The role of nitric oxide in hyperoxia-induced injury to the developing lung.

Abstract

Exogenous or inhaled NO (iNO) has been successfully used, as a selective pulmonary vasodilator, in a wide variety of clinical situations especially in the management of persistent pulmonary hypertension in the newborn. A better understanding of the role of endogenous and exogenous NO in the lungs of surfactant-deficient animals exposed to hyperoxia could result in novel strategies for the better management of RDS in premature babies with the ultimate aim to decrease chronic lung disease in these infants. This review will focus on the effects of NO, when used in combination with hyperoxia, on lung injury; information on the effects on cell culture systems and animal models will be used to highlight the unique responses of the developing lung. Most of the data from cell culture systems and adult animal models of hyperoxia-induced lung injury suggests that endogenous NO has a protective role. In the newborn animal, endogenous NO appeared to be harmful, had no effect or was protective in hyperoxia-induced lung injury. The data are conflicting on the issue of whether exogenous NO is protective or damaging in the presence of hyperoxia on lung cells and animal models. Despite the variability in the studies, it would appear that low dose exogenous NO for short duration is beneficial in hyperoxic lung injury in adult and newborn animals. In the human newborn, use of iNO in infants< 34 weeks of gestation should be considered experimental, pending results of ongoing trials.