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Biomedical subjects

D F Rochester

Publications and source records attributed to D F Rochester.

At least 73 records · Page 4Linked to original sources
PubMed1982

The influence of airway obstruction and respiratory muscle strength on maximal voluntary ventilation in lung disease.

To assess the effects of airway conductance (Gaw) and respiratory muscle strength (RMS) on maximal voluntary ventilation (MVV), we studied 8 normal subjects (N), 8 patients with interstitial lung disease (ILD), and 16 with chronic airflow limitation (CAL). In the patients with ILD, RMS explains 83% of the variance in MVV (p less than 0.005), but Gaw explains none. In the patients with CAL, Gaw and RMS explain, respectively, 65 and 34% of the variance in MVV (p less than 0.02). Considering Gaw and RMS together increases the explained variance to 77% (p less than 0.005). In groups CAL and N combined, Gaw and RMS explain 86% of the variance in MVV, with 71% explained by Gaw and 34% by RMS, which the other variable alone failed to explain (p less than 0.005). When the data are normalized for age, sex, height, and lung volume, the influence of %RMS on %MVV is halved, but remains significant (p less than 0.05). We conclude that RMS is a primary determinant of MVV in patients with ILD, and an important determinant in patients with CAL.

Adult↗
PubMed1981

Lung compliance and its transient elevations measured with pulse-flow method.

We describe a pulse-flow method of measuring static lung compliance (CL) that is sensitive to rapid transients in CL. CL is measured by blowing air at a constant flow into the mouth and lungs for 2 s and calculated by dividing airflow in 1/s by the change in transpulmonary pressure in CMH2O/s. Pulse and static inspiratory CL was measured in five normals, four obstructives, five obese, and two patients with pulmonary fibrosis, Pulse CL after tidal breathing was correlated with static CL measured after deep breaths (r = 0.96). Pulse CL after deep breaths was higher than pulse CL after tidal breathing (p less than 0.01) and then static CL after deep breaths (p less than 0.05). In all subjects the lower the forced expiratory volume in 1 s, expressed as a percentage of vital capacity (FEV1/FVC), the greater the increase in pulse CL after a deep breath will be (r = 0.93). After deep breaths pulse CL fell from maximum CL to base-line CL at a rate related to 1/t2 where t equals the time in seconds from the last deep breath. We conclude that the increase in CL after a deep breath is related to the degree of airway obstruction and that the subsequent fall in CL is related to 1/t2.

Adult↗
PubMed1981

Atypical mycobacterial infections: a clinical study of 92 patients.

Between July 1970 and December 1979, 92 patients with atypical mycobacterial infections of the lung were hospitalized 110 times at Blue Ridge Hospital (Charlottesville, Va). These patients comprised less than 3% of all patients hospitalized for active mycobacterial disease. Sixteen had Mycobacterium kansasii or group I disease, three had group II disease (two M scrofulaceum, one M szulgai), 70 had group III disease (68 M avium-intracellulare, two M xenopi), and three had M fortuitum or group IV disease. M kansasii infections comprised 23% of the total during the first five years, but only 6% during the second half of the decade. Clinical and roentgenographic findings were similar to those in patients with tuberculosis. As anticipated, most of the M kansasii organisms were sensitive to antimycobacterial drugs, and these patients generally responded well to chemotherapy. In contrast, most of the group III organisms, including one of the M xenopi, exhibited resistance to several drugs. Despite the high incidence of resistance, 59% of the patients with group III infections who were treated for at least three months in the hospital had sputum cultures converted to negative.

Adult↗
PubMed1978

Volume-pressure and morphometric observations after acute alveolar injury in the dog from N-nitroso-N-methylurethane.

Volume-pressure diagrams during inflation with air and saline were made with the lungs of 6 control dogs and 24 dogs with acute alveolar injury induced by subcutaneous injection of 6 mg of N-nitroso-N-methylurethane per kg of body weight 3 to 14 days before study. The extent of alveolar closure was estimated by measuring the mean linear intercept of the remaining open air spaces after inflation of the lung with liquid formalin at a pressure of 40 cm H2O. This alveolar closure was defined as irreversible. The volume-pressure diagrams and compliance data derived from them during the 3 to 4, 5 to 7, and 9 to 14 day periods after injection were analyzed and compared with the morphometric data. The diagrams with air inflation showed a progressive downward shift beginning with the 3 to 4 day period. This shift was at least partly independent of volume loss. The diagrams with saline inflation were unchanged during the 3 to 4 day period, but showed a downward shift, largely due to volume loss thereafter. Irreversible alveolar closure, reflected by an increased mean linear intercept, was present in the 3 to 4 day period, and its extent increased with time, correlating inversely with total lung capacity and saline compliance. The data indicate that decreased lung compliance and volume during the first 7 days of injury induced by injection of N-nitroso-N-methylurethane were due largely to increased surface tension and that tissue forces became a significant factor later. They suggest that the altered tissue forces were due principally to irreversible alveolar closure.

Animals↗