title: Functional alterations in NO, PGI2 and EDHF pathways in the aortic endothelium after myocardial infarction in rats.
abstract: BACKGROUND
  Previous work on endothelial dysfunction in post-MI heart failure has shown conflicting results.
  
  
  OBJECTIVE
  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).
  
  
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Experimental Pharmacology, Chair of Pharmacology, Jagiellonian University Medical College, Grzegorzecka Str. 16, 31-531 Krakow, Poland.
authors.forename: Gabor
authors.initials: G
authors.lastname: Csanyi
authors.forename: Michael
authors.initials: M
authors.lastname: Bauer
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Dietl
authors.forename: Magdalena
authors.initials: M
authors.lastname: Lomnicka
authors.forename: Tatiana
authors.initials: T
authors.lastname: Stepuro
authors.forename: Bruno K
authors.initials: BK
authors.lastname: Podesser
authors.forename: Stefan
authors.initials: S
authors.lastname: Chlopicki
mesh_terms: D000818:Animals; D001011:Aorta / Q000378:metabolism; D001685:Biological Factors / Q000378:metabolism*; D003577:Cytochrome P-450 Enzyme System / Q000378:metabolism; D004727:Endothelium / Q000378:metabolism; D011464:Epoprostenol / Q000378:metabolism*; D005260:Female; D008297:Male; D009203:Myocardial Infarction / Q000378:metabolism* / Q000503:physiopathology / Q000601:surgery; D009569:Nitric Oxide / Q000378:metabolism*; D015221:Potassium Channels / Q000378:metabolism; D011451:Prostaglandin-Endoperoxide Synthases / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D015854:Up-Regulation; D020257:Ventricular Remodeling
chemical_list: D001685:Biological Factors; D015221:Potassium Channels; C067410:endothelium-dependent hyperpolarization factor; D009569:Nitric Oxide; D003577:Cytochrome P-450 Enzyme System; D011464:Epoprostenol; D011451:Prostaglandin-Endoperoxide Synthases