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PubMed1994

The upper limit of alveolar capillary recruitment in a young man with lung growth impairment.

In order to obtain further insight into the adaptive mechanisms relating to gas exchange in anatomically small lungs, tests of mechanical lung function and gas exchange were made in an active young man, whose lung growth had been severely impaired due to pectus excavatum developed in childhood. We found our patient to have small (total lung capacity, 59% of predicted) but mechanically normal lungs. He had a normal cardiac output, a normal single-breath diffusing capacity (100% pred), and a high diffusion coefficient (148% pred) associated with a high pulmonary capillary blood volume (131% pred) at rest. Pulmonary distensibility (K) and elastic recoil were normal. During steady-state exercise he was unable to recruit further reserves of pulmonary capillaries, but this was not reflected in a plateau for oxygen consumption, which was presumably the result of an increased pulmonary capillary blood flow rather than volume. The recruitment of pulmonary capillary reserves in this young man has enabled him to maintain a normal maximum exercise capacity. In addition, the high stroke volume and a haemoglobin level in the high normal range (176 g.l-1) may have maintained his maximal exercise function, despite fewer alveolar units. This study suggests that, contrary to previous findings, loss of a major proportion of lung tissue need not impair exercise capacity. Patients with either small lungs or following pneumonectomy may benefit from physical training sufficient to optimize both an increase in cardiac output and recruitment of their existing alveolar capillary reserves.

Adult↗
PubMed1977

Regional intrapulmonary gas distribution in awake and anesthetized-paralyzed man.

Intrapulmonary distribution of ventilation/unit lung volume was studied in 28 volunteers in the sitting, supine, or right lateral decubitus position, either awake or anesthetized-paralyzed and mechanically ventilated. We found significant differences between the awake state and anesthesia-paralysis with mechanical ventilation in 1) intrapulmonary gas distribution, and 2) the vertical gradient of regional functional residual capacities for the subjects in the lateral decubitus position, but not for those in the sitting and supine positions. The effect of increasing the tidal volume on distribution of ventilation was significantly different 1) between the three body positions for a given state, and 2) between the two states for a given body position. The data suggest thoracoabdominal mechanics are different in the three body positions and that anesthesia-paralysis and mechanical ventilation may cause a different pattern of expansion of the respiratory system than spontaneous breathing in the awake state.

Adult↗
PubMed1994

Bronchoalveolar lavage immunoglobulin A and G and antiproteases correlate with changes in diffusion indices during the natural course of pulmonary sarcoidosis.

We wanted to determine whether cell populations and soluble components in bronchoalveolar lavage (BAL) could be useful in predicting the outcome of lung function and chest radiography in patients with untreated pulmonary sarcoidosis. Analysis of soluble proteins in BAL fluid, included the levels of immunoglobulins and the two major antiproteases, alpha 2-macroglobulin (alpha 2-M) and alpha 1-protease inhibitor (alpha 1-PI), expressed as a relative coefficient of excretion (RCE). Thirty one nonsmoking patients with biopsy proven sarcoidosis, who remained untreated, had reassessment of lung function tests after 6-54 months (median 21 months). No correlation was observed between initial BAL data and changes in lung volumes and radiographic opacities. By contrast, the initial BAL immunoglobulin A and G (IgA and IgG) RCE correlated inversely with the change in transfer factor for carbon monoxide (TLCO) in the whole group and in patients with sarcoidosis of recent origin (estimated disease duration < 6 months). In the whole group and in patients with longstanding disease (estimated disease duration > 24 months, or radiographic Stage 4), the change in carbon monoxide transfer coefficient (KCO) correlated negatively with the initial alpha 1-PI RCE and positively with the initial helper to suppressor T-cell (T4/T8) ratio. By contrast, no significant difference in BAL cellular and protein data was found between patients with recent and longstanding sarcoidosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

[Functional diagnosis of pulmonary sarcoidosis].

Restrictive disturbances of ventilation of various degree and disorders in diffusing capacity of the lung have been reported as the most frequent disorders in pulmonary sarcoidosis. Recently, however, several authors have found the obstructive disorders of ventilation being present as well, especially in the second stage of disease, and pointed out a possibility of the airways being affected very early at the onset of disease. Present study shows the results of functional tests carried out in 70 patients with histologically verified pulmonary sarcoidosis at all three stages of the disease (classification by Würm). All of them were nonsmokers, aged 20 to 55 years, and had no symptoms of chronic bronchitis, asthma or emphysema, either in case history or clinical findings. They included spirometry, flow-volume loop, body-plethysmography, blood gas analyses at rest and after exercise and pulmonary diffusing capacity for carbon monoxide obtained by single-breath method. Results from the study show the obstructive disorders of ventilation to be dominant in the early stage, while restrictive disturbances dominate in the third stage in pulmonary sarcoidosis. Diffusing capacity of the lung should be measured in the early stage of the disease as well as in those more advanced because of a possibility that interstitial space is being affected, although there is no visible damage on a radiograph. Measurement of pulmonary diffusing capacity together with radiological findings provide a highly valuable data which is of great importance in monitoring the dynamics of this disease.

Adult↗
PubMed1975

Relationship of arterial-alveolar nitrogen tension to alveolar-arterial oxygen tension, lung volume, flow measurements, and diffusing capacity in cystic fibrosis.

Pulmonary function in children with cystic fibrosis was assessed by the arterial-alveolar PN2 difference adjusted to sublingual temperature. The resulting values were compared with the alveolar-arterial PO2 difference, arterial PCO2, and standard measurements of lung volume, flow, and diffusing capacity. The arterial-alveolar PN2 difference was nearly one half of the PO2 difference, both early in the disease and at a more advanced stage. Analysis taking into account the O2 dissociation curve and the possibility that alveolar temperature is higher than sublingual temperature suggested that all of the PO2 difference could be explained in terms of ventilation-perfusion imbalance in gas-filled units of the lung. Reduction of fractional CO uptake with increasing PN2 difference suggested that the decrease in diffusing capacity in cystic fibrosis may be explained by ventilation-perfusion inequality. A significant relationship between arterial PCO2 and the PN2 difference supported the view that ventilation-perfusion inequality is the cause of CO2 retention when present. The PN2 and PO2 differences were abnormal before the standard tests of lung volume and flow, but in general, the correlation was excellent. Because the PN2 difference was not superior to the PO2 difference in detecting early disease, and because the technical problems in its measurement are considerable, it is not recommended as a routine measurement.

Adolescent↗
PubMed1993

Diffusing capacity decreases after heart transplantation.

We evaluated the following spirometric values: forced vital capacity (FVC), first second expiratory volume (FEV1), FEV1/FVC, the lung volumes, total lung capacity (TLC), residual volume (RV), and single breath diffusing capacity for CO in 22 patients, before and after heart transplant. We found abnormal pulmonary function in 21 patients before heart transplantation. Despite postoperative increases in lung volumes in 10 patients, abnormal pulmonary function persisted in 20 patients after heart transplant. Mean values for lung volumes and flow rates did not change but diffusion for CO decreased significantly after heart transplantation. Diffusion failed to correlate with ejection fraction, pulmonary arterial pressure, pulmonary capillary wedge pressure (PCWP), and pulmonary vascular resistance; however, in a subset of patients with improved postoperative lung volumes, preoperative diffusion for CO correlated with preoperative PCWP. We conclude that pulmonary function abnormalities are common among heart transplant recipients. Diffusion abnormalities are not linearly related to indices of cardiac function measured before transplantation and diffusion abnormalities appear to be multifactorial in cause. The posttransplant decrease in diffusion appears to result from the combined effects of decreased postoperative lung volumes in some patients and relief of heart failure induced pulmonary vascular engorgement in others. Improvement in lung volumes and flow rates may occur but cannot be expected after heart transplantation, and diffusion decreases after heart transplantation. The fact that pulmonary function and lung volumes do not improve following heart transplantation implies to underlying lung disease or permanent lung alterations result from chronic heart failure.

Adult↗
PubMed1992

Combined nitrofurantoin toxicity to liver and lung.

Nitrofurantoin is an antibiotic commonly used for prophylaxis and treatment of urinary tract infections. Pulmonary and hepatic toxicity are rare side effects of this agent. The simultaneous occurrence of pulmonary fibrosis and chronic active hepatitis in a patient undergoing long-term nitrofurantoin therapy is reported. The presence of pulmonary toxicity was evidenced by infiltrates on chest radiographs and impaired diffusion capacity during pulmonary function tests. Prolonged elevation of liver enzyme concentrations together with the presence of increased antibody titers (anti-smooth muscle antibody, antinuclear antibody) was suggestive of chronic hepatitis, a diagnosis corroborated by liver biopsy findings. After discontinuation of nitrofurantoin therapy, the patient had a full recovery. The infiltrates initially found on chest radiographs disappeared, and laboratory parameters normalized without the need for corticosteroid therapy.

Aged↗
PubMed1997

Effects of smoking and clinical status on lung function in human immunodeficiency virus (HIV)-seropositive subjects.

Lung function was measured at 3-month intervals for up to 1 yr in a group of Caucasian HIV-seropositive subjects. The objective was to document any deterioration in lung function and seek correlations between such deterioration and smoking history and Centers for Disease Control (CDC) status. Ninety-nine subjects were studied at enrollment; 43 were followed-up (mean duration 9 +/- 3 months). Ninety-five of the 99 enrolled subjects remained free of HIV-related respiratory disease and were included in the analysis. At enrollment, carbon monoxide diffusing capacity (TLCO) was significantly lower than predicted in non-smokers, smokers and ex-smokers (88, 77 and 88%, respectively, P < 0.001). The TLCO measurements in the smoking group were significantly lower than those of the life-long non-smoking subjects (P < 0.01). Residual volume (RV) was significantly higher than predicted in smokers (111%, P = 0.02). During follow-up, all three groups demonstrated significant declines in TLCO (7%, P = 0.01; 9%, P = 0.005; 13%, P < 0.001, respectively), and increases in RV (9%, P = 0.03; 13.5%, P = 0.02, 22%, P = 0.02, respectively). At enrollment, significantly lower than predicted values of TLCO were observed in groups stratified by CDC criteria: in asymptomatic HIV-seropositive subjects (CDC 11) 89%, P = 0.01; persistent generalized lymphadenopathy (PGL) 84%; AIDS-related complex (ARC) 81%; and in non-pulmonary AIDS (IV C1) 69%, P = 0.0001, respectively. Residual volume was significantly higher than predicted in CDC II (114%, P = 0.05). During follow-up, TLCO fell in groups PGL and ARC by 7 and 9%, respectively, while RV increased in groups CDC II, PGL and ARC by 17, 15 and 8%, respectively. Only the TLCO decline in PGL showed any linkage to clinical deterioration. This study demonstrates deficits at enrollment, and a continuing decline of TLCO and increase in RV in HIV-seropositive subjects without overt lung disease.

AIDS-Related Complex↗
PubMed2001

The lung diffusing capacity for nitric oxide in rats is increased during endotoxemia.

Rats, when injected with endotoxin, begin to exhale nitric oxide (NO) within 1 h. This study measured the diffusing capacity for NO in the lungs of rats (DL(NO)) under both control and endotoxemic conditions, and it also estimated the rate at which endogenous NO (VP(NO)) enters the distal compartment of the lung, both in control rats and during endotoxemia. DL(NO) increased from 0.68 +/- 0.12 (SE) ml. min(-1). mmHg(-1) in control rats to 1.17 +/- 0.25 ml. min(-1). mmHg(-1) in endotoxemic rats. VP(NO) was 2.6 +/- 0.5 nl/min in control rats and attained a value of 218.6 +/- 50.1 nl/min at the height of NO exhalation 3 h after the endotoxin. We suggest that increased DL(NO) reflects an increase in pulmonary membrane diffusing capacity, caused by a pulmonary hypertension that is due to neutrophil aggregation in the lung capillaries. DL(NO) may also be increased by an enlarged pulmonary capillary volume because of the vasodilatory effects of the endogenous NO that is produced by the lung in response to the endotoxin. NO production by the lungs in response to endotoxin is unique in that it is the only situation reported to date in which pathologically induced increases in NO exhalation originate from the alveolar compartment of the lung, as opposed to the small conducting airways.

Animals↗
PubMedDate not supplied

Diffusing capacity and spirometry following a 60-minute dive to 4.5 meters.

The purpose of this study was to assess the contribution of SCUBA to the pulmonary effects of diving to 4.5 meters depth in healthy subjects using a randomized crossover control condition. Ten healthy divers performed two 60-minute 'dives' using SCUBA in a swimming pool. The non-immersed 1 ATA SCUBA control exposure took place at ambient pressure in the laboratory. Thirty minutes prior to, and 30 and 90 minutes post-exposure, FVC (forced vital capacity), FEV1.0 (forced expired volume), peak expiratory flow rate (PEFR), diffusing capacity (DL(co)), heart rate (HR) and temperature were measured. No significant differences were noted in HR, temperature or spirometry between the two conditions. A significant reduction in diffusing capacity occurred at 30 and 90 minutes after the pool dive (9.3% and 15.1%, respectively, p < 0.05). There was no concordant change in DL(co) following the non-immersed 1 ATA SCUBA control. Thus, a pool dive to 4.5 meters for 60 minutes causes a decrease in DL(co), without a change in spirometry, while breathing from SCUBA equipment without immersion causes no significant change in lung function.

Adult↗