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Reticular basement membrane (RBM) thickness and airway responses to inhaled methacholine (MCh) were studied in perennial allergic asthma (n = 11), perennial allergic rhinitis (n = 8), seasonal allergic rhinitis (n = 5), and chronic obstructive pulmonary disease (COPD, n = 9). RBM was significantly thicker in asthma (10.1 +/- 3.7 microm) and perennial rhinitis (11.2 +/- 4.2 microm) than in seasonal rhinitis (4.7 +/- 0.7 microm) and COPD (5.2 +/- 0.7 microm). The dose (geometric mean) of MCh causing a 20% decrease of 1-s forced expiratory volume (FEV(1)) was significantly higher in perennial rhinitis (1,073 microg) than in asthma (106 microg). In COPD, the slope of the linear regression of all values of forced vital capacity plotted against FEV(1) during the challenge was higher, and the intercept less, than in other groups, suggesting enhanced airway closure. In asthma, RBM thickness was positively correlated (r = 0.77) with the dose (geometric mean) of MCh causing a 20% decrease of FEV(1) and negatively correlated (r = -0.73) with the forced vital capacity vs. FEV(1) slope. We conclude that 1) RBM thickening is not unique to bronchial asthma, and 2) when present, it may protect against airway narrowing and air trapping. These findings support the opinion that RBM thickening represents an additional load on airway smooth muscle.

Crimi, Emanuele, Riccardo Pellegrino, Manlio Milanese, and Vito Brusasco. Deep breaths, methacholine, and airway narrowing in healthy and mild asthmatic subjects. J Appl Physiol 93: 1384-1390, 2002. First published June 21, 2002 10.1152/japplphysiol.00209.2002Deep breaths taken before inhalation of methacholine attenuate the decrease in forced expiratory volume in 1 s and forced vital capacity in healthy but not in asthmatic subjects. We investigated whether this difference also exists by using measurements not preceded by full inflation, i.e., airway conductance, functional residual capacity, as well as flow and residual volume from partial forced expiration. We found that five deep breaths preceding a single dose of methacholine 1) transiently attenuated the decrements in forced expiratory volume in 1 s and forced vital capacity in healthy (n ϭ 8) but not in mild asthmatic (n ϭ 10) subjects and 2) increased the areas under the curve of changes in parameters not preceded by a full inflation over 40 min, during which further deep breaths were prohibited, without significant difference between healthy (n ϭ 6) and mild asthmatic (n ϭ 16) subjects. In conclusion, a series of deep breaths preceding methacholine inhalation significantly enhances bronchoconstrictor response similarly in mild asthmatic and healthy subjects but facilitates bronchodilatation on further full inflation in the latter.forced expiratory volume in 1 s; specific airway conductance; partial flow-volume curve; functional residual capacity; residual volume RECENT STUDIES HAVE SHOWN that deep breaths taken immediately before inhalation of methacholine (MCh) greatly modulate the bronchoconstrictor response in normal (10, 12, 21) but not in asthmatic (10) subjects. This would suggest that the shortening capacity of airway smooth muscle is reduced by previous lung stretching in healthy subjects, and the lack of such a bronchoprotective mechanism may be responsible for airway hyperresponsiveness in asthma. A mechanistic interpretation of the above studies is, however, limited by the use of forced expiratory volume in 1 s (FEV 1 ) and forced vital capacity (FVC), measurements that are highly and variably affected by the full lung inflation preceding the forced expiratory maneuver. During induced bronchoconstriction, a full inflation transiently increases airway caliber, and the magnitude of this increase depends on the relative magnitude of the distending force of lung parenchyma and the constrictor force of airway smooth muscle (17). Therefore, any parameter derived from a full forced expiratory maneuver, including FEV 1 and FVC, will depend on both airway smooth muscle shortening capacity and airway wall response to a deep breath.It is reasonable to postulate that, if the lack of a bronchoprotective effect by multiple deep breaths taken before inhaling a constrictor agent in asthma is due to the inability to reduce the shortening capacity of airway smooth muscle, then the different effects of the deep breaths on airway response to MCh between asthmati...

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