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Background and Objective:  Lung-protective mechanical ventilation is known to attenuate ventilator-associated lung injury (VALI), but often at the expense of hypoventilation and hypercapnia. It remains unclear whether the main mechanism by which VALI is attenuated is a product of limiting mechanical forces to the lung during ventilation, or a direct biological effect of hypercapnia.   Methods:  Acute lung injury (ALI) was induced in 60 anesthetized rats by the instillation of 1.25 M HCl into the lungs via tracheostomy. Ten rats each were randomly assigned to one of six experimental groups and ventilated for 4 h with: 1)  Conventional HighV   E   Normocapnia  (high V T , high minute ventilation, normocapnia), 2)  Conventional Normocapnia  (high V T , normocapnia), 3)  Protective Normocapnia  (V T  8 ml/kg, high RR), 4)  Conventional iCO   2   Hypercapnia  (high V T , low RR, inhaled CO 2 ), 5)  Protective iCO   2   Hypercapnia  (V T  8 ml/kg, high RR, added CO 2 ), 6)  Protective endogenous Hypercapnia  (V T  8 ml/kg, low RR). Blood gasses, broncho-alveolar lavage fluid (BALF), and tissue specimens were collected and analyzed for histologic and biologic lung injury assessment.   Results:  Mild ALI was achieved in all groups characterized by a decreased mean PaO 2 /FiO 2  ratio from 428 to 242 mmHg ( p  &amp;lt; 0.05), and an increased mean elastance from 2.46 to 4.32 cmH 2 O/L ( p  &amp;lt; 0.0001). There were no differences in gas exchange among groups. Wet-to-dry ratios and formation of hyaline membranes were significantly lower in low V T  groups compared to conventional tidal volumes. Hypercapnia reduced diffuse alveolar damage and IL-6 levels in the BALF, which was also true when CO 2  was added to conventional V T . In low V T  groups, hypercapnia did not induce any further protective effect except increasing pulmonary IL-10 in the BALF. No differences in lung injury were observed when hypercapnia was induced by adding CO 2  or decreasing minute ventilation, although permissive hypercapnia decreased the pH significantly and decreased liver histologic injury.   Conclusion:  Our findings suggest that low tidal volume ventilation likely attenuates VALI by limiting mechanical damage to the lung, while hypercapnia attenuates VALI by limiting pro-inflammatory and biochemical mechanisms of injury. When combined, both lung-protective ventilation and hypercapnia have the potential to exert an synergistic effect for the prevention of VALI.

frontiers in physiology

Lung-Protective Ventilation Attenuates Mechanical Injury While Hypercapnia Attenuates Biological Injury in a Rat Model of Ventilator-Associated Lung Injury