Influence of glottic mechanism on pulmonary function after acute lung injury.

We measured arterial gas tensions, respiratory timing, and intratracheal pressure in 12 rabbits to investigate the consequences of translaryngeal intubation with normal and subsequently injured lungs. Data were collected before, during, and after intubation. Intubation in normal rabbits precipitated no untoward effects on gas exchange or respiratory phase timing. However, there was significant elevation of subglottic pressure during expiration following extubation. Central venous injection of oleic acid (0.08 ml/kg) induced an acute lung injury that after 24 h was characterized by reduced PaO2 and dynamic lung-thorax compliance and tachypnea. Intubation in animals with acute lung injury was associated with a significant decline in arterial oxygenation, tachypnea, and increased PCO2. Expiratory tracheal pressure and expiratory time were greater and PaCO2 and respiratory rate were lower following extubation. We conclude that translaryngeal intubation following acute lung injury exacerbates already compromised pulmonary function by preventing a compensatory expiratory braking maneuver by the glottic apparatus.