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PubMed2004

8-Isoprostane, a marker of oxidative stress, is increased in the expired breath condensate of patients with pulmonary sarcoidosis.

STUDY OBJECTIVE: 8-Isoprostane is considered an index of oxidative stress. Measurement of 8-isoprostane in the expired breath condensate, a totally noninvasive method, has not been used to explore the level of inflammation in pulmonary sarcoidosis. Therefore, the aim of our study was to measure the levels of 8-isoprostane in the expired breath condensate of patients with sarcoidosis, and to investigate the relation of 8-isoprostane level to disease activity. PATIENTS: We investigated 30 patients with pulmonary sarcoidosis (active disease, n = 14; nonactive disease, n = 16) and 12 healthy subjects as control group. METHODS: 8-Isoprostane was measured in the expired breath condensate of all subjects, and its levels were compared between the control and sarcoidosis groups as well as between the subgroups of patients with active and nonactive disease. In the group with sarcoidosis, 8-isoprostane levels were further correlated with markers that may reflect disease activity, such as serum angiotensin-converting enzyme (sACE) level, serum calcium level, and pulmonary function test results. RESULTS: The concentration of 8-isoprostane was increased in patients with sarcoidosis compared to control subjects (mean, 64.23 pg/mL; 95% confidence interval [CI], 37.00 to 91.46 pg/mL; vs mean, 20.75 pg/mL; 95% CI, 16.06 to 25.44 pg/mL; p = 0.04). The difference was primarily due to the patients with active disease, who had significantly higher levels of 8-isoprostane (mean, 111.4 pg/mL; 95% CI, 62.56 to 160.30 pg/mL; p < 0.001) compared to patients with nonactive disease (mean, 22.94 pg/mL; 95% CI, 15.89 to 29.99 pg/mL) or healthy subjects. 8-Isoprostane levels in patients with nonactive disease did not differ from those in healthy subjects (p > 0.05). In the patients with sarcoidosis, 8-isoprostane levels were positively correlated with sACE level (p < 0.0001, r = 0.69), but was not correlated with serum calcium level or pulmonary function test values. CONCLUSIONS: Our data suggest that 8-isoprostane levels are increased in the expired breath condensate of patients with sarcoidosis and might serve as an index of disease activity.

Adult↗
PubMed1991

The effect of postural change on the coefficient of diffusion in sarcoidosis patients.

Granulomatous angiitis is common in sarcoidosis. To test the hypothesis that patients with sarcoidosis have an impaired ability to recruit or to distend the pulmonary vascular bed, the postural change in the coefficient of diffusion (ratio of DCO to alveolar volume) for carbon monoxide was measured in 20 patients with sarcoidosis and in 10 normal subjects. The normal control group increased the coefficient of diffusion (KCO) by 12.8% (p, 0.05), when values at sitting position were compared to values at supine position. The sarcoidosis group did not significantly increase the coefficient with change in position. The absence of an increase in the coefficient of diffusion (KCO) in sarcoidosis with change in position may indicate vascular involvement.

Adult↗
PubMed2005

Pulmonary function changes after radiotherapy in non-small-cell lung cancer patients with long-term disease-free survival.

PURPOSE: To evaluate the changes in pulmonary function after high-dose radiotherapy (RT) for non-small-cell lung cancer in patients with a long-term disease-free survival. METHODS AND MATERIALS: Pulmonary function was measured in 34 patients with inoperable non-small-cell lung cancer before RT and at 3 and 18 months of follow-up. Thirteen of these patients had a pulmonary function test (PFT) 36 months after RT. The pulmonary function parameters (forced expiratory volume in 1 s [FEV(1)], diffusion capacity [T(lcoc)], forced vital capacity, and alveolar volume) were expressed as a percentage of normal values. Changes were expressed as relative to the pre-RT value. We evaluated the impact of chronic obstructive pulmonary disease, radiation pneumonitis, mean lung dose, and PFT results before RT on the changes in pulmonary function. RESULTS: At 3, 18, and 36 months, a significant decrease was observed for the T(lcoc) (9.5%, 14.6%, and 22.0%, respectively) and the alveolar volume (5.8%, 6.6%, and 15.8%, respectively). The decrease in FEV(1) was significant at 18 and 36 months (8.8% and 13.4%, respectively). No recovery of any of the parameters was observed. Chronic obstructive pulmonary disease was an important risk factor for larger PFT decreases. FEV(1) and T(lcoc) decreases were dependent on the mean lung dose. CONCLUSION: A significant decrease in pulmonary function was observed 3 months after RT. No recovery in pulmonary function was seen at 18 and 36 months after RT. The decrease in pulmonary function was dependent on the mean lung dose, and patients with chronic obstructive pulmonary disease had larger reductions in the PFTs.

Aged↗
PubMed1996

Membrane diffusion and capillary blood volume in chronic thromboembolic pulmonary hypertension.

A reduced diffusing capacity for carbon monoxide (DCO) is common among patients with chronic thromboembolic pulmonary hypertension (CTEPH) and often persists for more than a year following successful pulmonary thromboendarterectomy (PTE). To determine the relative contribution the pulmonary membrane diffusing capacity (DM) and pulmonary capillary blood volume (VC) make to the reduction in DCO, we measured both in 29 patients with CTEPH before and approximately 3 weeks after PTE. Mean preoperative DM was reduced in patients with CTEPH (28 mL min-1 mm Hg-1 vs 43 mL min-1 mm Hg-1 in control subjects; p < 0.001) and dropped significantly following PTE (21 mL min-1 mm Hg-1; p < 0.001). Mean preoperative VC was mildly reduced in the CTEPH group compared with healthy control subjects (57 vs 67 mL; p = 0.044) and did not rise following PTE (57 mL pre-PTE vs 54 mL post-PTE; p > 0.05) despite substantial reduction in mean pulmonary artery pressure and increase in cardiac output after surgery. We conclude that the low DCO observed in patients with CTEPH before and after PTE is principally caused by a reduced DM and to a lesser extent by a low VC. The mechanisms responsible remain speculative but may reflect pathophysiologic changes in the pulmonary microcirculation caused by chronic pulmonary hypertension that did not improve in the postoperative period studied.

Adult↗
PubMedDate not supplied

[Pulmonary manifestations of lupus erythematodes visceralis].

Eight patients with SLE were found on clinical and roentgenological grounds or by respiratory function tests to have evidence of lung involvement. Great discrepancies were noted between clinical findings and the results of the respiratory function tests on the one hand and lacking or discrete radiological changes on the other hand. Four patients with pulmonary fibrosis without auscultatory signs showed decreased compliance values and decreased diffusion and vital capacities were noticed in two. In only 2 out of 4 patients with abnormal clinical signs could fibrotic changes be detected roentgenologically. Corresponding to the general diagnostic experience the measurement of compliance, diffusion capacity and vital capacity are the most appropriate methodes for assessing these visceral manifestations of SLE.

Adolescent↗
PubMed1991

Pulmonary diffusion limitation after prolonged strenuous exercise.

To determine the effect of strenuous prolonged exercise on alveolo-capillary membrane diffusing capacity, 11 marathon runners aged 37 +/- 7 years (mean +/- SD) were studied before and during early recovery (28 +/- 14 min) from a marathon race. Lung capillary blood volume (Vc) and the alveolo-capillary diffusing capacity (Dm) were determined in a one-step maneuver by simultaneous measurements of CO and NO lung transfer (DLCO and DLNO, respectively) using the single breath, breath-holding method. After the race, both DLCO and DLNO were significantly decreased in all subjects (-10.9 +/- 4.8%, P less than 10(-4) and -29.0 +/- 11.1%, P less than 10(-4), respectively). The mean value of the derived DmCO decreased by -29.3 +/- 11.1%, whereas Vc had not entirely returned to control resting value. Although these results do not indicate the detailed mechanism involved, interstitial lung fluid was suspected to accumulate, particularly in alveoli, during the race. We concluded that the high overall work load and the extended duration of the exercise both contributed to a transient change in the structure of the alveolo-capillary membrane thereby affecting the diffusing capacity of the alveolo-capillary membrane.

Adult↗
PubMed1980

Effect of thrombolytic therapy on pulmonary-capillary blood volume in patients with pulmonary embolism.

To compare the effects of heparin thrombolytic agents in pulmonary thromboembolic disease, we randomly assigned 40 patients with pulmonary emboli but without other clinical cardiopulmonary disease either to heparin followed by oral anticoagulants (21 patients) or to urokinse or streptokinase followed by heparin and then by oral anticoagulants (19 patients). The effects on pulmonary-capillary blood volume and diffusing capacity were compared at two weeks and at one year. The pulmonary-capillary blood volume (in milliliters per square meter of body-surface area) was abnormally low (30 +/- 2.4) [+/- S.E.]; normal, 47 +/- 1.5) in the heparin-treated group at two weeks and remained unchanged at one year. In contrast, it was normal (45 +/- 2.5) in the group receiving thrombolytic agents, both at two weeks and at one year (P < 0.001). The pulmonary diffusing capacity was reduced to 69% of the predicted value in the heparin group at two weeks and 72% at one year, whereas it was 85% of the predicted value in the thrombolytic group at two weeks and 93% at one year (P < 0.001). These results indicate that thrombolytic agents allow more complete resolution of thromboemboli than do heparin and anticoagulants and that they improve capillary perfusion and diffusion.

Blood Volume↗
PubMed1979

Pulmonary reaction to upper mantle radiation therapy for Hodgkin's disease.

To study the effects of upper mantle radiation therapy on pulmonary function, forced expiratory volume in one second (FEV1), vital capacity (VC), inspiratory capacity (IC), diffusing capacity for CO (DLCO) and diffusion per unit of alveolar volume (DL/VA were determined in 28 patients with Hodgkin's disease, stages 1--3, before therapy and at regular intervals thereafter. Within the first year of follow-up there were significant declines in DLCO, VC, and IC, whereas there were no significant changes in FEV1 or DL/VA. DLCO showed the greatest decline in the largest number of subjects (22/28). Eleven of the 22 had 20 to 60 percent decline of DLCO from baseline. The maximum mean decline in DLCO was -12.7 +/- 3 percent at the 87th +/- 3 days from initiation of therapy postradiation sustained through the 150th day and improving to pretreatment value (+/- 5 percent) by the 8th to 12th month. The changes in DLCO seemed to be independent of the radiation dose ranges evaluated, clinically apparent intrathoracic lymphoma, postradiation radiographic abnormalities and respiratory symptoms. We concluded that impairment in diffusing capacity and loss of vital capacity will develop in most patients receiving upper mantle radiation therapy, indicating that pulmonary reaction occurs despite lung shielding. The functional losses were prolonged and occasionally severe, but were transient and subclinical in most but not all cases. A case of fatal radiation pneumonitis affecting the lung beyond the field of irradiation is reported.

Adolescent↗
PubMed1977

Lung hypoplasia in congenital pulmonary valve stenosis.

The pulmonary function of ten adult patients with congenital pulmonary valvular stenosis was investigated. The patients clearly showed smaller lungs than healthy control subjects of equivalent age and height; lung elastic recoil pressure was normal at any given percentage of measured total lung capacity, indicating that postnatal parenchymal damage is not the cause of the small lungs. The lung diffusing capacity for carbon monoxide was reduced, reflecting the anatomical alterations of the pulmonary vascular bed. Finally, the maximal flow-static recoil curves showed a fixed (not dynamic) reduction of airway dimensions: the critical transmural pressure in the collapsible flow-limiting segment (Ptm') was normal, but the conductance of the S segment was lowered. These abnormalities most likely reflect inadequate development of the lung and suggest that pulmonary blood pressure may be an important determinant of lung growth in the postnatal period.

Adolescent↗
PubMed1976

Maximal oxygen consumption in patients with lung disease.

A theoretical model for oxygen transport assuming a series linkage of ventilation, diffusion, oxygen uptake by erythrocytes, cardiac output, and oxygen release was used to calculate expected values for maximal oxygen intake (VO2max) of patients with various pulmonary disorders 22 patients with either restrictive or obstructive ventilatory impairment were studied at rest and maximal exercise. When exercise measurements of maximal pulmonary blood flow (QCmax), oxygen capacity, membrane diffusing capacity for CO, pulmonary capillary blood volume, alveolar ventilation, and mixed venous oxygen saturation were employed as input values, predictions of VO2max from the model correlated closely with measured values (r = 0.978). Measured VO2max was 976+/-389 ml/min (45.3+/-13% of predicted normal), and VO2max predicted from the model was 1,111+/-427 ml/min. The discrepancy may in part reflect uneven matching of alveolar ventilation, pulmonary capillary blood flow, and membrane diffusing capacity for CO within the lung; uniform matching is assumed in the model so that mismatching will impair gas exchange beyond our predictions. Although QCmax was less than predicted in most patients (63.6+/-19.6% of predicted) the model suggests that raising QCmax to normal could have raised VO2max only 11.6+/-8.8% in the face of existent impairment of intrapulmonary gas exchange. Since pulmonary functions measured at rest correlated well with exercise parameters needed in the model to predict VO2max we developed a nomogram for predicting VO2max from resting CO diffusing capacity, the forced one second expired volume, and the resting ratio of dead space to tidal volume. The correlation coefficient between measured and predicted VO2max, by using this nomogram, was 0.942.

Adolescent↗
PubMed1993

Cardiopulmonary adaptations to pneumonectomy in dogs. II. VA/Q relationships and microvascular recruitment.

Ventilation-perfusion relationships, diffusing capacity for O2, and hemodynamic response were measured at rest and during exercise while five adult dogs breathed air and 15% O2 2 mo (Pnx-A, n = 2) or 12 mo (Pnx-B, n = 3) after right pneumonectomy (removal of 58% of lung tissue). Results were compared with those in five sham-operated controls. The multiple inert gas elimination technique was employed. Maximal O2 uptake was reduced by 50% in Pnx-A and by 15% in Pnx-B. Ventilation-perfusion matching was impaired in Pnx-A but not in Pnx-B. The increase in O2 diffusing capacity during exercise was significantly restricted in Pnx-A but was partially restored in Pnx-B. Mean pulmonary arterial pressure at a given blood flow through the remaining lung was normal in Pnx-A but lower than normal in Pnx-B compared with control values for a single lung. Stroke volume and cardiac output were lower in both Pnx-A and Pnx-B than in controls at a given exercise level. All functional abnormalities were more severe at 2 mo than at 12 mo postpneumonectomy. Gas phase diffusion resistance was present in both Pnx-A and Pnx-B but not in controls. We conclude that physiological compensation postpneumonectomy is progressive. Inability to recruit pulmonary vascular bed with incremental perfusion pressure or flow appears to be the major pathophysiological process that limits early functional capacity after right pneumonectomy.

Animals↗
PubMed1982

Diffusion in avian lungs.

Arterial PO2 in resting, normoxic avian lungs in not at the level of predicted for an ideal crosscurrent lung. In contrast to healthy alveolar lungs, such a reduction in efficiency of O2 exchange from optimal levels cannot be totally explained by ventilation/perfusion inequality, and the discrepancy is most likely related to diffusion resistances. The diffusing capacity of avian lungs (DLO2) will depend on: 1) stratification in the air capillaries, 2) blood-gas barrier morphology, 3) O2-Hb kinetics ( theta ), and 4) diffusive/perfusive conductance (D/ beta bQ) matching. Stratification in air capillaries, the membrane diffusing capacity, and time available in pulmonary capillaries for arterialization do not appear to be limiting at rest. D/ beta bQ inequality is expected in normoxic avian lungs but predictive models show that this should not limit O2 uptake. However, these resistances may interact in crosscurrent lungs or there may be other unknown diffusion limitations (e.g., theta ) to reduce PaO2 in birds. Recent morphologic evidence suggests DLO2 may increase in birds during exercise and V/Q and D/ beta bQ inequality would be expected to have less of an effect during hypoxia. Together, these factors may reconcile the relatively low PaO2 in resting birds at sea level and their ability to exercise at high altitudes.

Animals↗