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Airway narrowing, smooth muscle force and wall compliance at low and high mechanical strains

T.K. Ansell,1 P.K. McFawn,1 H.W. Mitchell1 and P.B. Noble,1,2 1School of Biomedical, Biomolecular and Chemical Sciences, University of Western Australia, Crawley, WA 6009, Australia and 2School of Women's and Infants' Health, University of Western Australia, Crawley, WA 6009, Australia.

In a normally inflated lung, airways are maintained under constant mechanical strain due to distending forces applied by the lung parenchyma. In obstructive disease (e.g. asthma) the magnitude of airway strain may be reduced due to mechanical 'uncoupling' or alternatively increased due to dynamic hyperinflation. While several studies have characterized the effect of mechanical strain in isolated airway smooth (ASM) strip preparations in vitro, the effect of mechanical strain on the intact airway wall has not been well studied.

Aim: To determine the effect of high and low mechanical strains on airway function

Methods: Whole bronchial segments were dissected from pig lungs and maintained in organ bath chambers. Mechanical strain on airways was controlled by modifying transmural pressure (Ptm). Airways were initially equilibrated to 5 cmH2O Ptm, approximating the mechanical environment present at functional residual capacity in vivo. Ptm was subsequently increased to 25 cmH2O or decreased to −5 cmH2O for 1 h, and then returned to 5 cmH2O for a further 1 h. Two recording systems were used on different groups of airways: (i) pressure controlled, where airways were allowed to narrow against a fixed pressure, and by which specific wall compliance was measured from volume changes to a 5 cmH2O cyclical pressure change; (ii) volume controlled, where airways contracted against a fixed lumen volume and the resultant increases in pressure were recorded as an index of ASM force. The desired pressure and volume conditions were applied by a servo controlled syringe pump.

Results: Increasing Ptm to 25 cmH2O produced an immediate expansion in airway volume of ∼25% and a reduction in wall compliance of 69.3 ±1.8% (n=6, P<0.001, paired t-test). Increased Ptm attenuated airway narrowing by 15.8 ±4.2% (n=6, P<0.05) and ASM force by 20.8 ±3.4% (n=5, P<0.05). Maintaining Ptm at 25 cmH2O for 1 h produced a further fall in narrowing (P<0.05, ANOVA) but did not affect ASM force or wall compliance. Decreasing Ptm to −5cmH2O produced an immediate reduction in airway volume of ∼30% and an increase in wall compliance of 30.2 ±2.6% (n=6, P<0.001). Reduced Ptm attenuated airway narrowing by 19.5 ±3.8% (n=6, P<0.001) and force by 20.0 ±2.7% (n=5, P<0.001). Maintaining Ptm at −5 cmH2O for 1 h produced a further decrease in airway narrowing (n=6, P<0.01) and ASM force (n=5, Pp<0.001), and an increase in wall compliance (n=6, P<0.01). In all cases upon return to Ptm of 5 cmH2O airway narrowing, ASM force and compliance were restored to the pre-strain levels in <20 min.

Conclusions: The findings suggest that changes in mechanical strain above or below that expected to occur in the normal healthy lung, and favor reduced airway narrowing and ASM force production. In comparison, increases in mechanical strain favor reduced airway wall compliance while lower strains may increase wall compliance. Acute changes in mechanical strain have no long lasting impact on airway wall properties.