title: Experimental hyperlipidaemia does not prevent preconditioning and it reduces ischemia-induced apoptosis.
abstract: BACKGROUND
  Although ischemic preconditioning (PC) is known to confer cardioprotection in healthy subjects, it is unclear whether this phenomenon exists in the presence of hyperlipidaemia. The goal of this study was to determine whether the cardioprotective effect of PC is affected by hyperlipidaemia in a guinea pig model.
  
  
  METHODS
  We investigated the influence of preconditioning in normo- and hyperlipidaemic animals on papillary muscle contractility and myocardial damage as expressed by the percentage of apoptotic cells. Guinea pigs were fed a normal diet or a hyperlipidaemic diet for 5 weeks. Experiments were performed on papillary muscles subjected to experimental ischemia-reperfusion with or without prior PC.
  
  
  RESULTS
  The dietary treatment resulted in significant changes in lipid parameters, which had not affected the functionality of the right ventricle papillary muscle, both at basal conditions and in response to ischemia-reperfusion injury. However, it was found that the hyperlipidaemic diet had an effect on ischemia-induced apoptosis. Papillary muscles of hyperlipidaemic animals with higher HDL plasma concentrations were less susceptible to ischemia-reperfusion injury.
  
  
  CONCLUSIONS
  This study demonstrates that hyperlipidaemia does not alter the benefits of ischemic preconditioning such as a reduction of apoptosis and preservation of myocardial contractility. Additionally, it has been shown that plasma HDL may protect cardiomyocytes against ischemia-induced apoptosis.
authors.affiliation: I Department of Cardiology, Medical University of Gdańsk, Poland. rdw1@amg.gda.pl
authors.forename: Rafal
authors.initials: R
authors.lastname: Dworakowski
authors.forename: Dorota
authors.initials: D
authors.lastname: Dworakowska
authors.forename: Ivan
authors.initials: I
authors.lastname: Kocic
authors.forename: Tomas
authors.initials: T
authors.lastname: Wirth
authors.forename: Marcin
authors.initials: M
authors.lastname: Gruchała
authors.forename: Maciej
authors.initials: M
authors.lastname: Kamiński
authors.forename: Robin
authors.initials: R
authors.lastname: Ray
authors.forename: Jacek
authors.initials: J
authors.lastname: Petrusewicz
authors.forename: Seppo
authors.initials: S
authors.lastname: Yla-Herttuala
authors.forename: Andrzej
authors.initials: A
authors.lastname: Rynkiewicz
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002784:Cholesterol / Q000096:biosynthesis / Q000097:blood; D008076:Cholesterol, HDL / Q000096:biosynthesis / Q000097:blood; D008078:Cholesterol, LDL / Q000096:biosynthesis / Q000097:blood; D004195:Disease Models, Animal; D006168:Guinea Pigs; D006949:Hyperlipidemias / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods*; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology; D017202:Myocardial Ischemia / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology*; D010210:Papillary Muscles / Q000378:metabolism / Q000473:pathology / Q000502:physiology; D014280:Triglycerides / Q000096:biosynthesis / Q000097:blood
chemical_list: D008076:Cholesterol, HDL; D008078:Cholesterol, LDL; D014280:Triglycerides; D002784:Cholesterol