transcutaneous PO2 (partial pressure of O2)]/PCO2 (partial pressure of CO2) monitoring system and optical NIRS (near-infrared spectroscopy) at graded levels of hypoxaemia using a rabbit model (n=6). The TCPO2/PCO2 probe was placed on the shaved hindlimb to record SPO2 (skin PO2) and SPCO2 (skin PCO2) continuously. A pair of NIRS probes were placed on the limb to monitor HbO2 (oxyhaemoglobin) and Hb (deoxyhaemoglobin). Graded hypoxaemia was achieved by stepwise reductions of FiO2 (fraction of inspired O2) from 30% to 6%. Animals were allowed to recover after each episode of hypoxia at an FiO2 of 30% as indicated by normalized arterial blood PO2. There was a significant (P<0.05) decrease in SPO2 with all grades of hypoxaemia and no significant changes in SPCO2. There was a significant (P<0.05) increase in muscle Hb with all grades of hypoxaemia and a significant (P<0.05) decrease in HbO2 when FiO2 was below 15%. A significant correlation was found between the SPO2 and HbO2 (r=0.92, P<0.001) and both were significantly correlated with arterial blood PO2 (P<0.001). The new TCPO2/PCO2 system, in addition to its application for the assessment of conditions such as chronic venous insufficiency where alteration in skin oxygenation occurs solely, also has potential in conditions such as peripheral vascular disease where both skin and muscle oxygenation may be affected.     

Circulating vascular endothelial growth factor and systemic inflammatory markers in patients with stable and exacerbated chronic obstructive pulmonary disease

The aim of the present study was to assess circulating levels of VEGF (vascular endothelial growth factor), a biomarker with prognostic significance in cardiovascular disease, and markers of systemic inflammation in patients with stable and exacerbated COPD (chronic obstructive pulmonary disease). Lung function parameters, arterial blood gas analysis and circulating levels of VEGF, IL-6 (interleukin-6), TNF-alpha (tumour necrosis factor-alpha), CRP (C-reactive protein), fibrinogen and the peripheral blood neutrophil cell count were assessed in 30 patients on admission to the hospital for acute exacerbation of COPD, in 30 age-, gender- and BMI (body mass index)-matched patients with stable COPD, and 30 matched controls with normal lung function. Patients with acute exacerbated COPD had higher circulating concentrations of VEGF (P<0.001), IL-6 (P<0.05) and CRP (P<0.01) and an increased blood neutrophil cell count (P<0.05) compared with patients with stable COPD and healthy controls. VEGF levels in exacerbated COPD correlated with systemic inflammatory markers, such as CRP (r=0.61, P<0.005), IL-6 (r=0.46; P<0.01) and fibrinogen (r=0.39, P<0.05). In patients with stable COPD, there was a significant relationship between circulating VEGF levels and the percentage of the predicted FEV(1) (forced expiratory volume in 1 s) (r=0.47, P<0.01). Recovery from the exacerbation resulted in a significant decrease in both circulating VEGF levels and markers of systemic inflammation. In conclusion, circulating levels of VEGF and markers of systemic inflammation are up-regulated in patients with acute exacerbated COPD and decrease after recovery from the exacerbation.     

COPD患者血清 Cav-1及 CXCL12水平检测与并发肺动脉高压的相关性研究

目的　探讨血清小窝蛋白 -1(caveolave-1,Cav-1)及趋化因子 C-X-C基元配体 12(chemokine C-X-C ligand 12,CXCL12)水平与慢性阻塞性肺疾病 (chronic obstructive pulmonary disease,COPD)并发肺动脉高压 (pulmonary hypertension,PH)的相关性。方法　收集 2019年 3月～ 2020年 3月期间在咸阳市第一人民医院和商洛市中心医院就诊的 115例 COPD 患者作为研究对象 ,依据患者是否并发 PH分为非 PH组 (NPH组 ,70例 )和 PH组 (45例 )。另选取 43例同期体检健康者作为对照组,采用酶联免疫吸附法测定血清 Cav-1和 CXCL12水平,所有患者均接受肺功能检测 ,用肺功能检测仪检测患者治疗前的 1s 用力呼气容积占预计值的百分比 (forced expiratory volume/predicted value,FEV1/Pre), FEV1占用力肺活量 (Forced vital capacity,FVC)的百分比 (FEV1/FVC)。通过彩色多普勒超声检查获得所有 COPD患者的肺动脉收缩压 (pulmonary artery systolic pressure,PASP)。收集患者的临床资料 ,包括二氧化碳分压 (PCO2)、氧分压 (PO2)、B型脑利钠肽 (brain natriuretic peptide,BNP)以及白介素 -6(interleukin- 6,IL-6)等,比较分析以上指标的变化与 COPD并发 PH的相关性。结果　在对照组 ,NPH组和 PH组中 ,血清 Cav-1和 CXCL12水平分别为 10.37±2.28,7.23±1 .72,4.81±0.90μg/L和 65.74±12.27, 175.36±26.19, 270.33±43.79pg/ml,与对照组比较 ,NPH组和 PH组的 CXCL12水平明显增高 ,且 PH组增高更显著 ;与对照组比较 ,NPH组和 PH组的 Cav-1水平则明显降低 ,且 PH组降低更显著,差异均有统计学意义 (F=103.71～ 130.67,均 P=0.000)。相关性分析显示 ,NPH组和 PH组的血清 Cav-1及 CXCL12水平分别呈负相关性 (r=-0.813,-0.827, 均 P <0.01),NPH组的 CXCL12水平分别与 PCO2,PASP,IL-6及 BNP水平呈正相关性 ,而与 FEV1/Pre,FEV1/FVC及 PO2呈负相关性。 NPH组的 Cav-1分别与 PCO2,PASP,IL-6及 BNP水平呈负相关性 ,而与 FEV1/Pre,FEV1/FVC及 PO2呈正相关性（ rCXCL12=0.845,0.810,0.807,0.783,-0.799,-0.775和 -0.793,均 P<0.01;rCav-1=-0.853,-0.828,-0.816,-0.792,0.763,0.803,0.822,均 P <0.01）。PH组的 CXCL12水平分别与 PCO2,PASP,IL-6及 BNP水平呈正相关性 ,而与 FEV1/Pre,FEV1/FVC及 PO2呈负相关性。 PH组的 Cav-1水平分别与 PCO2,PASP,IL-6及 BNP水平呈负相关性,而与 FEV1/Pre,FEV1/FVC及 PO2呈正相关性（ rCXCL12=0.839,0.816, 0.817,0.806,-0.782,-0.785,-0.809,均 P<0.01;rCav-1=-0.862,-0.821,-0.819,-0.797,0.782,0.811,0.829,均 P <0.01）。结论　血清 Cav-1及 CXCL12水平的差异性变化可能与 COPD患者 PH的形成有关,调节 Cav-1及 CXCL12水平能抑制炎症因子释放 ,缓解 COPD病情进展 ,改善患者的临床症状。     

Prediction of arterial blood gas values from venous blood gas values in patients with acute exacerbation of chronic obstructive pulmonary disease

Arterial blood gas (ABG) analysis has an important role in the clinical assessment of patients with acute exacerbation of chronic obstructive pulmonary disease (AECOPD). However, arterial puncture or insertion of an arterial catheter has many drawbacks. The aim of this study was to evaluate whether venous blood gas (VBG) values of pH, partial pressure of carbon dioxide (PCO(2)) and oxygen (PO(2)), bicarbonate (HCO(3)), and oxygen saturation (SO(2)) can reliably predict ABG levels in patients with AECOPD. One hundred and thirty-two patients with a prior diagnosis of COPD presenting with acute exacerbation according to AECOPD criteria were included in this prospective study. AECOPD is defined as a recent increase in cough, wheezing, the volume and purulence of sputum or shortness of breath necessitating a change in regular medication, including corticosteroids or antibiotics. ABG samples were taken immediately after venous sampling, and both were analyzed. Linear regression analysis was performed and equations were established for the estimation of arterial values. The Pearson correlation coefficients for pH, PCO(2), HCO(3), PO(2), and SO(2) were 0.934, 0.908, 0.927, 0.252, and 0.296, respectively. There was a significant correlation between ABG and VBG values of pH, PCO(2), and HCO(3) (p < 0.001). Linear regression equations for the estimation of pH, PCO(2), and HCO(3) were as follows: arterial pH = 1.004 x venous pH; arterial PCO(2) = 0.873 x venous PCO(2); and arterial HCO(3) = 0.951 x venous HCO(3). VBG analysis can reliably predict the ABG values of pH, PCO(2) and HCO(3) in patients with AECOPD.     

Carboxyhemoglobin and lactate levels do not correlate in critically ill patients

Endogenous carbon monoxide (CO) is produced in the degradation of heme by heme oxygenase. Studies have shown that hypoxia induces heme oxygenase production of CO in vascular tissue. Because elevated plasma lactate levels are associated with tissue hypoxia, we determined if there was any correlation between lactate and carboxyhemoglobin (COHb) levels in a group of critically ill patients with a high likelihood of hypoxia. In a 7.5-month period, 5322 simultaneous arterial COHb and lactate measurements were performed routinely on 183 patients with a blood gas analyzer in the Department of Veterans Affairs Medical Center, Bronx, New York, Surgical Intensive Care Unit. Sixty-one percent of the patients had elevated lactate levels (> 2.5mmol/L), and 46% had elevated COHb levels (> 1.5%). Lactate levels ranged from 0.12 to 22.7 mmol/L and COHb levels from 0% to 4.8%. There was no correlation between lactate and COHb levels (r = .07 with P < .0001). Levels of endogenous CO do not increase in situations in which lactate production is increased. It is possible that changes in endogenous production of CO may not significantly affect the circulating level of COHb. Although readily available, COHb levels do not seem to be clinically useful as markers of critical illness.     

Evidence that diffusion limitation determines oxygen uptake kinetics during exercise in humans.

To determine the role of arterial O2 content on the mechanism of muscle O2 utilization, we studied the effect of 2, 11, and 20% carboxyhemoglobin (COHb) on O2 uptake (VO2), and CO2 output (VCO2) kinetics in response to 6 min of constant moderate- and heavy-intensity cycle exercise in 10 subjects. Increased COHb did not affect resting heart rate, VO2 or VCO2. Also, the COHb did not affect the asymptotic VO2 in response to exercise. However, VO2 and VCO2 kinetics were affected differently. The time constant (TC) of VO2 significantly increased with increased COHb for both moderate and heavy work intensities. VO2 TC was positively correlated with blood lactate. In contrast, VCO2 TC was negatively correlated with increased COHb for the moderate but unchanged for the heavy work intensity. The gas exchange ratio reflected a smaller increase in CO2 stores and faster VCO2 kinetics relative to VO2 with increased COHb. These changes can be explained by compensatory cardiac output (heart rate) increase in response to reduced arterial O2 content. The selective slowing of VO2 kinetics, with decreased blood O2 content and increased cardiac output, suggests that O2 is diffusion limited at the levels of exercise studied.     

Mixed venous blood gases are superior to arterial blood gases in assessing acid-base status and oxygenation during acute cardiac tamponade in dogs.

Recent reports using anesthetized ventilator-dependent animal models, have suggested that in certain shock states, a disparity exists between arterial and mixed venous blood gases with regard to acid-base status and oxygenation. In a chronically instrumented unanesthetized canine model of acute cardiac tamponade breathing room air, we studied the effect of a graded decline in cardiac output on arterial and mixed venous pH, PCO2, and PO2. Cardiac tamponade resulted in a profound arterial respiratory alkalosis, whereas mixed venous pH, PCO2, and calculated serum bicarbonate levels remained relatively unchanged. As intrapericardial pressure increased and cardiac output declined, the difference between arterial and mixed venous PCO2 progressively increased. Further, whereas arterial oxygenation improved as cardiac output declined, mixed venous oxygenation steadily worsened. This disparity began early in cardiac tamponade (reductions in cardiac output of 20-40%) long before arterial blood pressure began to fall and progressively worsened as hemodynamic deterioration and lactic acidosis developed. Our findings are consistent with the hypothesis that a reduction in blood flow, resulting in decreased CO2 delivery to the lungs, is the primary mechanism responsible for the difference in pH and PCO2 observed between arterial and mixed venous blood. In this conscious, spontaneously breathing animal model, mixed venous blood gases thus are superior to arterial blood gases in assessing acid-base status and oxygenation, even early in acute cardiac tamponade when the decline in cardiac output is in the range of 20 to 40% and arterial blood pressure has not changed significantly.     

PAC-1、CD62P检测在慢性阻塞性肺疾病患者防治中的应用价值

目的探讨慢性阻塞性肺疾病(COPD)患者PAC-1、CD62P水平在肺心病发生发展过程中的意义。方法病例来自江苏省苏北人民医院呼吸科确诊的COPD患者60例,按有无肺心病分为肺心病组30例,单纯COPD组30例,另设20名健康体检者为对照组。应用流式细胞术检测全血活化血小板标记物PAC-1、CD62P的水平,以及与肺动脉压、血氧分压关系的分析。结果单纯COPD组,肺心病组PAC-1、CD62P表达水平均高于正常对照组(P0.01),肺心病组PAC-1C、D62P表达水平又高于单纯COPD组(P0.01)。PAC-1、CD62P的表达水平重度肺动脉高压组(45 mmHg)轻度肺动脉高压组(45mmHg)(P0.01)。PAC-1、CD62P的表达水平重度缺氧组(60 mmHg)轻度缺氧组(60 mmHg)(P0.01)。结论 COPD患者尤为合并肺心病患者存在血小板活化,PAC-1、CD62P可作为判断病情严重性及抗血小板药物治疗的依据。     

高原地区肺心病患者血清碱性成纤维细胞生长因子水平与肺动脉压的关系

目的探讨血清碱性成纤维细胞生长因子(bFGF)在低氧性肺动脉高压发病中的作用。方法采用双抗体夹心酶联免疫吸附法(ELISA)检测高原地区(海拔2260~3300m)38例慢性肺源性心脏病(肺心病)急性加重期患者、30例慢性阻塞性肺疾病(COPD)缓解期患者和30例当地健康人血清bFGF含量,并使用彩色多普勒超声心动仪测定肺动脉血流频谱,计算平均肺动脉压(MPAP),使用血气分析仪测定动脉血氧分压(PaO2)。结果肺心病组血清bFGF(87.54±12.15)ng/L、MPAP(45.86±5.63)mmHg(1mmHg=0.133kPa)显著高于COPD组分别为(55.72±9.08)ng/L和(22.95±2.56)mmHg,P均<0.01,COPD组显著高于健康对照组分别为(49.83±8.78)ng/L和(20.34±2.23)mmHg,P均<0.05;肺心病组PaO2(38.79±4.56)mmHg显著低于COPD组(58.22±6.18)mmHg,P<0.01,COPD组则显著低于健康对照组(66.57±5.48)mmHg,P<0.01。肺心病组和COPD组血清bFGF水平与MPAP均呈显著正相关(r肺心病=0.788,rCOPD=0.674,P均<0.01),与PaO2均呈显著负相关(r肺心病=-0.735,rCOPD=-0.587,P均<0.01)。结论慢性肺心病患者血清bFGF水平明显升高,可能与其慢性低氧性肺动脉高压形成有一定关系。     

Local metabolic effects of dopexamine on the intestine during mesenteric hypoperfusion

This self-controlled experimental study was designed to test the hypothesis that dopexamine, a synthetic catecholamine that activates dopaminergic (DA-1) and beta2-adrenergic receptors, improves oxygenation in the jejunal mucosa during intestinal hypotension. In six normoventilated barbiturate-anesthetized pigs, controlled reductions in superior mesenteric arterial pressure (PSMA) was obtained by an adjustable clamp around the artery. Dopexamine infusions (0.5 and 1.0 microg.kg(-1).min(-1)) were administered at a freely variable PSMA (i.e., with the perivascular clamp fully open) and at a PSMA of 50 mmHg and 30 mmHg. We continuously measured superior mesenteric venous blood flow (QMES; transit-time ultrasonic flowmetry), jejunal mucosal perfusion (laser Doppler flowmetry), and tissue oxygen tension (PO2TISSUE; microoximetry). Jejunal luminal microdialysate of lactate, pyruvate, and glucose were measured every 5 min. Measurements of mucosal PCO2 (air tonometry), together with blood sampling and end-tidal PCO2 measurements, enabled calculations of pHi and PCO2 gap. Dopexamine reduced mesenteric vascular resistance and increased QMES at a PSMA of 50 mmHg and 30 mmHg. At a PSMA of 30 mmHg, dopexamine increased mesenteric oxygen delivery but did not influence mesenteric oxygen uptake or extraction. In this situation, dopexamine had no beneficial effect on jejunal mucosal blood flow. On the contrary, dopexamine increased mesenteric net lactate production and PCO2 gap, whereas PO2TISSUE and pHi decreased. Jejunal luminal microdialysate data demonstrated an increased lactate concentration and a pattern of decreased glucose concentration and increased luminal lactate-pyruvate ratio. These negative metabolic effects of dopexamine should be taken into account in situations of low perfusion pressures.