title: Coenzyme Q10 protects against acute consequences of experimental myocardial infarction in rats.
abstract: OBJECTIVE
  Myocardial infarction (MI) due to sudden occlusion of a major coronary artery leads to a complex series of events that result in left ventricle (LV) impairment eventual heart failure. Therapeutic options are limited to reverse such trends post MI. The aim of this study was to compare the acute cardioprotective effects of the antioxidants, resveratrol (RES) and coenzyme Q10 (CoQ10), either individually or in combination, on infracts size, LV hemodynamics, inflammation and oxidative stress markers in rats with experimentally induced MI.
  
  
  METHODS
  Male Wistar rats were randomly divided into six groups: control without surgery, sham without occlusion, MI without antioxidants, RES pre-treated then MI (20 mg/kg, orally), CoQ10 then MI (20 mg/kg, intramuscular.), and combined RES and CoQ10 then MI with (each group n = 10). Pretreatment commenced 7 days prior to the permanent occlusion of the left anterior descending (LAD) coronary artery. Infarct area, hemodynamics, inflammation and oxidative stress markers were assessed 24 hours post-MI.
  
  
  RESULTS
  Compared to RES alone, CoQ10 pre-administration either by itself or in combination with RES, significantly reduced LV infarct area (57%), and normalized LV hemodynamic parameters like LVEDP (100%), LVSP (95.4%), LV +dp/dt and -dp/dt (102 and 73.1%, respectively). CoQ10 also decreased serum levels of brain natriuretic peptide (70%), and various circulating inflammatory markers like TNF-α (83.2%) and IL-6 (83.2%). Regarding oxidative stress, TBARS scores were lowered with a concurrent increase in both superoxide dismutase and glutathione peroxidase activities with CoQ10 alone or in combination with RES.
  
  
  CONCLUSIONS
  Coenzyme Q10 protects against the acute sequelae of myocardial infarction. It profoundly reduced infarct area, inflammation and oxidative stress while normalizing LV hemodynamics post MI.
authors.affiliation: Department of Applied Medical Sciences, College of Health Sciences PAAET, Kuwait.
authors.forename: Samy M
authors.initials: SM
authors.lastname: Eleawa
authors.affiliation: Department of Physiology, College of Medicine, King Khalid University Kingdom of Saudi Arabia ; Department of Biology, IK Barber School of Arts and Sciences UBC-Okanagan, Kelowna, BC, Canada.
authors.forename: Mahmoud
authors.initials: M
authors.lastname: Alkhateeb
authors.affiliation: Department of Biology, IK Barber School of Arts and Sciences UBC-Okanagan, Kelowna, BC, Canada.
authors.forename: Sanjoy
authors.initials: S
authors.lastname: Ghosh
authors.affiliation: Department of Physiology, College of Medicine, King Khalid University Kingdom of Saudi Arabia.
authors.forename: Fahaid
authors.initials: F
authors.lastname: Al-Hashem
authors.affiliation: Department of internal medicine, Cardiology section, College of Medicine, King Khalid University Kingdom of Saudi Arabia.
authors.forename: Abdullah S
authors.initials: AS
authors.lastname: Shatoor
authors.affiliation: Division of Physiology, Department of Basic Medical Sciences, Faculty of Medicine, King Saud bin Abdul Aziz University for Health Sciences King Fahad Medical City, Riyadh, Kingdom of Saudi Arabia.
authors.forename: Abdulmohsen
authors.initials: A
authors.lastname: Alhejaily
authors.affiliation: Division of Physiology, Department of Basic Medical Sciences, Faculty of Medicine, King Saud bin Abdul Aziz University for Health Sciences King Fahad Medical City, Riyadh, Kingdom of Saudi Arabia.
authors.forename: Mohammad A
authors.initials: MA
authors.lastname: Khalil
keywords: Myocardial infarction; apoptosis; coenzyme Q10; hemodynamics; oxidative stress; resveratrol