Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
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Target Concepts:
Gene/Protein
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Query: UMLS:C0242706 (
hyperoxia
)
5,219
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
We previously reported that neonatal blockade of angiotensin II AT
1
receptor prevents cardiac changes in 4 weeks rats with neonatal
hyperoxia
-induced cardiomyopathy, a recognized model of prematurity-related deleterious conditions. Considering the importance of AT
1
receptor and the renin angiotensin system (RAS) in normal development, the present study aimed to investigate the adult effects of neonatal AT
1
blockade on left ventricle (LV) in rats exposed to neonatal
hyperoxia
. Sprague-Dawley pups were exposed to 80% O
2
or room air from days 3-10. AT
1
blocker (losartan) or H
2
O were given by gavage from day 8-10. LV function (echo and intraventricular pressure), histology and expression of RAS components were examined in 15-16 weeks old adult males.
Losartan
treatment prevented myocardial fibrosis, LV wall thickening and stroke volume reduction in rats exposed to high O
2
in the neonatal period. However,
Losartan
treatment of O
2
-exposed pups led to reduced ejection fraction (EF) and fractional shortening (FS), and did not prevent changes in diastolic function.
Losartan
also did not prevent increased LV AT
2
and decreased angiotensin-(1-7) Mas receptors expression observed in high O
2
-exposed rats. Neonatal
Losartan
attenuated long-term impact of neonatal
hyperoxia
but also led to decreased EF and FS. Increased AT
2
and decreased Mas receptor expression observed in O
2
-exposed group were unaffected by
Losartan
treatment. Our results show that early life
Losartan
treatment aimed at preventing cardiac consequences of neonatal deleterious conditions may also comprise detrimental effects that require further investigation prior to clinical translation in developing children.
...
PMID:Impact of early life AT
1
blockade on adult cardiac morpho-functional changes and the renin-angiotensin system in a model of neonatal high oxygen-induced cardiomyopathy. 3137 67
