We used a computerized microscopic image analysis system to directly measure the surface area of distal air spaces in methacrylate-embedded blocks randomly selected from inflation-fixed lobes that were resected from 45 patients as treatment of their peripheral lung tumors. In 28 of these patients, a preoperative computer tomography (CT) scan, at 6 and 10 cm below the sternal notch, was used to generate frequency histograms of CT numbers (measured as EMI units), a measure of lung density, in pixels from the lung or lobe that was subsequently resected. A similar CT number histogram was also derived from the lateral two fifths of the area of lobe/lung that was to be resected. The EMI unit that defined the lowest fifth percentile of this latter histogram correlated (n = 28, r = -0.77, p less than 0.001) with the mean value of the surface area of the walls of distal airspaces per unit lung volume (AWUV) in the five 1 mm x 1 mm microscopic fields with the lowest AWUV values, out of the 20 to 35 such fields examined in each patient. In the 34 of the 45 patients in whom we also measured volume-corrected diffusing capacity (DLCO/VA), this also correlated (n = 34, r = 0.84, p less than 0.001) with this value of AWUV, which measures the surface area of airspaces distal to the terminal bronchioles--reflecting an increase in airspace size, a defining characteristic of emphysema. However, a low DLCO/VA is nonspecific, whereas an abnormally low regional lung density is more likely to be specific for emphysema. In addition, highlighting those pixels of the CT display with low CT numbers (i.e., EMI units -500 [air] to -450, where zero = water) can locate areas of macroscopic emphysema, as shown by subsequent pathologic examination. Thus the quantitative CT scan can diagnose, quantitate, and locate mild to moderate emphysema, in humans, in life, noninvasively.

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N-acetylcysteine (600 mg/day) was given to patients by mouth for five days before bronchoscopy and bronchoalveolar lavage to determine whether N-acetylcysteine could increase the concentrations of the antioxidant reduced glutathione in plasma and bronchoalveolar lavage fluid. Bronchoalveolar lavage was performed 1-3 hours (group 2, n = 9) and 16-20 hours (group 3, n = 10) after the last dose of N-acetylcysteine and the values were compared with those in a control group receiving no N-acetylcysteine (group 1, n = 8). N-acetylcysteine was not detected in plasma or lavage fluid. Plasma concentrations of cysteine, the main metabolite of Nacetylcysteine and a precursor of reduced glutathione, were greater in the groups receiving treatment (groups 2 and 3) than in group 1. Cysteine concentrations in lavage fluid were similar in the three groups. Concentrations of reduced glutathione were greater in both plasma and lavage fluid in group 2 than in group 1. These data suggest that Nacetylcysteine given by mouth is rapidly deacetylated to cysteine, with resulting increases in the concentrations of cysteine in plasma and of reduced glutathione in plasma and the airways, which thus temporarily increase the antioxidant capacity of the lung.

We measured ear oxygen saturation (SaO2), chest wall movement, and oronasal air flow, and took electroencephalographic tracings during nocturnal sleep in 20 healthy subjects and 20 similarly aged patients with chronic obstructive pulmonary disease (COPD), none of whom was obese. Thirteen of the patients with COPD were persistently hypoxemic and hypercapnic when awake ("blue and bloated", Type B); the remaining 7 maintained relatively normal arterial gas tensions when awake despite equally severe airways obstruction ("pink and puffing", Type A). Hypoxemic episodes (HE) (SaO2 falls of greater than 10%) occurred during sleep in all the blue bloaters but in only 3 of 7 pink puffers and 3 of 20 normal subjects. However, the maximal change in arterial oxygen tension (PaO2) (calculated from SaO2 values assuming normal pH) was similar in all 3 groups, averaging 24 mmHg. Furthermore, the cumulative duration of apnea and hypopnea was the same in each group. Only one patient COPD had more than 2 apneas per night, and obstructive apnea was seen only in the healthy subjects. Sleep apnea syndromes thus appear to be rare in nonobese patients with COPD. Of the 40 HE in patients with COPD, 29 occurred during periods of hypoventilation. In 10 blue bloaters whose arterial blood was sampled during sleep, the measured fall in PaO2 during the HE (mean, 11.2 mmHg) was greater than the rise in PaCO2 (mean, 4.2 mmHg). Although these changes in arterial gas tensions could be produced by an increase in ventilation-perfusion imbalance during the HE, it is suggested that unsteady-state gas exchange during transient hypoventilation could provide an alternative explanation.

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