title: [Effects of superoxide dismutase on ischemic reperfusion injury in isolated working heart and cultured myocardial cells of rats].
abstract: An isolated working rat heart underwent 40 min of normothermic ceasing perfusion and 25 min of reperfusion. Superoxide dismutase (SOD) or/and mannitol were added to the perfusate 15 min before ceasing perfusion and 15 min after reperfusion. The results indicate that SOD (37,000 IU/L) improved significantly the contractile function of heart and increased the aortic output and coronary flow. Mannitol 0.02 mol/L provided additional benefit. The rat myocardial cells were cultured in the medium for 3 h with hypoxia followed by 2 h of reoxygenation. The content of lactic dehydrogenase (LDH) in the medium was increased and the degree of fluorescence polarization of myocardial cell membrane was raised. SOD was effective in preventing LDH release and decreasing the degree of fluorescence polarization. These results clearly demonstrate that ischemic reperfusion are capable of causing significant myocardial injury, which can be reduced or prevented by administration of oxygen free radical scavenger SOD.
authors.affiliation: Department of Pharmacology, Suzhou Medical College, China.
authors.forename: M F
authors.initials: MF
authors.lastname: Xu
authors.forename: D S
authors.initials: DS
authors.lastname: Wang
authors.forename: X Z
authors.initials: XZ
authors.lastname: Chen
mesh_terms: D000818:Animals; D002463:Cell Membrane Permeability / Q000187:drug effects; D002478:Cells, Cultured; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D008297:Male; D008560:Membrane Fluidity / Q000187:drug effects; D015428:Myocardial Reperfusion Injury / Q000517:prevention & control*; D009206:Myocardium / Q000166:cytology; D051381:Rats; D011919:Rats, Inbred Strains; D013482:Superoxide Dismutase / Q000494:pharmacology* / Q000627:therapeutic use
chemical_list: D007770:L-Lactate Dehydrogenase; D013482:Superoxide Dismutase