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Functional alterations in NO, PGI 2 and EDHF pathways in the aortic endothelium after myocardial infarction in rats
Author(s) -
Csanyi Gabor,
Bauer Michael,
Dietl Wolfgang,
Lomnicka Magdalena,
Stepuro Tatiana,
Podesser Bruno K.,
Chlopicki Stefan
Publication year - 2006
Publication title -
european journal of heart failure
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.149
H-Index - 133
eISSN - 1879-0844
pISSN - 1388-9842
DOI - 10.1016/j.ejheart.2006.09.011
Subject(s) - medicine , endothelial dysfunction , cardiology , ventricle , basal (medicine) , ligation , myocardial infarction , aorta , vasodilation , endothelium , thoracic aorta , endocrinology , insulin
Background Previous work on endothelial dysfunction in post‐MI heart failure has shown conflicting results. Aim To analyze gender related alterations in NO‐, PGI 2 ‐ and EDHF‐dependent endothelial function in the thoracic aorta 7 and 42 days after myocardial infarction (MI). Methods and results MI was induced by coronary artery ligation in female and male Sprague–Dawley rats. There was no gender related difference in infarct‐size or in the impairment of fractional shortening of the left ventricle 42 days after coronary ligation. Neither acetylcholine‐induced (Ach) vasodilation nor basal PGI 2 production in the aorta was modified by coronary ligation. Interestingly, 7 days after MI, basal NO production was impaired and the EDHF component of Ach‐induced vasodilation was up‐regulated, in both male and female rats. However, 42 days post‐MI, basal NO was only impaired in male rats, while EDHF was only up‐regulated in female rats. Conclusion MI induced impairment of functional activity of basal NO production and adaptive up‐regulation of the EDHF component of Ach‐induced relaxation. The above alterations in endothelial function in the aorta were gender‐specific at 42 days but not 7 days after MI. Some of the previously reported discrepancies in the development of endothelial dysfunction in the post‐MI period may be gender related differences.