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.
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.
Authors: J S Pollock; U Förstermann; J A Mitchell; T D Warner; H H Schmidt; M Nakane; F Murad Journal: Proc Natl Acad Sci U S A Date: 1991-12-01 Impact factor: 11.205
Authors: Joshua R Sheak; Laura Weise-Cross; Ray J deKay; Benjimen R Walker; Nikki L Jernigan; Thomas C Resta Journal: Am J Physiol Heart Circ Physiol Date: 2017-07-21 Impact factor: 4.733
Authors: K A Fagan; B W Fouty; R C Tyler; K G Morris; L K Hepler; K Sato; T D LeCras; S H Abman; H D Weinberger; P L Huang; I F McMurtry; D M Rodman Journal: J Clin Invest Date: 1999-01 Impact factor: 14.808