Endothelial nitric oxide synthase in hypoxic newborn porcine pulmonary vessels

被引:28
|
作者
Hislop, AA
Springall, DR
Oliveira, H
Pollock, JS
Polak, JM
Haworth, SG
机构
[1] HAMMERSMITH HOSP, ROYAL POSTGRAD MED SCH, DEPT HISTOCHEM, LONDON W12 0HS, ENGLAND
[2] MED COLL GEORGIA, DEPT PHARMACOL & TOXICOL, VASC BIOL CTR, AUGUSTA, GA 30912 USA
来源
ARCHIVES OF DISEASE IN CHILDHOOD-FETAL AND NEONATAL EDITION | 1997年 / 77卷 / 01期
关键词
pulmonary circulation; nitric oxide synthase; hypoxia; endothelium; piglets;
D O I
10.1136/fn.77.1.F16
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
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 hom 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.
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页码:F16 / F22
页数:7
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