title: Determination of oxidative stress and cardiac dysfunction after ischemia/reperfusion injury in isolated rat hearts.
abstract: BACKGROUND
  Oxidative stress due to reactive oxygen species (ROS) is thought to play a considerable role in ischemia/reperfusion (I/R) injury that impairs cardiac function. The present study examined oxidative damage in I/R injury and investigated the correlation between oxidative stress and impaired cardiac function after I/R injury of the isolated rat heart.
  
  
  METHODS
  Hearts isolated from male Sprague-Dawley rats were mounted on a Langendorff apparatus. Hearts arrested using St. Thomas cardioplegic solution and then they were reperfused. The hearts were divided into three groups depending on the frequency (0-2) of I/R. After I/R, left ventricular developed pressure (LVDP), left ventricular end-diastolic pressure (LVEDP), positive maximum left ventricular developing pressure (max LV dP/dt) and coronary flow (CF) were measured. Creatine kinase (CK) was measured in the coronary effluent and 8-hydroxy-2'deoxyguanosine (8OHdG), a marker of oxidative DNA damage, was measured. Adenosine triphosphate (ATP) was measured from frozen myocardial tissue after experiment.
  
  
  RESULTS
  We immunohistochemically demonstrated and quantified levels of 8-OHdG after I/R injury of the heart. The frequency of I/R injury and cardiac dysfunction significantly and negatively correlated. The ATP products were similar among the three groups. The incidence of ventricular arrhythmias was not by affected oxidative stress.
  
  
  CONCLUSIONS
  The frequency of I/R injury had more of an effect on 8-OHdG products and on impaired cardiac function with less myocyte damage than ischemic duration within 30 minutes of ischemia.
authors.affiliation: Department of Thoracic and Cardiovascular Surgery, University of the Ryukyus, Nishihara, Okinawa, Japan. hitoshiinafuku@yahoo.co.jp
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Inafuku
authors.forename: Yukio
authors.initials: Y
authors.lastname: Kuniyoshi
authors.forename: Satoshi
authors.initials: S
authors.lastname: Yamashiro
authors.forename: Katsuya
authors.initials: K
authors.lastname: Arakaki
authors.forename: Takaaki
authors.initials: T
authors.lastname: Nagano
authors.forename: Yuji
authors.initials: Y
authors.lastname: Morishima
authors.forename: Yuya
authors.initials: Y
authors.lastname: Kise
mesh_terms: D000080242:8-Hydroxy-2'-Deoxyguanosine; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology; D015415:Biomarkers / Q000378:metabolism; D003326:Coronary Circulation; D003402:Creatine Kinase / Q000378:metabolism; D004249:DNA Damage; D003849:Deoxyguanosine / Q000031:analogs & derivatives / Q000378:metabolism; D004734:Energy Metabolism; D007150:Immunohistochemistry; D066298:In Vitro Techniques; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism*; D018384:Oxidative Stress; D010477:Perfusion; D051381:Rats; D017207:Rats, Sprague-Dawley; D013997:Time Factors; D016277:Ventricular Function, Left; D017725:Ventricular Pressure
chemical_list: D015415:Biomarkers; D000080242:8-Hydroxy-2'-Deoxyguanosine; D000255:Adenosine Triphosphate; D003402:Creatine Kinase; D003849:Deoxyguanosine