Protective effects of hypercapnic acidosis on ventilator-induced lung injury

To investigate whether respiratory acidosis modulates ventilator-induced lung injury (VILI), we perfused (constant flow) 21 isolated sets of normal rabbit lungs, ventilated them for 20 min (pressure controlled ventilation [PCV] = 15 cm H₂O) (Baseline) with an inspired CO₂ fraction adjusted for the partial pressure of CO₂ in the perfusate (Pco₂ ≅ 40 mm Hg), and then randomized them into three groups. Group A (control: n = 7) was ventilated with PCV = 15 cm H₂O for three consecutive 20-min periods (T1, T2, T3). In Group B (high PCV/normocapnia; n = 7), PCV was given at 20 (T1), 25 (T2), and 30 (T3) cm H₂O. The targeted Pco₂ was 40 mm Hg in Groups A and B. Group C (high PCV/hypercapnia; n = 7) was ventilated in the same way as Group B, but the targeted Pco₂ was ≅ 70 to 100 mm Hg. The changes (from Baseline to T3) in weight gain (ΔWG: g) and in the ultrafiltration coefficient (ΔK_f = gr/min/ cm H₂O/100g) and the protein and hemoglobin concentrations in bronchoalveolar lavage fluid (BALF) were used to assess injury. Group B experienced a significantly greater ΔWG (14.85 ± 5.49 [mean ± SEM] g) and ΔK_f (1.40 ± 0.49 g/min/cm H₂O/100 g) than did either Group A (ΔWG = 0.70 ± 0.43; ΔK_f = 0.01 ± 0.03) or Group C (ΔWG = 5.27 ± 2.03 g; ΔK_f = 0.25 ± 0.12 g/min/cm H₂O/ 100 g). BALF protein and hemoglobin concentrations (g/L) were higher in Group B (11.98 ± 3.78 g/L and 1.82 ± 0.40 g/L, respectively) than in Group A (2.92 ± 0.75 g/L and 0.38 ± 0.15 g/L) or Group C (5.71 ± 1.88 g/L and 1.19 ± 0.32 g/L). We conclude that respiratory acidosis decreases the severity of VILI in this model.