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Chronic allergic inflammation induces replication of airway smooth muscle cells in vivo in guinea pigs.

remodelling among individual animals.8 As shown in Figure 9, the severity of the functional abnormality (ie, airway constrictor hyperresponsiveness), manifest as lowering of the ED200ACh (the estimated dose of acetylcholine needed to double respiratory system resistance), does correlate with several indices of the magnitude of airway remodelling, including the smooth muscle layer thickness. Furthermore, when hyperoxia-exposed immature rats are removed from 8 days' oxygen exposure, both their airway constrictor hyperresponsiveness and their airway wall layer thickening resolve toward normal in parallel (Fig 10 and 11).9 This constant association between the magnitudes of hyperoxia-induced structural and functional airway abnormalities during both peak and resolution phases supports, though does not prove, the notion that hyperoxia-induced airway remodelling causes airway constrictor hyperresponsiveness in immature rats. A more definitive test of this potential causal relationship may come when, after identifying the precise nature of the mitogenic activity in hyperoxic animals' BAL fluid, specific interventions are designed to neutralize this activity during oxygen exposure. Still, it seems unlikely that airway remodelling can entirely explain hyperoxia-induced airway constrictor hyperresponsiveness, as we have also demonstrated epithelium-dependent increases in tracheal smooth muscle stress generation in vitro, in tissues obtained from hyperoxia-exposed rats (Fig 12).10 Thus, hyperoxiainduced airway constrictor hyperresponsiveness appears to be the complex result of multiple simultaneous mechanisms, which may include airway remodelling as a principal contributor.