Two groups of rats (young and old) were food-deprived for 3 wk and were compared with age-matched fed groups. Final body weight and dry and wet weights of lungs were significantly reduced in both young and old starved rats. As determined by saline volume-pressure (VP) curves, lungs of young starved rats accepted significantly less volume at all pressure levels compared with lungs of young fed rats. When expressed as a percent of maximum lung volume, the VP curve in young starved rats was significantly shifted upward at low lung volumes. In the old rats, the VP curves were similar in fed and starved rats. Total lung content of protein, DNA, crude connective tissue, hydroxyproline, and elastin were significantly reduced in young starved compared with young fed rats, whereas in old starved rats only protein and DNA contents were lower than those in old fed animals. It appears that in rapidly growing young rats starvation leads to growth retardation, loss of connective tissue components, and possibly reduction in tissue elastic forces at low lung volumes, whereas starvation has no significant effects on lung mechanics and connective tissue in old rats.
A substantial number of patients with COPD are underweight (UW); they comprise the clinical subtype of "dyspneic" or emphysematous. To determine whether these patients are more dyspneic than normal weight (NW) patients with COPD, we quantitated the severity of dyspnea, using a modified Medical Research Council (MRC) dyspnea scale, in 33 UW and 57 NW patients and compared their pulmonary function tests (PFTs), arterial blood gases (ABGs), and respiratory muscle strength as estimated by maximum static inspiratory (PI(max)) and expiratory (PE(max)) mouth pressures (all as means +/- SEM). Body mass index was 18.7 +/- 1.2 and 24.5 +/- 1.8 kg/m(2) in UW and NW patients, respectively (p < 0.0001). The MRC dyspnea scale was 3. 1 +/- 0.9 in UW and 2.5 +/- 1.2 in NW groups (p = 0.035). All PFT and ABG parameters were similar in the two groups except for DCO (36 +/- 11% in UW and 57 +/- 17% in NW, p < 0.001) and PI(max) (55 +/- 18 mm Hg in UW and 66 +/- 19 mm Hg in NW, p = 0.020). In a stepwise multiple regression model, %DCO and %MVV combined were the best predictors of dyspnea severity (R(2) = 0.30, p = 0.001). We conclude that UW patients with COPD are more dyspneic than NW patients. Although the origin of dyspnea in COPD is multifactorial, changes in DCO and respiratory muscle strength may contribute to its intensity.
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