The Effects of Lung Protective Ventilation or Hypercapnic Acidosis on Gas Exchange and Lung Injury in Surfactant Deficient Rabbits

• Published in: PloS one Vol. 11; no. 2; p. e0147807
• Main Authors: Hummler, Helmut D., Banke, Katharina, Wolfson, Marla R., Buonocore, Giuseppe, Ebsen, Michael, Bernhard, Wolfgang, Tsikas, Dimitrios, Fuchs, Hans
• Format: Journal Article
• Language: English
• Published: United States Public Library of Science 03.02.2016; Public Library of Science (PLoS)
• Subjects: Acidosis; Acidosis, Respiratory - etiology; Acidosis, Respiratory - physiopathology; Alveoli; Analysis; Animal models; Animals; Biology and Life Sciences; Biomarkers; Blood Gas Analysis; Bronchoalveolar lavage; Bronchoalveolar Lavage Fluid; Bronchus; Carbon dioxide; Critical care; Disease Models, Animal; Drug therapy; Engineering and Technology; Gas exchange; Hemodynamics; Histology; Hospitals; Hypercapnia; Hypercapnia - complications; Hypoventilation; Inflammation; Inflammatory response; Injury prevention; Interleukin; Interleukin 8; Laboratory animals; Lactic acid; Lung Injury - blood; Lung Injury - etiology; Lung Injury - pathology; Lung Injury - prevention & control; Lung Injury - therapy; Lungs; Mechanical ventilation; Medicine and Health Sciences; Newborn babies; Pediatric respiratory diseases; Pediatrics; pH effects; Physical Sciences; Pulmonary Surfactants; Rabbits; Respiration, Artificial - methods; Respiratory distress syndrome; Rodents; Surface active agents; Surfactants; Tidal Volume; Ventilation; Ventilators; Germany
• ISSN: 1932-6203; 1932-6203
• DOI: 10.1371/journal.pone.0147807

Permissive hypercapnia has been shown to reduce lung injury in subjects with surfactant deficiency. Experimental studies suggest that hypercapnic acidosis by itself rather than decreased tidal volume may be a key protective factor. To study the differential effects of a lung protective ventilatory strategy or hypercapnic acidosis on gas exchange, hemodynamics and lung injury in an animal model of surfactant deficiency. 30 anesthetized, surfactant-depleted rabbits were mechanically ventilated (FiO2 = 0.8, PEEP = 7cmH2O) and randomized into three groups: Normoventilation-Normocapnia (NN)-group: tidal volume (Vt) = 7.5 ml/kg, target PaCO2 = 40 mmHg; Normoventilation-Hypercapnia (NH)-group: Vt = 7.5 ml/kg, target PaCO2 = 80 mmHg by increasing FiCO2; and a Hypoventilation-Hypercapnia (HH)-group: Vt = 4.5 ml/kg, target PaCO2 = 80 mmHg. Plasma lactate and interleukin (IL)-8 were measured every 2 h. Animals were sacrificed after 6 h to perform bronchoalveolar lavage (BAL), to measure lung wet-to-dry weight, lung tissue IL-8, and to obtain lung histology. PaO2 was significantly higher in the HH-group compared to the NN-group (p<0.05), with values of the NH-group between the HH- and NN-groups. Other markers of lung injury (wet-dry-weight, BAL-Protein, histology-score, plasma-IL-8 and lung tissue IL-8) resulted in significantly lower values for the HH-group compared to the NN-group and trends for the NH-group towards lower values compared to the NN-group. Lactate was significantly lower in both hypercapnia groups compared to the NN-group. Whereas hypercapnic acidosis may have some beneficial effects, a significant effect on lung injury and systemic inflammatory response is dependent upon a lower tidal volume rather than resultant arterial CO2 tensions and pH alone.