Lung distension and carbon dioxide affect pulmonary nitric oxide formation in the anaesthetized rabbit.

Positive end-exspiratory pressure (PEEP) and nitric oxide (NO) can influence lung VA/Q-matching and pulmonary vascular resistance, and application of PEEP can increase exhaled NO in animals. To obtain a better understanding of these mechanisms, we examined how different types of ventilation or changes in CO2 affect the formation of endogenous NO. Exhaled NO in pentobarbital-anaesthetized rabbits was monitored by chemiluminescence. The animals were enclosed in a chamber and subjected to various modes of positive as well as negative pressure ventilation which was adjusted to induce similar changes in functional residual capacity (FRC) with maintained ventilatory rate and tidal volume. In addition, stepwise increase in FiCO2 (1.0-10%) was studied. Negative extrathoracic end-exspiratory pressure during negative extrathoracic pressure ventilation produced an increase in NO production similar to that of positive end-exspiratory pressure during positive pressure ventilation, the increase consisting of an initial peak followed by a plateau. The faster the FRC was increased, the higher was the initial peak in NO. The greater the increase in FRC, the higher was the plateau NO concentration. Increased FiCO2 caused a dose-dependent reduction in exhaled NO. The observations of lung distension effects on exhaled NO suggest the possibility of stretch receptors or -receptive mechanisms coupled to NO formation within the lung. In addition, NO formation in the lung is influenced by CO2 in a reciprocal fashion.