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Challenges with ouabain and histamine were performed a week apart in 10 patients with asthma and 5 normal subjects. Concentrations were increased cumulatively until specific airway conductance decreased by 30% or the maximal concentration of 1.0% was reached. At low concentrations, ouabain induced bronchodilatation in six patients who had asthma. Bronchodilatation gradually decreased with increasing concentrations and was followed by bronchoconstriction in two patients with asthma who had high airway sensitivity to histamine. Ouabain caused only bronchoconstriction in three patients with severe asthma. The normal subjects showed mild bronchodilatation or no response to ouabain. Several possible biochemical mechanisms may be responsible for the bronchodilatory response to low doses of ouabain, such as stimulation of adenylate cyclase or (Na + , K + )-adenosine triphosphatase. The absence of a bronchodilatory response to ouabain in patients with severe asthma suggests an impairment in the activity of these enzymes.

We determined regional (Vr) and overall lung volumes in six head-up anesthetized dogs before and after the stepwise introduction of saline into the right pleural space. Functional residual capacity (FRC), as determined by He dilution, and total lung capacity (TLC) decreased by one-third and chest wall volume increased by two-thirds the saline volume added. Pressure-volume curves showed an apparent increase in lung elastic recoil and a decrease in chest wall elastic recoil with added saline, but the validity of esophageal pressure measurements in these head-up dogs is questionable. Vr was determined from the positions of intraparenchymal markers. Lower lobe TLC and FRC decreased with added saline. The decrease in upper lobe volume was less than that of lower lobe volume at FRC and was minimal at TLC. Saline increased the normal Vr gradient at FRC and created a gradient at TLC. During deflation from TLC to FRC before saline was added, the decrease in lung volume was accompanied by a shape change of the lung, with greatest distortion in the transverse (ribs to mediastinum) direction. After saline additions, deflation was associated with deformation of the lung in the cephalocaudal and transverse directions. The deformation with saline may be a result of upward displacement of the lungs into a smaller cross-sectional area of the thoracic cavity.

Specific airway conductance (sGaw) was measured during quiet breathing and during panting in 21 normal subjects and 10 patients with obstructive lung disease. The direct method used does not require measuring thoracic gas volume (TGV). Coefficients of variation were 5.5% for panting and 5.1% for quiet breathing. Interobserver variability was 4.7% in the quiet-breathing method and 6.3% in the panting method. The two methods gave equivalent results for sGaw. A slightly greater sGaw was found by the panting method in normal subjects with the highest sGaw values, probably due to widening of the oropharynx-glottis during panting. In six normal subjects studied for intrasubject variability over time, no significant diurnal or day-to-day variability was seen by either method. We conclude that the quiet-breathing method is a simple valid means of determining sGaw and utilizes a physiological respiratory maneuver. Obviation of the need to measure TGV is advantageous. Results are equivalent to those of the panting method and variability is similar.

When faced with a critically ill patient with new pulmonary infiltrates on chest roentgenograms, the physician must choose the appropriate diagnostic procedure on the basis of the expected yields versus the potential complications. The first steps in any patient should include discontinuation of any nonessential medications, careful evaluation of fluid status to exclude cardiogenic pulmonary edema, and a review of likely diagnoses based on the patient's underlying disease. Although not likely to be of immediate utility, obtaining cultures of blood and other body fluids or sites and serologic testing may provide helpful information when combined with other procedures. Bronchoscopy is a reasonable first step in patients with a slow progression of disease or in those in whom the pulmonary process is discovered early in its course. As these patients often present with several of the known risk factors for complications with bronchoscopy, the decision to perform this procedure should not be made lightly. Transbronchoscopic lung biopsy adds additional risk to bronchoscopy but also increases the diagnostic yield considerably over lavages, brushing, and bronchial washings. Open lung biopsy offers high diagnostic yields and relatively low rates of serious complications. Because of the invasive nature of the procedure, there is often reluctance to perform it. In patients with rapidly progressive disease or conditions that make the risk of bronchoscopy unacceptably high, such as severe hypoxemia, bleeding diathesis, or cardiac compromise, prompt diagnosis requires that the physician consider open lung biopsy as a first diagnostic procedure. The physician must also consider whether making a specific diagnosis will be of benefit to the patient. Potential benefits of a specific diagnosis include stopping unnecessary empirical (and potentially toxic) therapies, instituting correct and specific therapy, and thus decreasing morbidity and mortality. The impact of specific diagnosis on morbidity and survival is often difficult to demonstrate. Discouraging notes have been sounded by studies of the effect of bronchoscopic or surgical diagnosis on the ultimate outcome for patients. For bronchoscopy with transbronchoscopic lung biopsy, although the overall diagnostic rate was 60 per cent, no difference in survival was noted between patients in whom a diagnosis was made and those in whom the nature of the pulmonary process remained unknown. Similarly, in a series of patients who underwent open lung biopsy, although the results of biopsy led to a therapeutic change in 70 per cent of the patients, only 16.5 per cent of the patients benefited from this change.(ABSTRACT TRUNCATED AT 400 WORDS)

The pulmonary mechanics and bronchoscopic findings in 5 patients with relapsing polychondritis were studied to evaluate the mechanism of obstruction. Two of the patients did not have clinical symptoms referable to the respiratory tract: pulmonary function was normal in 1 patient and was suggestive of mild restriction in the other. Three patients had dyspnea; pulmonary function studies revealed expiratory and inspiratory obstruction in all 3. The maximal flow-static recoil curves demonstrated that the expiratory obstruction was due predominantly to airway abnormality and not to loss of elastic recoil forces of the lung. The bronchoscopic appearance of the extrathoracic airway during quiet breathing did not accurately reflect pulmonary function results. One patient had a visually normal upper airway but greatly reduced maximal inspiratory flow rates, whereas another patient had pronounced narrowing of the upper airway but only a modest reduction of maximal inspiratory flow rates. The bronchoscopic appearance of the intrathoracic airway during quiet breathing did relate well to maximal expiratory flow rates. We conclude that in our group of patients the predominant mechanism of expiratory obstruction in relapsing polychondritis is due to airway abnormality. Although the bronchoscopic and radiographic findings are useful, spirometry is more important in determining functional abnormality.

Lobar functional residual capacity-to-total lung capacity ratios (FRC/TLC) and strains in five supine anesthetized dogs were determined from volumes and side lengths of tetrahedra formed by multiple intraparenchymal markers whose positions were determined roentgenographically. Strain is related to fractional changes in length of elements in a Cartesian coordinate system and was used to describe parenchymal distortion. Volumes and strain patterns were compared in three states: intact dogs, after transection of forelimb structures to relieve traction on the chest wall, and in dogs' excised lungs. Removing traction (NT) decreased the plethysmographically determined FRC and the upper-to-lower lobe ratio (UL/LL) for FRC/TLC. The ratio in the NT state was more like the ratio in the excised lungs (UL/LL approximately equal to 1) than in the intact dog (UL/LL greater than 1). Strain patterns were similar between the intact and the NT states, indicating no lobar shape change at FRC between these two states. Strain in the excised lungs differed greatly from strains in the intact and NT states. We conclude that forelimb traction alters volume distribution between lobes and that lung-chest wall interactions are important in determining volume and strain patterns.