title: Tolerance of the developing cyanotic heart to ischemia-reperfusion injury in the rat.
abstract: OBJECTIVE
  Whether chronic hypoxia attenuates myocardial ischemia-reperfusion injury remains controversial because conflicting data have been reported probably due to the existence of many factors influencing the functional recovery of hearts. These factors include the differences of species, the time at which hypoxia begins, the degree of hypoxia, and so on. Regarding chronic hypoxia from birth, so far the only available data are based on findings in rabbit hearts. The purpose of this study was to describe the effect of chronic hypoxia from birth on myocardial reperfusion injury in the rat heart.
  
  
  METHODS
  Normoxic hearts were obtained from rats housed in ambient air for 6 weeks (normoxic group); hypoxic hearts were obtained from rats housed in a hypoxic chamber (13%-14% oxygen) from birth for 6 weeks (hypoxic group). Isolated, crystalloid perfused working hearts were subjected to 30 min of global normothermic ischemia followed by 15 min of reperfusion; functional recovery was then measured in the two groups. The excretion of cyclic guanosine monophosphate (cGMP) in the coronary drainage was measured at the end of the preischemia and reperfusion periods.
  
  
  RESULTS
  The percent recovery of the left ventricular developed pressure and the first derivative of left ventricular pressure were significantly better in the hypoxic group than in the normoxic group. cGMP excretion in the coronary drainage was significantly increased during both the preischemia and reperfusion periods.
  
  
  CONCLUSIONS
  Chronic hypoxia from birth increased myocardial tolerance to ischemia-reperfusion injury with increased cGMP synthesis in the isolated heart model in rats.
authors.affiliation: Department of Cardiovascular Surgery, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science, 2-5-1 Shikata-cho, Okayama, 700-8558, Japan. GZE00572@nifty.ne.jp
authors.forename: Yasuhiro
authors.initials: Y
authors.lastname: Fujii
authors.forename: Kozo
authors.initials: K
authors.lastname: Ishino
authors.forename: Tomoko
authors.initials: T
authors.lastname: Tomii
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Kanamitsu
authors.forename: Hideya
authors.initials: H
authors.lastname: Mitsui
authors.forename: Shunji
authors.initials: S
authors.lastname: Sano
mesh_terms: D000818:Animals; D002908:Chronic Disease; D003490:Cyanosis / Q000378:metabolism / Q000503:physiopathology*; D006152:Cyclic GMP / Q000378:metabolism; D004195:Disease Models, Animal; D006321:Heart / Q000254:growth & development / Q000503:physiopathology*; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology*; D054086:KATP Channels / Q000378:metabolism; D008297:Male; D009200:Myocardial Contraction; D015428:Myocardial Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D009206:Myocardium / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function; D015854:Up-Regulation; D016277:Ventricular Function, Left; D017725:Ventricular Pressure
chemical_list: D054086:KATP Channels; D006152:Cyclic GMP
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