Lung mechanics in antigen-induced asthma.

Increased Vascular Permeability during Passive Peritoneal Anaphylaxis in the Rat

“…Extravasation of serous fluid into the bronchial lumen of an asthmatic is thought to contribute to bronchial plugging, reduction in ciliary action in bronchial mucous membrane, and the shedding of the mucosal cells in the bronchi [4], and there is evidence that bronchial provocation with an tigen can induce serous transudation into the smaller airways of some asthmatics [10]. In short-term clinical trials with DSCG there seems to be no significant correlation between therapeutic effectiveness and improve ments in lung function, assessed in most studies by changes in upper air ways resistance; and therapeutic benefit from treatment with DSCG can be slow to develop and can extend into the period of placebo treatment [2], It is perhaps worth considering that the ability of DSCG to protect against an increase in extravasation following antigen challenge might be relevant to its clinical efficacy.…”

Physiologic similarities and differences between asthma and chronic obstructive pulmonary disease

“…As previously noted [1], several investigators have reported the transient but reversible loss of lung elastic recoil and hyperinflation at residual volume, FRC and TLC during acute exacerbations of asthma [21][22][23][24][25][26][27]. With eventual clinical recovery and return of spirometry to baseline values, there was nearly always complete recovery of the previously noted loss of lung elastic recoil, except in isolated cases [21][22][23].…”

“…With eventual clinical recovery and return of spirometry to baseline values, there was nearly always complete recovery of the previously noted loss of lung elastic recoil, except in isolated cases [21][22][23]. This reversible phenomenon has been noted during acute attacks of asthma, whether spontaneous [21][22][23][24], precipitated by exercise [25], or antigen induced [26,27], and has evaded a unifying physiologic explanation. Previous attempts to induce small airway bronchoconstriction with histamine in the presence of negative pressure around the chest wall failed to cause loss of lung elastic recoil [21].…”

Budesonide reverses lung hyperinflation in childhood asthma: a controlled study

“…Based on the inflammatory theory of asthma, it was hypothesised that this was due, not only to an increase in airway calibre [23][24][25], but also to a reduction in peribronchial and alveolar inflammation [26] which, when present, causes a temporary loss of the relationship between small bronchi and parenchyma, thus reducing elastic recoil [27,28]. This is suggested in this study by the fact that a small improvement in airway calibre after budesonide, demonstrated by the increase in sG aw , was not accompanied by a change in RV, which remained higher and not different from placebo.…”