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At least 955 records · Page 53Linked to original sources
PubMed1980

Structure and function in tracheal stenosis.

The mechanism of airflow obstruction was investigated in 21 patients with tracheal stenosis using tantalung tracheograms and pulmonary function studies, including flow-volume (FV) loops. In 4 patients with severe obstructive pulmonary disease, FV loops failed to demonstrate radiographically visible tracheal stenosis. In 17 patients, both FV loops and tracheograms demonstrated central airway obstruction. In three of the 17 patients, the stenotic segment was a rigid lesion at the thoracic outlet with similar limitation of inspiratory and expiratory flow. In nine of the 17 patients, the lesion was extrathoracic (rigid in 6 patients and pliable in 3). The 3 pliable extrathoracic lesions produced marked limitation of inspiratory flow but normal expiratory flow. Three rigid extrathoracic lesions produced inspiratory flow that was more limited than expiratory flow, suggesting dynamic inspiratory compression of the normal extrathoracic trachea. The one rigid intrathoracic lesion caused expiratory flow limitation greater than inspiratory flow limitation, suggesting dynamic compression of the intrathoracic trachea on expiration. The position of the obstructing lesion and dynamic compression of the normal, compliant trachea may be the major determinants of the difference in flow limitation between expiration and inspiration in some patients.

Adolescent↗
PubMed1981

Inspiratory flow and intrapulmonary gas distribution.

The effect of flow of inspired gas on intrapulmonary gas distribution was examined by analysis of regional pulmonary 133Xe clearances and of total pulmonary 133Xe clearance measured at the mouth after equilibration of the lungs with 133Xe. Five awake healthy volunteers (24 to 40 yr of age) and another 5 healthy, anesthetized-paralyzed volunteers (26 to 28 yr of age) were studied while they were in the right lateral decubitus position. The awake subjects were studied at 3 inspiratory flows (0.4, 0.7, and 1.0 L/s) and the anesthetized-paralyzed subjects at 4 inspiratory flows (0.2, 0.5, 1.1, and 1.6 L/s). Interregional differences in 133Xe clearances along the vertical axis were significantly less during anesthesia-paralysis and mechanical ventilation than during spontaneous breathing in the awake state. No differences in the regional or total pulmonary 133Xe clearances were detected at these different flows in either of the two states, i.e., the difference between the awake and anesthetized-paralyzed states persisted.

Adult↗
PubMed1982

Comparison of physiologic dead space/tidal volume ratio and alveolar-arterial PO2 difference during incremental and constant work exercise.

We prefer 1-min incremental exercise testing on a cycle ergometer rather than constant work studies because of its speed, repeatability, and ease of identification of the anaerobic threshold. Although values such as VO2 and anaerobic threshold from both types of studies are reported to be comparable, we questioned whether VD/VT and AaPO2, which depend on simultaneous arterial blood and mixed expired gas sampling, would also be reliable during incremental testing. In 23 patients we did both a constant work test at below the anaerobic threshold and a 1-min incremental test. At matched VO2 we found no difference between VD/VT and AaPO2 despite anticipated differences in VE, VCO2, and R because of differences in their rates of increase. We conclude that VD/VT and AaPO2, determined during 1-min incremental exercise tests, are equivalent to those from constant work tests and that a separate constant work study is not needed for these measurements if determined below the anaerobic threshold.

Adult↗
PubMed2003

Enhanced expression of vascular endothelial growth factor in pulmonary arteries of smokers and patients with moderate chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is associated with structural and functional changes in the pulmonary circulation that commence at an early stage. To investigate whether vascular endothelial growth factor (VEGF) might be implicated as a mediator in COPD-associated pulmonary vascular changes, we studied surgical specimens obtained from 19 nonsmokers, 21 smokers with normal lung function, 28 patients with moderate COPD, and 10 patients with severe emphysema. The expression of VEGF in pulmonary muscular arteries was evaluated by immunohistochemistry, its protein content in lung tissue by Western blot analysis, and VEGF mRNA and its isoforms were analyzed by reverse transcription-polymerase chain reaction. The immunohistochemical expression of VEGF was increased in pulmonary arteries of smokers (median, 68% [interquartile range, 60-88]) and patients with moderate COPD (77% [63-82]), compared with nonsmokers (53% [40-63]) (p < 0.05 each). The expression of VEGF in smooth muscle cells correlated with the thickness of the vessel wall (r = 0.38, p < 0.01). VEGF protein content in lung tissue was reduced in severe emphysema, where reverse transcription-polymerase chain reaction demonstrated a lower proportion of the VEGF189 isoform. In conclusion, the expression of VEGF varies according to the severity of COPD and might be involved in the pathogenesis of pulmonary vascular remodeling at early stages of the disease.

Aged↗
PubMed2004

Recurrence of pulmonary emphysema in an alpha-1 proteinase inhibitor-deficient lung transplant recipient.

Several types of primary disease may recur after lung transplantation, but recurrence of pulmonary emphysema has so far never been published. We report the case of a 49-year-old white male who underwent single lung transplantation for emphysema related to alpha-1 antitrypsin deficiency and to superimposed smoking. The postoperative course was complicated by several rejection episodes. Subsequently, the patient remained stable without evidence of graft dysfunction for more than 10 years, but he resumed light smoking at 8 years after transplant. At 11 years after transplant, although the patient was still asymptomatic and had a stable lung function, recurrence of emphysema on the grafted side was diagnosed on computerized tomography of the thorax. One year later, the patient began to experience a moderate decline in lung function. Two separate bronchoalveolar lavages performed after the onset of the recurrence disclosed a significant elastolytic activity related to neutrophil serine-elastase in lavage fluid. In summary, we describe a case of recurrence of pulmonary emphysema in a patient with alpha-1 antitrypsin deficiency. The resumption of smoking has probably played a central role in the presence of elastolytic activity in lavage fluid and in the recurrence of emphysema.

Acute Disease↗
PubMed2005

Six-minute walk, maximal exercise tests: reproducibility in fibrotic interstitial pneumonia.

Resting pulmonary function and exercise variables are widely used to stage and monitor idiopathic interstitial pneumonia (IIP). However, the variability of exercise data (maximal exercise and the 6-minute walk test) has not been evaluated definitively. We have prospectively quantified the reproducibility of resting and exercise functional data in fibrotic IIP (idiopathic pulmonary fibrosis, fibrotic nonspecific interstitial pneumonia) and have evaluated interrelationships between variables. Thirty consecutive patients with fibrotic IIP underwent serial resting pulmonary function tests, 6-minute walk (n = 29), and maximal exercise (n = 24) at an interval of 1 week, with all testing performed in accordance with American Thoracic Society standards. Within-subject reproducibility was excellent for 6-minute walk distance (SD/mean = 4.2%) and clinically acceptable for resting pulmonary function indices and VO(2)max on maximal exercise testing. However, the amplitude of oxygen desaturation at the end of exercise was poorly reproducible in both 6-minute walk and maximal exercise testing (SD/mean > 25%). There was a highly significant relationship between VO2max on maximal exercise testing and 6-minute walk distance (r(s) = 0.78, p < 0.0001). In fibrotic IIP, the excellent reproducibility of the 6-minute walk distance is a major advantage in routine staging and monitoring, whereas maximal exercise variables are poorly reproducible.

Aged↗
PubMed2004

Sildenafil inhibits altitude-induced hypoxemia and pulmonary hypertension.

Exposure to high altitude induces pulmonary hypertension that may lead to life-threatening conditions. In a randomized, double-blind, placebo-controlled study, the effects of oral sildenafil on altitude-induced pulmonary hypertension and gas exchange in normal subjects were examined. Twelve subjects (sildenafil [SIL] n = 6; placebo [PLA] n = 6) were exposed for 6 days at 4,350 m. Treatment (3 x 40 mg/day) was started 6 to 8 hours after arrival from sea level to high altitude and maintained for 6 days. Systolic pulmonary artery pressure (echocardiography) increased at high altitude before treatment (+29% versus sea level, p < 0.01), then normalized in SIL (-6% versus sea level, NS) and remained elevated in PLA (+21% versus sea level, p < 0.05). Pulmonary acceleration time decreased by 27% in PLA versus 6% in SIL (p < 0.01). Cardiac output and systemic blood pressures increased at high altitude then decreased similarly in both groups. Pa(O(2)) was higher and alveolar-arterial difference in O(2) lower in SIL than in PLA at rest and exercise (p < 0.05). The altitude-induced decrease in maximal O(2) consumption was smaller in SIL than in PLA (p < 0.05). Sildenafil protects against the development of altitude-induced pulmonary hypertension and improves gas exchange, limiting the altitude-induced hypoxemia and decrease in exercise performance.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1976

Effects of antihistamines on the lung vascular response to histamine in unanesthetized sheep. Diphenhydramine prevention of pulmonary edema and increased permeability.

To see whether antihistamines could prevent and reverse histamine-induced pulmonary edema and increased lung vascular permeability, we compared the effects of a 4-h intravenous infusion of 4 mug/kg per min histamine phosphate on pulmonary hemodynamics, lung lymph flow, lymph and plasma protein content, arterial blood gases, hematocrit, and lung water with the effects of an identical histamine infusion given during an infusion of diphenhydramine or metiamide on the same variables in unanesthetized sheep. Histamine caused lymph flow to increase from 6.0+/-0.5 to 27.0+/-5.5 (SEM) ml/h (P less than 0.05), lymph; plasma globulin concentration ratio to increase from 0.62+/-0.01 to 0.67+/-0.02 (P less than 0.05), left atrial pressure to fall from 1+/-1 to -3+/-1 cm H2O (P less than 0.05), and lung lymph clearance of eight protein fractions ranging from 36 to 96 A molecular radius to increase significantly. Histamine also caused increases in lung water, pulmonary vascular resistance, arterial PCO2, pH, and hematocrit, and decreases in cardiac output and arterial PO2. Diphenhydramine (3 mg/kg before histamine followed by 1.5 mg/kg per h intravenous infusion) completely prevented the histamine effect on hematocrit, lung lymph flow, lymph protein clearance, and lung water content, and reduced histamine effects on arterial blood gases and pH. 6 mg/kg diphenhydramine given at the peak histamine response caused lymph flow and lymph: plasma protein concentration ratios to fall. Metiamide (10 mg/kg per h) did not affect the histamine lymph response. We conclude that diphenhydramine can prevent histamine-induced pulmonary edema and can prevent and reverse increased lung vascular permeability caused by histamine, and that histamine effects on lung vascular permeability are H1 actions.

Animals↗
PubMed1980

Noninvasive measurement of pulmonary transvascular protein flux in normal man.

Onset of lung edema is usually associated with increase in the pulmonary transvascular flux of water and proteins. Clinical measurement of these parameters may aid in early diagnosis of pulmonary edema, and allow differentiation between "cardiogenic" and "noncardiogenic" types base on the magnitude of the detected changes. We have previously described a noninvasive method for estimating transvascular protein flux in lung (Gorin, A. B., W. J. Weidner, R. H. Demling, and N. C. Staub, 1978. Noninvasive measurement of pulmonary transvascular protein flux in sheep. J. Appl. Physiol. 45: 225-233). Using this method we measured the net transvascular flux of [113mIn]transferrin (mol wt, 76,000 in lungs of nine normal human volunteers. Plasma clearance of [113In]transferrin occurred with a T1/2 = 7.0 +/- 2.6 h (mean +/- SD). The pulmonary transvascular flux coefficient, alpha, was 2.9 +/- 1.4 X 10(-3) ml/s (mean +/- SD) in man, slightly greater than that previously measured in sheep (2.7 +/- 0.7 X 10(-3) ml/s; mean +/- SD). The pulmonary transcapillary escape rate is twofold greater than the transcapillary escape rate for the vascular bed as a whole, indicating a greater "porosity" of exchanging vessels in the lung than exists for the "average" microvessel in the body. Time taken to reach half-equilibrium concentration of tracer protein in the lung interstitium was quite short, 52 +/- 13 min (mean +/- SD). We have shown that measurement of pulmonary transvascular protein flux in man is practical. The coefficient of variation of measurements of alpha (between subjects) was 0.48, and of measurements of pulmonary transcapillary escape rates was 0.39. In animals, endothelial injury commonly results in a two- to threefold increase in transvascular protein flux. Thus, external radioflux detection should be a suitable means of quantitating lung vascular injury in human disease states.

Adult↗