Endothelial nitric oxide synthase in hypoxic newborn porcine pulmonary vessels
b
H Oliveira,b
J S Pollock,c
J M Polak,b
S G Hawortha
a Developmental
Vascular Biology and Pharmacology Unit, Institute of Child
Health, 30 Guilford Street, London WC1N 1EH, b Department of
Histochemistry, Royal Postgraduate Medical School,
Hammersmith Hospital, London, c Vascular
Biology Center, Department of Pharmacology and Toxicology,
Medical College of Georgia, Augusta, USA
Correspondence to: Dr Hislop.
Accepted 4 February 1997
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.
Deceased
© 1997 by Archives of Disease in Childhood
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