1c:I[419806,["/_next/static/chunks/bb923814e1f4d2e9.js","/_next/static/chunks/dd3ee9f5b7716ca6.js","/_next/static/chunks/4204a0ae82542ca8.js","/_next/static/chunks/1270dead247da766.js","/_next/static/chunks/6e1aa89a642f40be.js","/_next/static/chunks/2d7aa753e81324a8.js","/_next/static/chunks/8ffd0b71567920d8.js","/_next/static/chunks/67ea6dfd21f16c5f.js","/_next/static/chunks/24eb4379f68013fd.js","/_next/static/chunks/b8cd775ffdf935bd.js","/_next/static/chunks/983103cd9eb7b428.js","/_next/static/chunks/263f2cdcb9aa2341.js","/_next/static/chunks/294b9525248c8e5f.js"],"default"] 1d:T404,THE DIAGNOSIS of bronchial asthma can ordinarily be made with assurance by employing the standard criteria of history, physical examination, and the demonstration of reversible airway obstruction.¹Occasionally, the diagnosis of asthma is suspected from the history, but the physical examination is normal, and spirometry shows no airway obstruction at the time of the evaluation. When it is not possible for the physician to observe the patient during an acute episode, the diagnosis cannot be made with certainty. Consequently, a test for bronchial asthma is needed. More than 20 years ago Dautrebande and Philpott²and Tiffeneau³demonstrated that the asthmatic patient is much more sensitive than normal persons to the bronchoconstrictive effects of histamine and cholinergic agents. This increased response has since been amply confirmed and has been used many times to investigate the pathophysiology and pathogenesis of the disease.^4-17 Tiffeneau^18,19has suggested that1e:T414,Recruitment and derecruitment (R/D) of air spaces within the lung is greatly enhanced in lung injury and is thought to be responsible for exacerbating injury during mechanical ventilation. There is evidence to suggest that R/D is a time-dependent phenomenon. We have developed a computer model of the lung consisting of a parallel arrangement of airways and alveolar units. Each airway has a critical pressure (Pcrit) above which it tends to open and below which it tends to close but at a rate determined by how far pressure is from Pcrit. With an appropriate distribution of Pcrit and R/D velocity characteristics, the model able to produce realistic first and second pressure-volume curves of a lung inflated from an initially degassed state. The model also predicts that lung elastance will increase transiently after a deep inflation to a degree that increases as lung volume decreases and as the lung becomes injured. We conclude that our model captures the time-dependent mechanical behavior of the lung due to gradual R/D of lung units.1f:T419,Fifteen mild to moderate attacks of asthma were induced in 12 asymptomatic asthmatic subjects by nebulization of an allergen. Serial measurements were made of maximal expiratory flow-volume curves and total respiratory resistance; both were related to absolute lung volume. At the height of the attack, total lung capacity was unchanged, vital capacity decreased, residual volume increased, maximal flows decreased, and resistance increased. Maximal flow at 60 per cent of control total lung capacity was the most sensitive indicator of response. Total respiratory resistance corrected for volume was also sensitive and tended to change with maximal flow at 60 per cent of total lung capacity. In many subjects, the first effect of the inhaled allergen was to cause a parallel shift in the maximal expiratory flow-volume curve, with no change in slope. The mechanical explanation for this behavior is uncertain. A possible explanation is that closure of susceptible lung units occurred but the mechanical behavior of uninvolved units was unaffected.20:T712,

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