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Morphometry of methacholine-induced bronchoconstriction in the rat
D H Eidelman1, M Lei, R H Ghezzo
1Meakins-Christie Laboratories, Royal Victoria Hospital, Montreal, Quebec, Canada.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|October 1, 1993
Summary
Lung hyperinflation, not airway narrowing, significantly impacts mechanical changes during methacholine-induced bronchoconstriction. This suggests parenchymal viscoelasticity plays a larger role than previously thought in respiratory resistance.
Area of Science:
- Pulmonary physiology
- Respiratory mechanics
- Morphometry
Background:
- Smooth muscle agonists can induce resistive pressure losses, potentially due to parenchymal viscoelasticity.
- Understanding the relative contributions of lung parenchyma and airways to these changes is crucial.
Purpose of the Study:
- To evaluate the roles of lung parenchyma and airways in mechanical changes during methacholine-induced bronchoconstriction.
- To quantify the impact of airway narrowing and parenchymal changes on pulmonary resistance and elastance.
Main Methods:
- Open-chest, mechanically ventilated rats were exposed to saline, low-dose, or high-dose methacholine aerosols.
- Pulmonary resistance (RL) and elastance (EL) were calculated using pressure-volume data.
- Lung morphometry assessed airway lumen area and air space size (mean linear intercept, Lm).
Main Results:
- Methacholine induced progressive airway narrowing (aBM/ABM) and increased air space size (Lm).
- Multiple regression analysis revealed that air space size (Lm) explained more variance in mechanical parameters than airway narrowing.
- Parenchymal distortion (SDi) had minimal impact once Lm was accounted for.
Conclusions:
- Lung hyperinflation, indicated by increased Lm, is a major contributor to mechanical changes during methacholine-induced bronchoconstriction.
- Parenchymal viscoelasticity appears to play a significant role in respiratory resistance, potentially exceeding the contribution of airway narrowing.