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HIGHLIGHTED TOPIC

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Reflexes from the Lungs and Airways

CO₂ relaxes parenchyma in the liquid-filled rat lung

Departments of Physiology and Biophysics and of Medicine (Pulmonary and Critical Care Medicine), University of Washington School of Medicine; and the Department of Veterans Affairs Puget Sound Health Care System, Seattle, Washington

Submitted 2 February 2006 ; accepted in final form 7 April 2007

ABSTRACT

CO₂ regulation of lung compliance is currently explained by pH- and CO₂-dependent changes in alveolar surface forces and bronchomotor tone. We hypothesized that in addition to, but independently of, those mechanisms, the parenchyma tissue responds to hypercapnia and hypocapnia by relaxing and contracting, respectively, thereby improving local matching of ventilation (A) to perfusion (). Twenty adult rats were slowly ventilated with modified Krebs solution (rate = 3 min^–1, 37°C, open chest) to produce unperfused living lung preparations free of intra-airway surface forces. The solution was gassed with 21% O₂, balance N₂, and CO₂ varied to produce alveolar hypocapnia (PCO₂ = 26.1 ± 2.4 mmHg, pH = 7.56 ± 0.04) or hypercapnia (PCO₂ = 55.0 ± 2.3 mmHg, pH = 7.23 ± 0.02). The results show that lung recoil, as indicated from airway pressure measured during a breathhold following a large volume inspiration, is reduced 30% when exposed to hypercapnia vs. hypocapnia (P < 0.0001, paired t-test), but stress relaxation and flow-dependent airway resistance were unaltered. Increasing CO₂ from hypo- to hypercapnic levels caused a substantial, significant decrease in the quasi-static pressure-volume relationship, as measured after inspiration and expiration of several tidal volumes, but hysteresis was unaltered. Furthermore, addition of the glycolytic inhibitor NaF abolished CO₂ effects on lung recoil. The results suggest that lung parenchyma tissue relaxation, arising from active elements in response to increasing alveolar CO₂, is independent of (and apparently in parallel with) passive tissue elements and may actively contribute to A/ matching.

alveolar; pulmonary mechanics; ventilation-to-perfusion matching