Submitted on February 1, 2006
Accepted on April 7, 2007
CO2 relaxes parenchyma in the liquid-filled rat lung
Michael J Emery1*, Randy L Eveland2, Seong S Kim3, Jack Hildebrandt4, and Erik R Swenson5
1 Physiology & Biophysics, University of Washington School of Medicine, Seattle, Washington, United States; Pulmonary & Critical Care Medicine, Department of Veteran's Affairs Puget Sound Health Care System, Seattle, Washington, United States
2 Pulmonary & Critical Care Medicine, Department of Veteran's Affairs Puget Sound Health Care System, Seattle, Washington, United States
3 Anesthesiology, University of Ulsan College of Medicine, Asan Medical Center, Kangnung, Korea, Republic of
4 Physiology & Biophysics, University of Washington School of Medicine, Seattle, Washington, United States
5 Pulmonary & Critical Care Medicine, Department of Veteran's Affairs Puget Sound Health Care System, Seattle, Washington, United States; Physiology & Biophysics, University of Washington School of Medicine, Seattle, Washington, United States
* To whom correspondence should be addressed. E-mail: mjemery{at}u.washington.edu.
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 independent of, those mechanisms the parenchymal tissue responds to hypercapnia and hypocapnia by relaxing and contracting, respectively, thereby improving local matching of alveolar ventilation ( VA) to perfusion (Q). Twenty adult rats were slowly ventilated with modified Krebs solution (rate = 3 min-1, 37C, open chest) to produce unperfused, but living lung preparations free of intra-airway and alveolar surface forces. The solution was gassed with 21% O2, CO2 varied to produce either 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), and balance N2. The results show that lung recoil, indicated from airway pressure measured during breathhold following large volume inspiration, is reduced ~30% during hypercapnia versus hypocapnia (p < .0001, paired t-test), while stress relaxation and flow-dependent airway resistance were not altered. Increasing CO2 from hypo- to hypercapnic levels caused a substantial, significant decrease in the quasi-static pressure-volume relationship, measured after inspiration and expiration of several volumes, but hysteresis was unaltered. Furthermore, addition of the glycolytic inhibitor, NaF, abolished the CO2 effect 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 matching of VA to Q.
