The American review of respiratory disease
-
Am. Rev. Respir. Dis. · Mar 1993
Comparative StudyAirway responsiveness to adenosine 5'-monophosphate in chronic obstructive pulmonary disease is determined by smoking.
In contrast to methacholine, a stimulus that induces airway constriction mainly by "direct" stimulation of airway smooth muscle cells, AMP airway responsiveness reflects "indirectly" induced airway narrowing via inflammatory or neural reflex mechanisms. In order to determine inflammatory contribution to airway narrowing in COPD, we performed AMP and methacholine inhalation provocation tests in nonatopic subjects with COPD and compared the results with those obtained from atopic nonsmoking asthmatics and from healthy smoking volunteers. AMP caused airway narrowing in all but two subjects with COPD and in only three of the 12 healthy smoking subjects. ⋯ In the nonatopic nonsmoking subjects with COPD, PC20 AMP was significantly higher than in the atopic nonsmoking asthmatics (3.8 mg/ml), whereas they responded similar to methacholine provocation. These results indicate that most subjects with COPD respond to AMP provocation and that smoking determines the degree of airway responsiveness to AMP in COPD. We suggest that increased susceptibility to mediator release by mast cells or neural reflex mechanisms are involved in AMP-induced airway constriction in asthma and in COPD.
-
Am. Rev. Respir. Dis. · Mar 1993
Comparative StudyPrediction equations for single-breath carbon monoxide diffusing capacity from a Chinese population.
Most available prediction equations for the single breath carbon monoxide diffusing capacity, or DLCO, are based on white populations and do not account for racial differences. We performed this test on 436 Chinese adults. The method of measurement essentially followed the American Thoracic Society recommendations. ⋯ The predicted values from this study for DLCO and alveolar volume (VA), were significantly lower than those of most equations for white subjects, but were not for DLCO/VA. Although a portion of the differences may be explained by the additive effects of technical factors, the discrepancies can also be attributed to the smaller body size in this ethnic group, and consequently to the smaller lung volumes. Equations derived from whites, with inclusion of smokers, provided predicted values comparable to, or even lower than, those from this study.(ABSTRACT TRUNCATED AT 250 WORDS)
-
Am. Rev. Respir. Dis. · Mar 1993
Comparative StudyThe effect of respiratory and lactic acidosis on diaphragm function.
The relative effects of respiratory and metabolic acidosis on diaphragm function are not known. To determine these effects, we compared the effects of respiratory and lactic acidosis on the contractile properties of the diaphragm. We estimated diaphragmatic performance from the change in transdiaphragmatic pressure after supramaximal stimulation of the phrenic nerves in an open-chested, casted-abdomen dog. ⋯ There was a fall in diaphragm performance with respiratory acidosis (77.1 +/- 16.9 cm H2O versus 93.8 +/- 15.0 cm H2O baseline), but not with lactic acidosis (96.7 +/- 15.7 cm H2O versus 93.8 +/- 15.0 cm H2O baseline); and the gastrocnemius was unaffected by either acidosis. The changes with respiratory acidosis were similar to those seen with diaphragmatic fatigue and had similar relaxation rate changes, suggesting that intracellular pH may play a mechanistic role in respiratory muscle fatigue. In addition, the absence of a respiratory acidosis effect on a non-diaphragmatic skeletal muscle's function represents another physiologic difference between the diaphragm and other skeletal muscles.
-
Am. Rev. Respir. Dis. · Jan 1993
Physiologic effects of positive end-expiratory pressure in patients with chronic obstructive pulmonary disease during acute ventilatory failure and controlled mechanical ventilation.
Dynamic hyperinflation and intrinsic positive end-expiratory pressure (PEEPi) are observed in patients with chronic obstructive pulmonary disease (COPD) and flow limitation. Several reports suggest that PEEP levels approaching PEEPi reduce inspiratory load due to PEEPi, without further hyperinflation. Hence PEEP should not increase intrathoracic pressure or affect hemodynamics and gas exchange. ⋯ PEEPtot,rs and PEEPtot,cw also increased. Under these circumstances, PEEP increased static elastance in both the respiratory system and the chest wall, reducing cardiac index and affecting hemodynamics and gas exchange. Our data show that in mechanically ventilated COPD patients with PEEPi due to flow limitation, PEEP levels exceeding the 85% of PEEPi (Pcrit) caused further hyperinflation and compromised hemodynamics and gas exchange.