The effect of nitroglycerin in gas exchange on chronic obstructive pulmonary disease.

Nitroglycerin was administered to a group of 11 patients with chronic obstructive pulmonary disease in a dose of 0.4 mg sublingually. Arterial blood gases and blood pressure and pulse were measured at 5-min intervals for 30 min after nitroglycerin. There was a slight decrease in arterial O2 tension for the duration of the study; the maximal change was from a mean pre-nitroglycerin value of 53.5 mm Hg to 50.3 mm Hg at 20 min. In addition, there was a slight reduction in arterial CO2 tension and bicarbonate for 25 min. It is postulated that decreased O2 transport (due to increased hypoxemia and probably decreased cardiac output) plus hypocapnia were a sufficient stimulus to raise blood lactate. It is recommended that in patients receiving nitroglycerin who have obstructive airway disease, attention be directed toward the effect on arterial blood gases.     

The effect of exercise on pulmonary gas exchange in patients with severe chronic obstructive pulmonary disease

The effect of low level, steady-state exercise on pulmonary gas exchange was studied in 7 patients with severe chronic obstructive pulmonary disease and pulmonary hypertension. Exercise led to a significant fall in the arterial PO2 from 76 +/- 10 to 63 +/- 8 mm Hg, a rise in the arterial PCO2 from 56 +/- 6 to 62 +/- 8 mm Hg, and a fall in the mixed venous PO2 from 38 +/- 2 to 32 +/- 2 mm Hg. There was, however, no significant change in the degree of ventilation-perfusion inequality as quantified by the multiple inert gas technique and no evidence that impaired O2 diffusion was playing a role in the increased hypoxemia. We conclude that the worsening hypoxemia with exercise in patients with severe COPD is due to an inadequate ventilatory response (leading to a rise in arterial PCO2) and the impact of a decreased mixed venous PO2 on the end-capillary PO2 of low VA/Q lung units and shunt.     

Hypoxic pulmonary vasoconstriction and gas exchange during exercise in chronic obstructive pulmonary disease

In patients with chronic obstructive pulmonary disease (COPD) studied at rest, nifedipine releases hypoxic pulmonary vasoconstriction (HPV) and worsens gas exchange. During exercise, this drug lowers pulmonary hypertension, but the effects of this lower pulmonary vascular tone on ventilation-perfusion (VA/Q) relationships are still poorly understood. To analyze them, we determined the VA/Q distributions in eight patients with stable COPD (FEV1, 36 percent of predicted) at rest and during exercise (60 percent VO2 max), before and after nifedipine (20 mg sublingually). Nifedipine shifted to the right the pulmonary pressure-flow relationship (p less than 0.01) and increased the dispersion of the blood flow distribution at rest and during exercise (p less than 0.005). These observations strongly suggest that nifedipine released HPV under both conditions. However, even after releasing HPV by nifedipine, exercise distributed blood flow more homogeneously than at rest (p less than 0.05). Besides, exercise greatly decreased the overall degree of VA/Q mismatching (p less than 0.001) not only before but also after nifedipine. Thus, we postulate that most of the VA/Q improvement that exercise may induce in patients with COPD, as it is shown here, is due to improvement in the ventilation distribution. Interestingly, this VA/Q improvement was not paralleled by a significant decrease of P(A-a)O2. This apparent paradox could be explained by 20 percent of the actual P(A-a)O2 during exercise due to diffusion limitation, as assessed through the inert gas approach. Taken all together, these results help to better understand the mechanisms that govern pulmonary gas exchange during exercise in COPD.     

Effects of nifedipine in patients with unstable chronic obstructive pulmonary disease

The hemodynamic and gas exchange effects of 20 mg of nifedipine (NFD), at rest and exercise were evaluated in seven patients with unstable COPD and pulmonary hypertension. The cause of instability was pulmonary infection (n = 6) and pulmonary emboli (n = 1). At rest, pulmonary hypertension (Pp = 40 +/- 3 mmHg), severe hypoxemia (PaO2 +/- 2 mmHg) and elevated pulmonary vascular resistance (Rp) = 9 +/- .6 u.sq.m, were found. At exercise, Pp raised to 52 +/- 5 mmHg with no change in cardiac index (CI), Rp or gas exchange. After NFD at rest, significant (p less than 0.05) increases in CI, oxygen transport and venous admixture occurred. Also, Rp and systemic arterial pressure and resistance decreased significantly. Pp and blood gas exchange did not vary. Rp and systemic resistance were lower at exercise after NFD than without the drug with no change in blood gas exchange. The pulmonary flow pressure relationship showed a right shift after NFD in both, rest and exercise conditions. We conclude that NFD can be of value for the management of pulmonary hypertension that aggravates COPD.     

Influence of posture on pulmonary gas exchange and heart rate in chronic obstructive lung disease.

Sixteen subjects with chronic obstructive lung disease were studied in supine and sitting position. VT, VE, VD and VD/VT were definitely higher in the sitting position (p less than 0.001). PaCO2 was slightly lower in the sitting position, whereas Pa?O2 was the same in both positions. P(A-a)O2 was essentially the same in both positions, but the estimated QS/QT was definitely lower in the sitting position. In patients with low FEV1.0 the heart rate showed a tendency towards higher values in the sitting position.     

慢性阻塞性肺疾病患者运动高峰时肺内气体交换对运动能力的影响

目的 探讨COPD患者在运动高峰时肺内气体交换对最大运动能力的影响.方法 对42例男性稳定期COPD患者及26例健康男性进行功率递增至症状自限的踏车运动,同步实时测定摄氧量和二氧化碳产生量,在运动高峰时抽取桡动脉血,测定并计算PaO2、PaCO2、死腔容积与潮气容积比值(VD/VT)和P(A-a)O2.分别对两组资料进行正态性检验,符合正态分布的资料以x-±s表示,两组间比较采用独立样本t检验,最大摄氧量与运动高峰时的血气参数进行相关因素分析.结果 COPD组的最大摄氧量[(16±4)ml·kg-1·min-1]明显低于对照组[(19±6)ml·kg-1·min-1];PaCO2[(43±3)mm Hg,1 mm Hg=0.133 kPa]、VD/VT(0.35±0.11)和P(A-a)O2[(33±11)mm Hg]均明显高于对照组[(40±5)mm Hg、0.27±0.08和(15±7)mm Hg];最大摄氧量与VD/VT呈显著负相关(r=-0.734,P＜0.01).结论 VD/VT增加导致通气效率降低,这是引起COPD患者运动能力减低的一个重要原因.     

他汀类药物治疗慢性阻塞性肺疾病的作用

COPD是以进行性气流受限及肺功能下降为特征的肺部炎症性疾病.由于肺功能受到损害,COPD患者的日常生活能力减退,住院率及病死率增加[1].COPD的发病率呈逐年上升趋势,预计在2020年COPD将成为世界第3位致死原因.     

Effect of medroxyprogesterone on ventilatory control and pulmonary gas exchange in chronic obstructive patients

Chronic obstructive hypercapnic patients were monitored for blood gases and breathing pattern, before, during and after a 7-day treatment with 75 mg/day of medroxyprogesterone (MPA). In 9 out of the 15 patients the PaCO2 level decreased (+/- 8 mm Hg) significantly with return to nearly control values at stop. 4 subjects still continued to improve after cessation of therapy and were considered as not being stable. In 2 patients PaCO2 did not change. We were unable to find any significant difference between the control values of these three categories. The study of the breathing pattern in responsive subjects showed an increase in minute ventilation and tidal volume, with a small increase in mean inspiratory flow and no change in inspiratory time as a function of total respiratory cycle time. We conclude that MPA lowers the PaCO2 of hypercapnic chronic obstructive pulmonary disease patients through an increased tidal volume, which could result from an increased central nervous inspiratory output, or from better mechanical performance of the respiratory muscles due to the same central stimulation.     

他汀类药物治疗慢性阻塞性肺疾病的作用

COPD是以进行性气流受限及肺功能下降为特征的肺部炎症性疾病.由于肺功能受到损害,COPD患者的日常生活能力减退,住院率及病死率增加[1].COPD的发病率呈逐年上升趋势,预计在2020年COPD将成为世界第3位致死原因.     

Effects of hydralazine on hemodynamics, ventilation, and gas exchange in patients with chronic obstructive pulmonary disease and pulmonary hypertension

Reports on hemodynamic effects of hydralazine on pulmonary hypertension (primary or secondary) usually include cases with severe disease or with mixed varieties of pulmonary vascular disease. Serious side effects and death have been reported. Effects of this drug on ventilation and gas exchange are unknown. We investigated the short-term effects of hydralazine treatment on hemodynamics, ventilation, and gas exchange in a relatively homogeneous group of patients with severe chronic obstructive pulmonary disease and moderate exertional pulmonary hypertension (mean pulmonary artery pressure, 43 +/- 3 mmHg). Hydralazine produced significant improvement in cardiac index, total pulmonary resistance, and oxygen transport. We also observed significant improvement in alveolar ventilation (mean PaCO2, decreased from 47 +/- 2 to 40 +/- 3 mmHg at rest and from 51 +/- 3 to 43 +/- 3 mmHg during exercise). The severe exertional hypoxemia of the group (mean PaO2, 48 +/- 2 mmHg) improved significantly (mean PaO2, 57 +/- 3 mmHg). Four of 11 patients showed increased exercise tolerance after hydralazine. This change is probably related to a combined improvement in hemodynamics plus a newly observed improvement in gas exchange and ventilation. Three of 14 patients could not tolerate hydralazine because of marked tachycardia. Serious side effects were not observed in the remaining group.     

The effects of urapidil therapy on hemodynamics and gas exchange in exercising patients with chronic obstructive pulmonary disease and pulmonary hypertension

To examine the hemodynamic changes induced by vasodilator therapy with urapidil during exercise in patients with chronic obstructive pulmonary disease (COPD) and their potential impact on symptom-limited maximal oxygen consumption, we studied 12 clinically stable patients using a randomized, crossover design. Placebo or urapidil (60 mg orally thrice a day) was given during 48 h preceding each incremental maximal exercise testing. Urapidil compared to placebo consistently lowered the pulmonary artery pressure either at rest from 29 +/- 2.5 to 24 +/- 1.5 mm Hg (p less than 0.001) or during exercise from 55 +/- 3 to 46 +/- 2 mm Hg (p less than 0.01). At rest, the systemic arterial pressure was reduced from 97.5 +/- 4 to 88.5 +/- 3 mm Hg (p less than 0.001) with no significant difference in heart rate or cardiac index. During exercise, systemic arterial pressure decreased from 135 +/- 4 to 119 +/- 3 mm Hg (p less than 0.001). As compared to placebo, urapidil tended to increase the cardiac index from 6.1 +/- 0.4 to 6.6 +/- 0.4 L/min.m2 (NS) and to decrease heart rate, from 122 to 116 beats/min (NS); the resulting stroke volume index increased with urapidil from 49 +/- 3 to 57 +/- 4 ml/m2 (p less than 0.01); at rest, urapidil did not induce alteration in gas exchange, while during exercise, C(a-v)O2 decreased from 8.6 +/- 0.5 to 7.7 +/- 0.4 vol% (p less than 0.01), SVO2 increased from 39.5 +/- 2 to 44.5 +/- 1.5% (p less than 0.01), and SaO2 from 82 +/- 2 to 85 +/- 2% (p less than 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)     

One-year clinical study on nifedipine in the treatment of pulmonary hypertension in chronic obstructive lung disease

The advantages of long-term administration of vasodilators in the treatment of chronic cor pulmonale were investigated after informed consent in 60 patients with obstructive respiratory insufficiency (56 men, 4 women, mean age 63.5 +/- 1.5 years; mean pulmonary pressure 30.4 mm Hg). They were randomly divided into two groups of 30, a control group and a group treated with nifedipine, 10 mg three times a day. The following parameters were recorded every 3 months for a year: dyspnea, degree of right ventricular failure, number of days spent in hospital, survival and arterial blood gas tension. On the first day of study, no significant difference existed between the control and the treated groups. After 1 year 22 patients in the control group were still followed and 8 were dead. In the treated group 19 were followed, 7 were dead and 4 stopped treatment, generally due to ankle edema. At the end of the study, the only significant modification was improvement of the dyspnea in the nifedipine group (p less than 0.01). In conclusion, in spite of an improvement in the dyspnea index, clinical study for 1 year failed to demonstrate any objective benefit of nifedipine treatment.     

Oral nifedipine in chronic cor pulmonale secondary to severe chronic obstructive pulmonary disease (COPD)

Hemodynamic effects of orally-administered nifedipine were evaluated in 12 patients with pulmonary hypertension secondary to severe COPD after short-term (30 and 60 minutes) treatment and then again in eight of these 12 patients after long-term (average 55 days) treatment. Pulmonary vascular resistance (PVR) decreased from 426 +/- 52 to 294 +/- 28 dynes.s.cm-5 (p less than 0.001) after therapy with 20 mg sublingual nifedipine (at 60 minutes). Cardiac index (CI) increased from 3.7 +/- 0.2 to 4.6 +/- 0.3 L/min/m2 (p less than 0.001). There was a decrease in mean pulmonary artery pressure (MPAP) only in 4/12 patients after Nifedipine. There was no significant fall in PaO2, while PvO2 and oxygen delivery (CI X CaO2) increased significantly 60 minutes after administration of sublingual nifedipine. PVR decreased from 482 +/- 82 to 374 +/- 44 dynes.s.cm-5 (p less than 0.05) after long-term nifedipine therapy. The changes in PVR and CI 60 minutes after administration of nifedipine in the patients on long-term treatment were similar to those observed with the same doses of nifedipine before initiation of therapy. Despite beneficial hemodynamic effects in two of eight patients, there was progressive clinical worsening. The benefit of long-term administration of nifedipine is difficult to predict on the basis of short-term effects.     

Repetitive hemodilution in chronic obstructive pulmonary disease and pulmonary hypertension: effects on pulmonary hemodynamics, gas exchange, and exercise capacity.

BACKGROUND: In cor pulmonale associated with severe chronic obstructive pulmonary disease (COPD), disturbances of pulmonary microcirculation may contribute significantly to hypoxemia, pulmonary hypertension, and exercise intolerance. OBJECTIVE: It was tested whether reduction of blood viscosity induced by repetitive hemodilution might improve pulmonary hemodynamics and oxygen uptake. METHODS: Seven patients with stable COPD (forced expiratory volume in 1 s 33 +/- 3 % of predicted, means +/- SE) and pulmonary hypertension were phlebotomized 5-6 times over a period of 3 months with substitution of 6% hydroxyethyl starch (molecular weight 40, 000). This resulted in a stepwise reduction of the hematocrit from 53.3 +/- 2.6 to 45.8 +/- 3.1% and a reduction of whole blood viscosity from 9.8 +/- 0.6 to 8.8 +/- 0.7 mPa x s at a shear rate of 2.0 s-1. Before and after the treatment period, patients underwent cardiopulmonary exercise testing and right heart catheterization. RESULTS: Mean pulmonary artery pressure (PAm) decreased from 30 +/- 3 to 22 +/- 2 mm Hg and arterial oxygen partial pressure (PaO2) increased from 63.2 +/- 2.2 to 71.8 +/- 3.7 mm Hg at rest. During peak exercise, PAm decreased from 59 +/- 7 to 53 +/- 7 mm Hg and PaO2 increased from 54.0 +/- 5.7 to 63.2 +/- 2.4 mm Hg after hemodilution. Peak oxygen consumption rose from 573 +/- 84 to 750 +/- 59 ml x min-1, corresponding to an increase in cardiac index from 4.25 +/- 0.5 to 5.88 +/- 0.76 liters x min-1 x m-2. Pulmonary vascular resistance fell from 345 +/- 53 to 194 +/- 32 dyn x s x cm-5. The patients' peak exercise capacity increased from 9.2 +/- 2. 0 before to 13.5 +/- 3.2 kJ at the end of the study (p < 0.05 for all differences, paired t test). CONCLUSION: The findings suggest that a prolonged improvement of pulmonary microcirculation by reducing blood viscosity may improve pulmonary gas exchange, central hemodynamics, and exercise tolerance in patients with severe COPD and pulmonary hypertension.     

慢性阻塞性肺疾病评估测试评分对预后的评估意义

目的探讨慢性阻塞性肺疾病评估测试(CAT)评分与慢性阻塞性肺疾病(COPD)患者预后因素之间的相关性,明确CAT评分对COPD患者预后评估的应用价值。方法选取2013年1月至2015年1月我院呼吸内科住院及门诊就诊的106例COPD患者为研究对象。对106例患者治疗前后进行CAT评分、6 min步行实验(6MWD)、改良英国MRC呼吸困难指数(m MRC)、BODE(B为体质量指数,O为气道阻塞程度,D为呼吸困难分数,E为运动耐力)指数、圣乔治呼吸问卷(SGRQ)评分及肺功能的测定。采用单因素线性相关分析CAT评分与患者各临床特征之间的相关性。结果随着CAT评分的升高,患者6MWD、用力呼气容积(FVC)实测值、FVC实测/预测值、一秒用力呼气容积(FEV1)实测值、FEV1实测/预测值、FEV1/FVC、呼气峰流速(PEF)实测值、PEF实测/预测值均明显降低(P0.05),而m MRC评分、BODE指数及SGRQ总评分明显升高(P0.05);患者经短期治疗后,CAT评分、BODE指数及SGRQ总评分均显著低于治疗前(P0.05),而6MWD、FEV1实测值、FEV1实测/预测值、FEV1/FVC则均显著高于治疗前(P0.05);单因素相关分析发现,治疗前CAT评分与m MRC评分(r=0.254,P=0.018)、BODE指数(r=0.426,P=0.009)及SGRQ总评分(r=0.563,P=0.007)呈显著正相关,与6MWD(r=-0.387,P=0.008)、FVC实测值(r=-0.181,P=0.023)、FVC实测/预测值(r=-0.192,P=0.021)、FEV1实测值(r=-0.201,P=0.016)、FEV1实测/预测值(r=-0.214,P=0.013)及FEV1/FVC(r=-0.223,P=0.012)呈显著负相关;治疗后CAT评分与m MRC评分(r=0.304,P=0.011)、BODE指数(r=0.382,P=0.010)及SGRQ总评分(r=0.621,P=0.004)呈显著正相关,与6MWD(r=-0.407,P=0.007)、FEV1实测值(r=-0.211,P=0.014)、FEV1实测/预测值(r=-0.228,P=0.012)及FEV1/FVC(r=-0.231,P=0.011)呈显著负相关。结论 CAT评分与COPD患者m MRC评分、BODE指数、SGRQ总评分、6MWD及肺功能指标均有较好的相关性,具有较好的预测COPD患者预后的应用价值。     

奥扎格雷钠对慢性阻塞性肺疾病合并慢性肺源性心脏病的临床治疗研究

目的观察奥扎格雷钠注射液对慢性肺源性心脏病患者血小板功能和心肺功能的影响。方法将80例COPD三级合并慢性肺源性心脏病急性发作的患者,随机分为对照组和干预组各40例,对照组给予吸氧、平喘、祛痰、利尿等支持治疗,纠正水电解质失衡,并根据病原学选择有效的抗生素。干预组在上述治疗的基础上给予奥扎格雷钠注射液160mg,1次／天,15天为1疗程。观察两组患者心功能、血小板功能指标、纤溶指标、肺功能、血气分析变化情况。结果干预组治疗后心功能、血小板各项参数改善情况明显好于对照组。FEV1／FVC升高幅度显著大于对照组,血氧分压和血氧饱和度的升高幅度及二氧化碳分压下降幅度显著大于对照组。结论奥扎格雷钠能有效改善肺心病患者血液高凝和低氧状态,降低肺循环阻力。     

吸入糖皮质激素对慢性阻塞性肺疾病的抗炎效应

目的　研究二丙酸氯地米松 (BDP)短疗程吸入对慢性阻塞性肺疾病 (COPD)的抗炎疗效。方法　 30例COPD患者分两组 (治疗组和安慰剂组 ) ,分别予BDP(10 0 0 μg·d-1)与安慰剂吸入治疗 6周 ,治疗前后测定肺功能 1秒钟用力呼气容积 (FEV1)、血浆内皮素 (ET 1)的质量浓度 ,诱导痰细胞总数 ,中性粒细胞 (PMN)分类及ET 1质量浓度 ,并记录临床症状记分。选择正常对照组 14例予以上指标测定。结果　COPD组诱导痰细胞总数、PMN分类、ET 1质量浓度均高于正常对照组 (P均 <0 0 1) ,且均与FEV1占预计值 %呈显著负相关 (P均 <0 0 1)。 2 7例完成实验 ,治疗组 14例临床症状改善 (P <0 0 5 ) ,FEV1提高 (P <0 0 1) ,诱导痰中细胞总数、PMN分类均明显下降 (P均 <0 0 1)。血浆ET 1和诱导痰ET 1质量浓度均无明显改变 ;安慰剂组 (13例 )治疗前后各项指标无明显差异。结论　气道炎性细胞在气道内活化聚集对COPD病理发生发展有重要作用。短期BDP吸入治疗COPD患者可抑制呼吸道炎性细胞浸润 ,缓解临床症状 ,提高肺功能 ,但不影响血浆与诱导痰的ET 1水平。