title: Cardioprotective effects of ozone oxidative preconditioning in an in vivo model of ischemia/reperfusion injury in rats.
abstract: BACKGROUND
  Several studies have demonstrated the beneficial effects of ozone oxidative preconditioning in several pathologies characterized by cellular oxidative and inflammatory burden. The present study was designed to investigate the cardioprotective effects of oxidative preconditioning in ischemia/reperfusion (I/R) injury.
  
  
  METHODS
  Rats were randomly assigned into five groups. Groups 1 and 2 were normal and I/R groups, respectively. Two of the other groups received two different doses of ozone therapies by rectal insufflations. The last group received vehicle (oxygen). Rats were subjected to myocardial I/R (40 min/10 min). Heart rate and ventricular arrhythmias were recorded during I/R progress. At the end of reperfusion, plasma creatine kinase-MB (CK-MB) activity and total nitrate/nitrite (NO(x)) were determined. In addition, lactate, adenine nucleotides, thiobarbituric acid reactive substances (TBARS), reduced glutathione (GSH) and myeloperoxidase (MPO) activity were estimated in the heart left ventricle. Histological examination was also performed to visualize the protective cellular effects.
  
  
  RESULTS
  Both doses of ozone therapy were equally protective in reducing CK-MB release. However, the higher dose was more effective in reducing oxidative stress, lactate accumulation, elevated MPO activity and plasma NO(x) as well as preserving myocardial adenine nucleotides. Histological examination also revealed better improvement with a higher dose of ozone therapy compared to the I/R group.
  
  
  CONCLUSIONS
  Ozone therapy can afford significant cardioprotection against biochemical and histological changes associated with I/R injury.
authors.affiliation: Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt. lamiaahmed2004@yahoo.com
authors.forename: Lamiaa A
authors.initials: LA
authors.lastname: Ahmed
authors.forename: Hesham A
authors.initials: HA
authors.lastname: Salem
authors.forename: Mohamed N
authors.initials: MN
authors.lastname: Mawsouf
authors.forename: Amina S
authors.initials: AS
authors.lastname: Attia
authors.forename: Azza M
authors.initials: AM
authors.lastname: Agha
mesh_terms: D000227:Adenine Nucleotides / Q000378:metabolism; D000818:Animals; D002316:Cardiotonic Agents / Q000494:pharmacology* / Q000627:therapeutic use; D052279:Creatine Kinase, MB Form / Q000097:blood; D005978:Glutathione / Q000378:metabolism; D006321:Heart / Q000187:drug effects / Q000503:physiopathology; D006339:Heart Rate / Q000187:drug effects; D006352:Heart Ventricles / Q000378:metabolism / Q000473:pathology; D019344:Lactic Acid / Q000378:metabolism; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000097:blood / Q000378:metabolism / Q000517:prevention & control*; D018384:Oxidative Stress; D010126:Ozone / Q000494:pharmacology* / Q000627:therapeutic use; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism
chemical_list: D000227:Adenine Nucleotides; D002316:Cardiotonic Agents; D017382:Reactive Oxygen Species; D017392:Thiobarbituric Acid Reactive Substances; D019344:Lactic Acid; D010126:Ozone; D052279:Creatine Kinase, MB Form; D005978:Glutathione