SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
To determine the magnitude of functional compensation after pneumonectomy and whether compensation is related to maturity of the animal at the time of resection, we performed left pneumonectomy in either adult or 10-wk-old beagles. Studies were performed in adults 7-9 mo after surgery and in puppies 18-23 mo after surgery when the dogs reached full maturity. Results were compared with those in age- and sex-matched unoperated controls. Measurements included pressure-volume relationships, pulmonary hemodynamics, rebreathing studies of lung volume, diffusing capacity and its components, lung tissue volume, and pulmonary blood flow. Computerized-tomographic scans were performed in the puppy groups to determine changes in thoracic shape and size. Morphometric analysis of the lungs was performed under light microscopy. There was partial compensation for loss of one lung by functional improvement in the remaining lung. Compensation was greater in those pneumonectomized as puppies than as adults. Volume of the remaining lung was larger than predicted for a given transpulmonary pressure in both groups. Diffusing capacity, pulmonary capillary blood volume, and lung tissue volume were larger than expected for the normal right lung. After pneumonectomy, compliance of the rib cage was greater in puppies than in adults. Weight of the costal diaphragm was reduced in pneumonectomized puppies. Pulmonary hypertension at rest did not develop, and pulmonary vascular reactivity to hypoxia was unchanged after pneumonectomy in both groups. Significant correlations were obtained between physiological and morphometric measurements.
Kirby and Downs are to be congratulated for introducing a technique that has greatly extended the principles of the old Engström ventilator. IMV permits diagnostic distinction and therapeutic choice between lung distention, for mechanical improvement and oxygen exchange, and mechanical ventilation for pH homeostasis. They have stimulated great interest on the part of manufacturers and clinicians. Factual physiological support is still relatively slim, hypotheses greatly outstripping their supporting data. Much of the existing data are as yet either poorly based or, in one or two instances, in error. Where data do exist, their clinical importance is frequently unclear--effects on cardiac output being a good example. The obvious popularity of this technique certainly justifies its further study, and I look forward to seeing the results. I hope that, if studies being carried out in our own intensive care unit are subject to a similar degree of criticism, my resilience will equal that of the authors of these very interesting chapters.
The acute (30 min postexposure) and delayed (24 and 48 h postexposure) effects of a 4-h exposure to 1.0 ppm O3 (n = 10), 0.3 ppm O3 (n = 9) were evaluated using an inert multiple gas rebreathing method as well as arterial blood gas determinations in anesthetized dogs. Rebreathing parameters included pulmonary capillary blood flow (Qc), diffusing capacity, functional residual capacity, pulmonary tissue plus capillary blood volume (VTPC), and oxygen consumption. The Qc and PaO2 were significantly decreased 30 min after exposure to O3 and remained decreased 24 and 48 h after exposure only in the 1.0 ppm O3 group. After exposure to 1.0 ppm O3 only, a 33% increase in VTPC was found at 24 but not at 48 h and was confirmed by autopsy lung water determinations. No changes in rebreathing parameters or arterial blood gas measurements occurred in the air exposure control group. Therefore, an acute exposure to O3 resulted in adverse cardiopulmonary effects in dogs. Five additional dogs were exposed to 1.0 ppm O3 for 4 h while breathing spontaneously rather than with ventilation being assisted by electrophrenic stimulation (as done in the other exposures), and no changes in VTPC occurred. Thus, the ventilatory pattern used during O3 exposure is also an important factor in causing critical degrees of parenchymal lung injury.
Explore the source record for details and available documents.
The alveolar-arterial O2 pressure difference (AaDO2) is composed of three parts which depend on inhomogeneities of the ventilation-perfusion ratio (AaD(distr.) 1), on size and distribution of the diffusing capacity-perfusion ratio (AaD(distr.) 2), and on the effect of the shunt perfusion (AaD(sh)). These three parts can be calculated for normal, hypoxic and hyperoxic breathing conditions if the inhomogeneities of the function parameters and the size of the shunt perfusion are known. The calculation based on experimental data in 28 healthy subjects shows the following results: (1) Under hypoxic breathing conditions the AaD(distr.) 2 due to diffusion dominates. However, even at alveolar O2 pressures below 45 mm Hg the AaD(distr.) 1 must not be ignored. (2) Under normal breathing conditions AaD(distr.) 2 may be ignored and will under pathological conditions become relevant only if the diffusing capacity-perfusion ratio is below 3.10(-3) mm Hg(-1). (3) Under hyperoxic breathing conditions the AaD(sh) is predominant. However, even with the inhalation of pure oxygen, the AaD(distr.) 1 contributes 10% of the total AaDO2. (4) When evaluating the methods of measurement of the O2 diffusing capacity and of the shunt perfusion the inhomogeneities of ventilation, perfusion and diffusion must be considered.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
OBJECTIVES: To estimate the value of diffusing capacity for carbon monoxide (T(LCO)) in patients with cystic fibrosis and to evaluate its ability to predict arterial desaturation during exercise. METHOD: Fourty-four patients (9-30 years) with cystic fibrosis performed pulmonary function tests with measure of T(LCO) and a bicycle incremental exercise test. They represent a wide variation in disease severity: mean Shwachman score: 77.8 (range: 40-100), mean FEV1%: 72.8 (range: 17-131). This study investigated the relationship between T(LCO), lung volumes and exercise data. RESULTS: T(LCO) remained normal for a long time in patients with cystic fibrosis: 82% of them show a normal T(LCO) (mean value: 91.3% of predicted). T(LCO) was significantly correlated with FEV(1), residual volume, maximal work load and maximum oxygen uptake. A fall in arterial oxygen saturation was uncommon in our study (five patients) and not significantly correlated with T(LCO). CONCLUSIONS: T(LCO) is a good criter of severity of cystic fibrosis but remains unreliable to predict values above which physical activity is safe, without arterial desaturation. Exercise tests should be proposed in order to evaluate exercise adaptation of each patient and determine which factor limits maximal performance.
Thirteen patients were exposed to accidental zinc chloride inhalation during an army exercise. Smoke bombs were released in open air. The exposure was modest ranging from "taking a few inhalations" to "5-10 minutes in a house with smoke drifting in through unshuttered windows". Initial symptoms were scanty. All patients received inhalation steroid on admittance followed by i.v. bolus of hydrocortisone. Four patients continued systemic steroid treatment (prednisolone 40 mg with stepwise reduction to zero over four weeks) because exposure was judged significant (> 1 minute of unprotected inhalation). No respiratory symptoms developed within an eight week observation period. However, a gradual decline in pulmonary CO diffusion capacity (to 85% (76-99 of initial capacity) was observed within the first four weeks. It is concluded that a very modest inhalation of zinc chloride smoke may induce prolonged impairment of pulmonary function.
OBJECTIVE: To demonstrate the change of pulmonary function in patients with end-stage renal disease(ESRD) before and after peritoneal dialysis (PD). METHODS: In this study were measured the forced vital capacity (FVC), maximum breathing capacity (MBC), the forced expiratory volume of the first second (FEV1), maximal expiratory flow (MEF), maximal mid-expiratory flow rate (MMEF), 25% of maximal expiratory flow (V25), and the diffusion of co in lung (DLco) for 50 patients with end-stage renal disease and 20 normal subjects. All the indexes were determined again in 30 ESRD patients two months after peritoneal dialysis. RESULTS: The indexes of pulmonary ventilation (FVC, MBC, FEV1, PEF, MMEF, V25) and the pulmonary diffusion DLco were lower in the ESRD patients than in the controls. FEV1, PEF, MMEF and V25 were improved markedly after peritoneal dialysis in ESRD patients (P < 0.05); FVC, MBC, and DLco were of no change (P > 0.05). CONCLUSION: The function of pulmonary ventilation and diffusion are decreased in patients with ESRD accompanied with airways obstruction. Peritoneal dialysis can improve airways obstruction remarkably, but it has no effect on the function of pulmonary ventilation and diffusion.
We used the dual capability of hyperpolarized 129Xe for spectroscopy and imaging to develop new measures of xenon diffusing capacity in the rat lung that (analogously to the diffusing capacity of carbon monoxide or DLCO) are calculated as a product of total lung volume and gas transfer rate constants divided by the pressure gradient. Under conditions of known constant pressure breath-hold, the volume is measured by hyperpolarized 129Xe MRI, and the transfer rate is measured by dynamic spectroscopy. The new quantities (xenon diffusing capacity in lung parenchyma (DLXeLP)), xenon diffusing capacity in RBCs (DLXeRBC), and total lung xenon diffusing capacity (DLXe)) were measured in six normal rats and six rats with lung inflammation induced by instillation of fungal spores of Stachybotrys chartarum. DLXeLP, DLXeRBC, and DLXe were 56 +/- 10 ml/min/mmHg, 64 +/- 35 ml/min/mmHg, and 29 +/- 9 ml/min/mmHg, respectively, for normal rats, and 27 +/- 9 ml/min/mmHg, 42 +/- 27 ml/min/mmHg, and 16 +/- 7 ml/min/mmHg, respectively, for diseased rats. Lung volumes and gas transfer times for LP (TtrLP) were 16 +/- 2 ml and 22 +/- 3 ms, respectively, for normal rats and 12 +/- 2 ml and 35 +/- 8 ms, respectively, for diseased rats. Xenon diffusing capacities may be useful for measuring changes in gas exchange associated with inflammation and other lung diseases.
BAL was performed in different courses of sarcoidosis in order to evaluate the importance of this examination. We found a higher degree of lymphocytosis in Löfgren's syndrome and in relapses than in the others. Probably there is a direct connection between high intensity alveolitis and reduction of diffusing capacity. There could not be found any correlation to other markers of activity (lung function, SACE, 67-Gallium-Scan).
The purpose of these experiments was to quantify stagnant intrapulmonary blood caused by a pulmonary arterial occlusion (PAO). The hypothesis was that the diffusing capacity of the lung for CO (DLCO) would be altered little by PAO when measured with the usual inspired concentrations (0.3%) of CO, since stagnant blood distal to the occlusion takes up CO for 20 s or more before significant CO backpressure would develop. However, higher levels of CO (i.e., greater than or equal to 3%) would equilibrate faster with capillary blood (within 5-10 s), and DLCO measured 10-20 s subsequent to the high CO exposure would reflect only the DLCO in the unoccluded regions. Thus the fractional reduction in DLCO measured with 3% CO, with respect to that measured with 0.3% CO, should be related to the fractional occlusion of the pulmonary artery in a predictable way. We occluded the right pulmonary artery (RPAO), the left pulmonary artery (LPAO), or the left lower lobar artery (LLPAO) and found that DLCO measured during rebreathing a 0.3% CO mixture was 80, 87, and 94%, respectively, of the preocclusion value, whereas the DLCO measured during rebreathing a 3.3% CO mixture was 59, 73, and 87% of the preocclusion value. A computer model was developed to predict the reduction in DLCO at different levels of CO exposure that would be caused by varying fractions of PAO. Our data indicated that RPAO corresponded to a 42% vascular occlusion, LPAO a 35% occlusion, and LLPAO a 20% occlusion. Measurement of DLCO using low and high concentrations of CO might be useful in assessing the fraction of vascular bed occluded and in following noninvasively the course of vascular occlusion in a variety of pulmonary diseases.
The presence of anti-lung antibody was evaluated in 20 patients with farmer's lung disease. Antibody was found in 14. In patients with disease of less than five years' duration, there was no evidence of any significant differences in vital capacity, total lung capacity, diffusion capacity, and PaO2 between those with and without anti-lung antibody. However, in patients with disease of longer than five years' duration, the diffusion capacity was lower in the anti-lung antibody-positive group (p less than 0.05). The prevalence of abnormalities of vital capacity and diffusion capacity and fibrosis on chest roentgenograms was higher in those who had anti-lung antibody and disease of more than five years' duration. The study suggests that anti-lung antibody is present before permanent measurable physiologic abnormality occurs and may potentiate the pulmonary damage during subsequent episodes.
Pulmonary function data, including diffusing capacity, were evaluated in 56 patients with chronic severe cardiomyopathy before heart transplantation. Cardiac catheterization data were used to describe the relationship between cardiac and pulmonary function. Of 56 patients 44 had some abnormality in pulmonary function. The majority, 30 of 56, had a restrictive impairment alone. Of 28 patients in whom diffusing capacity was measured, 64% had a diffusion impairment. There was no association of pulmonary function impairment with type of cardiomyopathy or smoking history. Pulmonary capillary wedge pressure correlated positively with DLCO, but not with FVC or TLC. Cardiac index and ejection fraction did not correlate with diffusing capacity. This precardiac transplantation cardiomyopathy patient group demonstrated frequent pulmonary function abnormalities not previously recognized.
We studied lung function tests during euhydration (Days 1 and 2), hypohydration (Days 3 and 4), and rehydration (Days 5, 6, and 7) in 6 normal subjects. Hypohydration was induced by administering chlorthalidone, and this resulted in a 4.5% loss of body weight. During hypohydration, lung volumes increased significantly. Interestingly, ventilatory lung function tests including peak expiratory flow rate, FEV1, maximal voluntary ventilation, and flow rates at low lung volumes also increased significantly and returned to normal upon rehydration. Diffusing capacity for carbon monoxide remained unchanged. The improvement in ventilatory lung function tests during hypohydration was surprising, and it is suggested that this was related to loss of water within and/or around the airways. This mechanism is opposite to that which occurs in pulmonary edema with excess lung water where reduction in flow rates occurs.
Pulmonary inflammation secondary to oxidant generation catalyzed by transition metals associated with inhaled particles is one factor postulated to underlie the acute health effects of particulate air pollution. We postulated that inhaled iron oxide particles with associated amounts of soluble iron should induce mild pulmonary inflammation and lead to altered alveolar epithelial integrity and altered gas exchange. To test this hypothesis we examined the effects of inhaled iron oxide particles on alveolar epithelial permeability. Sixteen healthy subjects inhaled aerosols of iron oxide particles (1.5 microm mass median aerodynamic diameter) having either high or low water-soluble iron content [3.26 +/- 0.25 (SE) and 0.14 +/- 0.04 microg soluble iron/mg of particles, respectively] for 30 min at an average mass concentration of 12.7 mg/m(3). Alveolar epithelial permeability was assessed by measuring the pulmonary clearance of an inhaled radiolabeled tracer molecule ((99m)Tc-DTPA, diethylene triamine pentaacetic acid) using a gamma camera at 1/2 h and 24 h post particle exposure. Carbon monoxide lung diffusing capacity (DL(CO)) and spirometry were also performed before and after breathing the iron oxide. As a control, on a separate day, the procedures were duplicated except that the subject breathed particle-free air. For those subjects breathing aerosols with high soluble iron, we found no significant difference in DTPA clearance half-times after breathing particles versus particle-free air either at 1/2 h (97.4 +/- 15.4 vs. 116.1 +/- 15.5 min, respectively) or 24 h postinhalation (105.1 +/- 13.8 vs. 106.9 +/- 12.9 min, respectively). Likewise, for those subjects breathing aerosols with low soluble iron content we found no significant difference in DTPA clearance half-times after breathing particles versus particle-free air either at 1/2 h (108.6 +/- 31.9 vs. 95.6 +/- 10.8 min, respectively) or 24 h postinhalation (130.0 +/- 18.0 vs. 105.8 +/- 13.7 min, respectively). We found no significant differences in DL(CO) between particle exposures and air exposures. Minor differences in spirometric measurements were noted but were not statistically significant. We conclude that inhalation of iron oxide particles did not cause an appreciable alteration of alveolar epithelial permeability, lung diffusing capacity, or pulmonary function in healthy subjects under the studied conditions.