title: L-ascorbic acid and alpha-tocopherol attenuates liver ischemia-reperfusion induced of cardiac function impairment.
abstract: OBJECTIVE
  The Pringle maneuver is a surgical procedure to minimize hemorrhage during hepatectomy, which however, can induce production of reactive oxygen species causing remote organ injury. We sought to study the impact of the Pringle maneuver on cardiac function as well as the protective effects of L-ascorbic acid and α-tocopherol pretreatments.
  
  
  METHODS
  Rats were divided into four study groups: L-ascorbic acid (60 mg/kg/d) or α-tocopherol (200 mg/kg/d), and surgical interventions (Sham-operated or liver ischemia-reperfusion [I/R]). Liver ischemia was performed by clamping the hepatic artery and portal vein for 30 minutes, followed by reperfusion by releasing the clamps for 2 hours. Cardiac function was evaluated by a high-fidelity pressure-volume catheter positioned in the left ventricle. Myocardial injury was assessed through plasma creatine kinase-MB (CKMB) and troponin I (cTnI). Cardiac lipid peroxidation and systemic hydroxyl radical levels were assessed by cardiac tissue malondialdehyde and plasma methylguanidine, respectively.
  
  
  RESULTS
  Cardiac function was significantly depressed in the I/R group, where plasma CKMB and cTnI were markedly increased (P < .05). L-ascorbic acid and α-tocopherol pretreatments improved cardiac function and significantly reduced cardiac injury (P < .05). L-ascorbic acid pretreatment demonstrated better heart protection than α-tocopherol, in terms of cTnI and CKMB (P < .05), but no significant difference in terms of cardiac functional improvement.
  
  
  CONCLUSIONS
  L-ascorbic acid and α-tocopherol pretreatment 3 days prior to the Pringle maneuver attenuated myocardial injury and protected cardiac function by scavenging hydroxyl radical and reducing lipid peroxidation. L-ascorbic acid demonstrated better protection than α-tocopherol.
authors.affiliation: Division of Cardiovascular Surgery, Department of Surgery, Chi-Mei Foundation Hospital, Tainan, Taiwan.
authors.forename: C-C
authors.initials: CC
authors.lastname: Hsu
authors.forename: J-J
authors.initials: JJ
authors.lastname: Wang
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology*; D015415:Biomarkers / Q000097:blood; D006328:Cardiac Catheterization; D052279:Creatine Kinase, MB Form / Q000097:blood; D004195:Disease Models, Animal; D006331:Heart Diseases / Q000209:etiology / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D006498:Hepatectomy / Q000009:adverse effects*; D017665:Hydroxyl Radical / Q000097:blood; D015227:Lipid Peroxidation / Q000187:drug effects; D008107:Liver Diseases / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D008315:Malondialdehyde / Q000378:metabolism; D008760:Methylguanidine / Q000097:blood; D009200:Myocardial Contraction / Q000187:drug effects; D009206:Myocardium / Q000378:metabolism; D018384:Oxidative Stress / Q000187:drug effects*; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000188:drug therapy* / Q000209:etiology / Q000378:metabolism; D013997:Time Factors; D019210:Troponin I / Q000097:blood; D016277:Ventricular Function, Left / Q000187:drug effects; D017725:Ventricular Pressure / Q000187:drug effects; D024502:alpha-Tocopherol / Q000494:pharmacology*
chemical_list: D000975:Antioxidants; D015415:Biomarkers; D019210:Troponin I; D017665:Hydroxyl Radical; D008315:Malondialdehyde; D008760:Methylguanidine; D052279:Creatine Kinase, MB Form; D024502:alpha-Tocopherol; D001205:Ascorbic Acid