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 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We prospectively elucidated the effect of home oxygen therapy (HOT) on the prognosis of patients with chronic pulmonary disease associated with pulmonary hypertension. One hundred and twenty-seven patients with pulmonary hypertension (mean pulmonary arterial pressure > or = 20 Torr) participated in this study. Fifty-four patients had chronic pulmonary emphysema, 5 chronic bronchitis, 19 diffuse panbronchiolitis, 29 old tuberculosis, 8 pulmonary fibrosis, and 12 other diseases. Fifty-one patients died of respiratory failure. The survival curve of patients who received HOT was not different from that of patients who did not receive HOT, although FEV1 and PaO2, both prognostic factors, were significantly worse in the patients who received HOT than in the patients who did not receive HOT. In the patients with COPD, the survival rate of patients who received HOT was significantly higher than that of those who did not receive HOT. The mean survival time of the patients who received HOT was significantly longer than that of the patients who did not received HOT (1971 +/- 217 SEM days and 978 +/- 156 days, respectively). From these data, we conclude that HOT improves the survival of patients with chronic pulmonary disease, especially COPD, associated with pulmonary hypertension.
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PMID:[Effect of home oxygen therapy on prognosis of patients with chronic pulmonary disease associated with pulmonary hypertension]. 130 22

We have shown that in patients with COPD, myocardial efficiency during exercise is enhanced following acute elevations of plasma phosphate (Pi). A decrease in Hb-O2 affinity (increase in P50) was not responsible for the improvement. We postulated that the physiologic benefit was due to the acute reversal of a subclinical myocardial Pi depletion. To further test this hypothesis in a chronic state, we studied nine stable hypoxemic (PaO2 = 64 +/- 2 mm Hg [+/- SEM]) patients with COPD over five weeks: two weeks at normal plasma Pi; and three weeks at elevated plasma Pi, induced by etidronate disodium (Didronel; 750 mg orally daily). Administration of etidronate disodium increased (p less than 0.05) plasma level of Pi (4.4 +/- 0.2 to 5.8 +/- 0.1 mg/dl), RBC level of Pi (3.1 +/- 0.2 to 4.1 +/- 0.2 mg/dl), RBC level of 2,3-DPG (16.2 +/- 1.1 to 21.3 g+/- 1.3 mumol/g of Hb) and P50 (23.7 +/- 0.5 to 26.0 +/- 0.8 mm Hg). At the end of the treatment, the widening of the C(a-v)O2 with exercise (7.1 +/- 0.8 to 8.9 +/- 0.6 ml/dl) was less pronounced than under control conditions (6.9 +/- 0.4 to 10.1 +/- 0.6 ml/dl; p less than 0.02); concomitantly, the crossover point (COP; the PaO2 below which a rightward-shifted Hb-O2 curve causes the C(a-v)O2 to become narrower rather than wider) increased (37 +/- 2 to 49 +/- 1 mm Hg). Indicators of myocardial work efficiency were not affected by etidronate disodium at rest or during exercise. We postulate that during exercise the potential beneficial effect of the rightward shift of the Hb-O2 curve upon cardiac function was negated by the fall of PaO2 to or below the COP level, a situation which would limit increases in tissue O2 extraction.
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PMID:Pharmacologic elevation of blood inorganic phosphate in hypoxemic patients with COPD. 190 14

This study reports on the relationship of airway hyperresponsiveness (AH) with respiratory symptoms and diurnal peak flow expiratory (PEF) variation in 221 hyperresponsive patients with moderately severe airways obstruction. The disease was in a stable phase in all patients. Closely adhering to the American Thoracic Society criteria, patients were divided into three syndrome diagnoses based on a standardized history: asthma (n = 81), asthmatic bronchitis (AB, n = 69), and chronic obstructive pulmonary disease [( COPD] n = 44); 27 subjects could not be placed in any group. Mean (+/- SEM) log2 PC20 histamine values were significantly lower in the asthmatic group (-2.77 +/- 0.20 mg/ml) than in the COPD (-0.89 +/- 0.29 mg/ml) and AB groups (-1.37 +/- 0.25 mg/ml; one-way ANOVA, p less than 0.001). However, considerable overlap of individual responses existed. Differences between the groups could not be attributed to differences in prechallenge FEV1 levels. For every level of FEV1, asthmatic subjects were more hyperresponsive than patients with COPD. The dependence of PC20 on prechallenge FEV1 was comparable in all groups. There was a significant correlation between the degree of AH and diurnal PEF variation (rho = -0.401, p less than 0.001), which was stronger in asthma (rho = -0.409) than in COPD (rho = -0.325). Despite this obvious association, a wide range of diurnal PEF variation values existed for every level of PC20, indicating that PEF variability and AH are not interchangeable. The relationships between symptoms and both AH levels and PEF variation were weak. No significant differences were found between syndrome diagnosis groups with respect to diurnal PEF variation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relationship of airway hyperresponsiveness to respiratory symptoms and diurnal peak flow variation in patients with obstructive lung disease. The Dutch CNSLD Study Group. 202 43

The diagnosis of emphysema has been associated with changes in the appearance of the pressure-volume (P-V) curve: reduced maximal recoil pressure, increased lung volume, and a shift in the position of the curve to the left. In our clinical practice, we have observed that patients with chronic obstructive lung disease (COPD) commonly had P-V curves with reduced maximal elastic recoil that are difficult to classify according to the classic description of the P-V curve in emphysema. In order to study the variability of P-V curves, we studied 39 cigarette smokers attending a pulmonary clinic (age, 61 +/- 1 yr; smoking history, 45 +/- 3 pack-years; mean +/- SEM) and compared them with 20 patients with alpha-1-antitrypsin deficiency (AATD) (age, 41 +/- 2 yr; 13 smokers with a smoking history of 17 +/- 2 pack-years, and seven nonsmokers). Subjects underwent spirometry, lung volume, and diffusing capacity measurements as well as static deflation P-V curves. To characterize the P-V curves, we used transpulmonary pressure at 90% of TLC (PL90) as a measure of overall recoil and specific compliance (Csp) as a measure of the slope of the initial part of the P-V curve. The curves of non-AATD smokers were classified into three groups: 13 had PL90 greater than or equal to 80% predicted (Group I), 13 had PL90 less than 80% predicted and Csp greater than or equal to 0.08 (Group II), and 13 had PL90 less than 80% predicted and Csp less than 0.08 (Group III).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pressure-volume curves in smokers. Comparison with alpha-1-antitrypsin deficiency. 278 62

Frequently, patients with COPD with similar spirometric impairment have marked differences in dyspnea and exercise limitation. As the classic "blue bloater" with attenuated respiratory drive is described as being less dyspneic than his "pink puffer" counterpart, we wondered whether the variability in dyspnea and exercise tolerance in a group of patients with COPD with relatively similar degrees of air-flow obstruction might be partly explained by the variability in resting respiratory drives (unstimulated P0.1 and hypoxic and hypercapnic P0.1 responses). Therefore, we measured unstimulated mouth occlusion pressure (P0.1), hypoxic response (-delta P0.1/delta SaO2), hypercapnic response (delta P0.1/delta PCO2), 6-min walk distance, VO2max, steady-state exercise VE/VO2, exercise SaO2, and dyspnea using an oxygen cost diagram in 15 subjects with severe COPD (mean FEV1% 35.2 +/- 1.9 SEM). No correlations between spirometric impairment and either dyspnea or exercise performance were seen. Unstimulated P0.1 correlated inversely with spirometric impairment but did not correlate with dyspnea, VO2max or 6-min walk distance. Both hypoxic and hypercapnic responses were significantly correlated with greater exercise ventilation (VE/VO2), less exercise O2 desaturation, and a greater VO2max, but not with dyspnea or 6-min walk distance. The results of this study do not support the concept that depressed respiratory drives are associated with less dyspnea or greater exercise capability in COPD.
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PMID:Relationship of respiratory drives to dyspnea and exercise performance in chronic obstructive pulmonary disease. 311 45

To investigate the effect of theophylline on cardiac electrophysiology, electrophysiologic testing was performed before and during aminophylline (theophylline ethylenediamine) infusions in 10 male patients with stable COPD. This produced a mean plasma theophylline concentration of 15.6 +/- 0.9 micrograms/ml (mean +/- SEM) and increases in plasma catecholamine concentrations consistent with activation of the sympathetic nervous system. Plasma epinephrine increased from 40 +/- 6 to 57 +/- 9 pg/ml (p less than 0.05), and plasma norepinephrine increased from 406 +/- 63 to 522 +/- 90 pg/ml (p less than 0.01) during the aminophylline infusion. Significant reductions were seen in the atrioventricular (81.4 +/- 6.8 to 73.0 +/- 5.6 ms, p less than 0.05) and His-Purkinje (40.7 +/- 4.3 to 36.1 +/- 3.8 ms, p less than 0.02) conduction intervals, sinoatrial conduction time (81.3 +/- 10.3 to 65.0 +/- 7.6 ms, p less than 0.05), corrected sinus node recovery time (199.0 +/- 13.4 to 148.2 +/- 22.9 ms, p less than 0.05), shortest atrial pacing interval producing 1:1 atrioventricular conduction (391.0 +/- 25.5 to 325.0 +/- 15.5 ms, p less than 0.001), and atrial effective refractory period (ERP) (224.0 +/- 7.0 to 201.0 +/- 7.2 ms, p less than 0.01), but there was no change in the intraatrial (PA) conduction interval or ventricular ERP. Although no arrhythmias were induced, 5 patients had symptoms (3 presyncope and 2 chest pain) with rapid atrial pacing during but not prior to the aminophylline infusion. These changes could be caused by direct action of theophylline on cardiac conduction tissue or they may be caused at least in part by the associated increase in sympathetic tone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Theophylline-induced alterations in cardiac electrophysiology in patients with chronic obstructive pulmonary disease. 381 92

Primary pulmonary hypertension (PPH) is characterized by the proliferation of smooth-muscle cells, fibroblasts, and endothelial cells in the walls of small pulmonary arteries. In order to evaluate a role for proinflammatory cytokines in this process, we studied the concentration of interleukin-1 beta (IL-1 beta), IL-6, and tumor necrosis factor-alpha (TNF alpha) in the serum of 29 patients with severe PPH referred to our center for lung transplantation. Results were compared with those obtained in 15 normal controls and nine patients with pulmonary hypertension secondary to chronic obstructive pulmonary disease (COPD-PH). TNF alpha serum levels were within the normal range in each group. This contrasted with increased IL-1 beta serum levels in severe PPH (118 +/- 36 pg/ml, mean +/- SEM) as compared with controls (3 +/- 1 pg/ml, p < 0.001) or COPD-PH patients (3 +/- 1 pg/ml, p < 0.001). IL-6 serum concentrations were also higher in severe PPH (66 +/- 20 pg/ml) than in controls (14 +/- 6 pg/ml, p < 0.01). This study demonstrates increased serum levels of IL-1 beta and IL-6 in severe PPH, and suggests a role for proinflammatory cytokines in PPH.
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PMID:Increased interleukin-1 and interleukin-6 serum concentrations in severe primary pulmonary hypertension. 773 24

In order to study the efficiency of individual training programs at the ventilatory threshold level, twenty COPD patients were randomized into two groups and studied over a two-month period. At the start, during, and at the end of the study all subjects performed incremental exercise tests. The trained group (59.60 SEM +/- 2.75 years) walked four times a week at the heart rate corresponding to the metabolic level of ventilatory threshold. The other group served as controls (58.2 +/- 1.80 years). A marked increase in the symptom-limited oxygen consumption (+/- 25%) (p < 0.01), the maximal ventilation (+20%) (p < 0.01), and the ventilatory threshold (+19%) (p < 0.05) was found in the trained group. No modification was recorded in the control group. The ventilatory pattern at submaximal intensities expressed in percentage of the initial oxygen consumption showed significant differences between groups, the trained-group ventilation decreased at 50% and 75% VO2 sl (p < 0.05). The breathing frequency also decreased at 50% and 75% VO2 sl (p > 0.05). Moreover, we observed an increase in the oxygen pulse at 50% VO2 sl (p < 0.05). In conclusion, this study demonstrates that individualized training at the ventilatory threshold level increases exercise tolerance and produces better ventilatory comfort in COPD patients.
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PMID:[Value of individualized rehabilitation at the ventilatory threshold level in moderately severe chronic obstructive pulmonary disease]. 781 93

Eighteen patients with severe COPD and seven healthy control subjects 64.0 +/- 2.2 and 66.8 +/- 1.4 yr of age, respectively (mean +/- SEM), were investigated. Arterial blood gas analysis, dynamic lung volumes, and muscle biopsy specimens from the quadriceps femoris muscle were performed. The muscle biopsies were analyzed for citrate synthase (CS), succinic acid dehydrogenase (SDH), 3-hydroxyacyl-CoA dehydrogenase (HAD), phosphofructokinase (PFK), and lactate dehydrogenase (LDH) activities and related to protein content. The PFK activity was higher in the COPD group than in the control group (+34%, p < 0.05). CS showed a group difference in the opposite direction (-29%, p < 0.05). LDH activity followed PFK and tended to be higher in the patient group (+27%, NS), whereas SDH (-31%, NS) and HAD (-28%, NS) mirrored the CS results. Muscle protein concentration tended to be lower in the COPD group (-14%, NS). There were no significant changes in enzyme activity after 7 mo of long-term oxygen therapy (n = 6). These results indicate adaptation in the form of augmented glycolysis (PFK), and decreased aerobic metabolism (CS) in the quadriceps femoris muscle in patients with advanced COPD.
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PMID:Metabolic enzyme activity in the quadriceps femoris muscle in patients with severe chronic obstructive pulmonary disease. 766 93

Pulmonary rehabilitation has been shown to improve exercise capacity in patients with COPD. It has been suggested that this improvement applies to all age groups; however, to our knowledge, the effects of pulmonary rehabilitation on older elderly patients (> or = 75 years of age) have not been studied. We compared changes in 12-min walking distance (12MD) and self-assessment scores in 47 older elderly patients with moderate to severe COPD who completed inpatient or outpatient pulmonary rehabilitation with those achieved by 87 younger patients who participated in the same programs from 1987 to 1992. There were 28 older elderly individuals (mean +/- SEM, 78 +/- 1 years) in the outpatient group and 56 younger patients (64 +/- 1 years). There were no differences between older and younger outpatients with respect to FEV1, FEV1/FVC, maximum inspiratory pressure (PImax), baseline 12MD, or baseline self-assessment score. After outpatient pulmonary rehabilitation, 12MD and self-assessment scores improved significantly in both groups. Inpatients included 19 older elderly individuals (81 +/- 1 years) who were also similar to the 31 younger inpatients (64 +/- 1 years) in FEV1, FEV1/FVC, PImax, and baseline self-assessment score, but they tended to be more limited in terms of baseline 12MD (p = 0.09). After inpatient pulmonary rehabilitation, significant improvements in 12MD and self-assessment were seen in both groups. We conclude that comprehensive outpatient and inpatient pulmonary rehabilitation programs are as beneficial in older elderly patients with COPD as they are in younger patients with similar lung function abnormalities. Patients 75 years of age or older should be considered for comprehensive pulmonary rehabilitation.
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PMID:Pulmonary rehabilitation improves exercise capacity in older elderly patients with COPD. 787 45


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