Continuous Positive Airway Pressure Modulates Effect of Inhaled Nitric Oxide on the Ventilation-Perfusion Distributions in Canine Lung Injury: Content

Continuous Positive Airway Pressure Modulates Effect of Inhaled Nitric Oxide on the Ventilation-Perfusion Distributions in Canine Lung Injury: ContentThis effect has been attributed to selective vasodilation in ventilated lung regions It has been suggested that inhaled NO by its lipophilic properties diffuses directly into the smooth muscle of the pulmonary resistance vessels in the proximity of alveoli, and activates soluble guanylate cyclase. This increases intracellular guanosine 3,5-cyclic monophosphate (cGMP) and causes smooth muscle relaxation. Simultaneously, inactivation of NO in the blood seems to be fast enough to prevent an effect on hypoxic pulmonary vasoconstriction in nonventilated lung areas

Application of CPAP with and without NO inhalation converted shunt units directly to normal Va/Q units without creating regions of low Va/Q. Similar phenomena have been observed previously when PEEP was applied2 or NO was added in the inspiratory gas in mechanically ventilated patients >vith adult respiratory distress syndrome. However, in this study, inhalation of NO did not significantly affect the distribution of pulmonary blood flow and Va/Q matching in the absence of CPAP. These findings are not in conflict with previous clinical observations that NO inhalation decreases perfusion of shunt units by redistribution of the blood flow to well-ventilated lung units. However, in patients with adult respiratory distress syndrome, inhalation of NO was always provided during mechanical ventilation with 10 to 15 cm H2O of PEEP. Our results indicate that adequate recruitment of gas exchange units is essential to get the gaseous NO in contact with enough pulmonary blood vessels and to cause vasodilation affecting significantly Va/Q matching.
The effect of NO inhalation on Va/Q distributions also has been attributed to relaxation of bronchial smooth muscles. However, bronchodilation, as inferred from measurements of Paw, Pes, and corresponding gas flow, was not noted in our dogs with oleic acid lung injury. Furthermore, dispersion of pulmonary blood flow (logSDQ) did not indicate lower Va/Q inequality of below normal and low Va/Q areas, as might be expected during NOinduced bronchodilation.
Recent development in the treatment of acute lung injury has introduced NO inhalation to improve pulmonary gas exchange by better Va/Q matching and to decrease PVR. The results of this study demonstrate that although PVR can be lowered with NO inhalation alone, recruitment of gas exchange units with CPAP is necessary to produce an effect of NO inhalation on Va/Q matching and oxygenation. A clinical study is necessary to evaluate the validity of these results in critically ill patients.

This entry was posted in Lung injury and tagged acute lung injury, continuous positive airway pressure, Nitric oxide, pulmonary gas exchange, ventilation-perfusion distribution.