No evidence for an increased lipid peroxidation during reoxygenation in Langendorff hearts and isolated atria of rats.
Rat left atria or Langendorff hearts were kept at 37 degrees C and stimulated at a rate of 3.33 Hz. They were subjected to hypoxia (deprivation of oxygen) or ischemia (deprivation of oxygen and glucose + acidosis + increased extracellular potassium concentration) for 15 min or 1 h and subsequent reoxygenation for 5 or 15 min. Tissue concentrations of proteins, reduced and oxidized glutathione and conjugated dienes were measured at the end of the experiment. Hypoxia and ischemia decreased the excitability and contractility of the preparations and caused contracture. These effects were partly reversible during reoxygenation. However, in Langendorff hearts reoxygenation caused an increased release of CPK, LDH and glutathione into the perfusion fluid. Ischemia and reoxygenation in atria lowered the tissue concentration of reduced glutathione and increased its oxidized form. Similar changes were seen in atria and Langendorff hearts when oxygen radical production was accelerated by hypoxanthine and xanthine oxidase. No treatment raised significantly the concentration of conjugated dienes. These results seem to exclude an important role of an increased lipid peroxidation for reperfusion injury of isolated heart preparations.
Brasch
H
H
Department of Pharmacology, Medical University of Lübeck, Federal Republic of Germany.
Schoenberg
M H
MH
Younes
M
M
D000818:Animals; D003327:Coronary Disease / Q000378:metabolism*; D003402:Creatine Kinase / Q000378:metabolism; D066298:In Vitro Techniques; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D015227:Lipid Peroxidation; D008297:Male; D015428:Myocardial Reperfusion Injury / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D007770:L-Lactate Dehydrogenase; D003402:Creatine Kinase