Evaluation of lung mechanics in epidemiologic studies.
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Airway Resistance↗
Biomedical subjects
N L Lapp
Publications and source records attributed to N L Lapp.
The effect of diffuse pulmonary fibrosis on lung mechanics.
Maximum expiratory flow-volume curves (MEFV), inflational and deflational pressure-volume curves, dynamic compliance at 20, 40, and 60 breaths per minute, closing volume (single-breath oxygen method), standard lung volumes are airway resistance measurements were made in eleven subjects with a clinical diagnosis of diffuse interstitial fibrosis (DIF) and eleven control subjects. No subject was a current cigarette smoker. Maximum flow-static recoil pressure curves (MFSR) were constructed and calculations of upstream resistance (Rus) were made. Comparison of the mean values showed no significant differences in airway resistance or FEV1/FVC% between the two groups; however, significant differences were noted in total lung capacity (TLC), forced expiratory volume in one second (FEV1) and expiratory flow rates. Nine of the diseased subjects had pressure-volume curves shifted to the right of the normal range, and a significant decrease in static expired and inspired compliance was noted in the diseased group. Six subjects with DIF showed increased Rus. The single-breath oxygen test results revealed an increased slope of phase III (delta N2/I) in the diseased group. Decreases in the static compliance may be explained by loss of lung volume in some patients with DIF. There is also evidence that the small airways may be affected by this disease process.
Adult↗
The effects of coal workers' pneumoconiosis on lung mechanics.
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Adult↗
How silicosis and coal workers' pneumoconiosis develop--a cellular assessment.
In vitro and in vivo animal studies, as well as human investigations, strongly support the role of macrophage products in the development and progression of silicosis and coal workers' pneumoconiosis. Such products include enzymes and reactive oxygen species which may cause lung damage; cytokines which recruit and/or activate polymorphonuclear leukocytes and thus result in further oxidant damage to the lung; and fibrogenic factors which induce fibroblast proliferation and collagen synthesis. This mechanistic understanding of pulmonary disease should assist in developing strategies for prevention and treatment.
Animals↗