Abstract

AIMS To determine if the failure of neonatal pulmonary arteries to dilate is due to a lack of nitric oxide synthase (NOS).

METHODS A monoclonal antibody to endothelial NOS was used to demonstrate the distribution and density of NOS in the developing porcine lung after a period in hypobaric hypoxia. Newborn piglets were made hypertensive by exposure to hypobaric hypoxia (50.8 kPa) from < 5 minutes of age to 2.5 days of age, 3–6 days of age or 14–17 days of age. A semiquantitative scoring system was used to assess the distribution of endothelial NOS by light microscopy.

RESULTS NOS was present in the arteries in all hypoxic animals. However, hypoxia from birth caused a reduction in NOS compared with those lungs normal at birth and those normal at 3 days. Hypoxia from 3–6 days led to a high density of NOS compared with normal lungs at 6 days. Hypoxia from 14–17 days had little effect on the amount of NOS. On recovery in room air after exposure to hypoxia from birth there was a transient increase in endothelial NOS after three days of recovery, mirroring that seen at three days in normal animals.

CONCLUSIONS Suppression of NOS production in the first few days of life may contribute to pulmonary hypertension in neonates.