CO2 relaxation of the rat lung parenchymal strip

Evidence from liquid-filled rat lungs supported the presence of CO2-dependent, active relaxation of parenchyma under normoxia by unknown mechanisms (Emery et al., 2007). This response may improve matching of alveolar ventilation (V˙A) to perfusion (Q˙) by increasing compliance and V˙A in overperfused (high CO2) regions, and decrease V˙A in underperfused regions. Here, we have more directly studied CO2-dependent parenchymal relaxation and tested a hypothesized role for actin-myosin interaction in this effect. Lung parenchymal strips (∼1.5 mm × 1.5 mm × 15 mm) from 16 rats were alternately exposed to normoxic hypocapnia (PCO2≈20mmHg) or hypercapnia (PCO2≈53mmHg). Seven specimens were used to construct length-tension curves, and nine were tested with and without the myosin blocker 2,3-butanedione monoxime (BDM). The results demonstrate substantial, reversible CO2-dependent changes in parenchyma strip recoil (up to 23%) and BDM eliminates this effect, supporting a potentially important role for parenchymal myosin in V˙A/Q˙ matching.

► We investigated the CO2 effects on recoil in normoxic rat lung parenchymal strips. ► We also investigated the role of myosin in CO2-dependent parenchymal strip recoil. ► Increasing PCO2 (20-53 mmHg) produced reversible parenchymal relaxation. ► Myosin blocker, 2,3-BDM (30 mM) eliminated CO2-dependent parenchymal strip recoil. ► Non-smooth muscle myosin may underlie CO2-dependent parenchymal recoil.