title: Effects of reperfusion and superoxide dismutase on myocardial infarct size in a closed chest pig model.
abstract: OBJECTIVE
  The aim was to study the effects on myocardial infarct size of reperfusion alone or of CuZn superoxide dismutase (SOD) as an adjunct to reperfusion.
  
  
  METHODS
  Occlusion was induced in closed chest, pentobarbitone anaesthetised, mechanically ventilated pigs by injection of a 2 mm ball into a preselected coronary artery. Reperfusion was achieved by retraction of the ball via an attached filament. Twenty nine placebo treated and 25 SOD treated animals were subjected to 30 (n = 21), 60 (n = 21), and 90 (n = 12) min of coronary occlusion followed by reperfusion to 24 h; a control group of 24 pigs was subjected to a sustained occlusion for 24 h. Infarct size was assessed by tetrazolium staining and plasma creatine kinase (CK), aspartate aminotransferase (ASAT), and lactate dehydrogenase (LD). In the CuZn SOD group, 200 mg bovine CuZn SOD was given as a bolus intravenously immediately before reperfusion followed by a continuous infusion (100 mg) for 60 min. The size of the ischaemic myocardium at risk was measured from post mortem autoradiograms.
  
  
  RESULTS
  Infarct size as percent of myocardium at risk was 46.0(SD 15.5)%, 80.1(9.9)%, and 88.9(5.0)% respectively in placebo animals with 30, 60, and 90 min occlusion, and 94.2(5.1)% in pigs with 24 h sustained occlusion. Compared to 24 h sustained occlusion, limitation of infarct size by reperfusion was only demonstrated in the 30 (p less than 0.001) and 60 min groups (p less than 0.001). Plasma values of CK, ASAT, and LD at 90 min post-reperfusion correlated closely with infarct size as assessed by tetrazolium staining and were related to occlusion duration. No myocardial salvage, as assessed by plasma ASAT, CK, or LD, was shown in the SOD treated groups.
  
  
  CONCLUSIONS
  Early reperfusion resulted in myocardial salvage as assessed by tetrazolium staining and peak ASAT, CK, and LD at 90 min after the reperfusion. No limitation of infarct size by SOD could be demonstrated from analyses of plasma CK, ASAT, or LD.
authors.affiliation: University Hospital, Umeå, Sweden.
authors.forename: U
authors.initials: U
authors.lastname: Näslund
authors.forename: S
authors.initials: S
authors.lastname: Häggmark
authors.forename: G
authors.initials: G
authors.lastname: Johansson
authors.forename: K
authors.initials: K
authors.lastname: Pennert
authors.forename: S
authors.initials: S
authors.lastname: Reiz
authors.forename: S L
authors.initials: SL
authors.lastname: Marklund
mesh_terms: D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood; D003402:Creatine Kinase / Q000097:blood; D004195:Disease Models, Animal; D007770:L-Lactate Dehydrogenase / Q000097:blood; D009203:Myocardial Infarction / Q000201:enzymology / Q000473:pathology / Q000628:therapy*; D015425:Myocardial Reperfusion / Q000379:methods*; D009206:Myocardium / Q000473:pathology; D013482:Superoxide Dismutase / Q000494:pharmacology*; D013552:Swine; D013997:Time Factors
chemical_list: D007770:L-Lactate Dehydrogenase; D013482:Superoxide Dismutase; D001219:Aspartate Aminotransferases; D003402:Creatine Kinase