title: Resistance of endothelial cells to anoxia-reoxygenation in isolated guinea pig hearts.
abstract: The release of cytosolic enzymes from myocardial and endothelial cells in the anoxic-reoxygenated guinea pig heart was investigated. Isolated hearts were perfused with Tyrode solution in the Langendorff mode. Sixty-minute anoxic perfusion with or without glucose (5 mM) was followed by 15-min normoxic perfusion with glucose. The losses of purine-nucleoside phosphorylase (PNP) from endothelial cells and of lactate dehydrogenase (LDH) and creatine kinase (CK) from the mass of myocardial cells were determined. After 30-min anoxia, the release of LDH and CK but not of PNP increased. Reoxygenation after 60-min anoxia with glucose caused a partial recovery of tissue ATP but also an increase in leakage of LDH (11% of total in 15 min) and CK (10%) and a sudden rise in coronary resistance, indicating contracture development ("oxygen paradox"). PNP release remained low (0.5%). In hearts subjected to glucose-free anoxia, ATP levels did not rise during 15-min reoxygenation, contracture development was delayed, and the release of LDH and CK was diminished (3.1 and 2.7%, respectively). Leakage of PNP was again low (0.5%). The results indicate that cardiomyocytes are more severely injured by anoxia-reoxygenation than the coronary endothelium. The rapidly developing reoxygenation-induced injury of cardiomyocytes seems to be an energy-dependent phenomenon, since it was attenuated in hearts deprived of substrate in anoxia.
authors.affiliation: Physiologisches Institut I, Universität Düsseldorf, Federal Republic of Germany.
authors.forename: S
authors.initials: S
authors.lastname: Buderus
authors.forename: B
authors.initials: B
authors.lastname: Siegmund
authors.forename: R
authors.initials: R
authors.lastname: Spahr
authors.forename: A
authors.initials: A
authors.lastname: Krützfeldt
authors.forename: H M
authors.initials: HM
authors.lastname: Piper
mesh_terms: D000227:Adenine Nucleotides / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D002478:Cells, Cultured; D003326:Coronary Circulation; D003402:Creatine Kinase / Q000378:metabolism; D004730:Endothelium, Vascular / Q000502:physiology*; D000860:Hypoxia / Q000503:physiopathology; D007770:L-Lactate Dehydrogenase / Q000378:metabolism; D007773:Lactates / Q000378:metabolism; D008297:Male; D008833:Microcirculation / Q000502:physiology; D010477:Perfusion; D011683:Purine-Nucleoside Phosphorylase / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D014655:Vascular Resistance
chemical_list: D000227:Adenine Nucleotides; D007773:Lactates; D000255:Adenosine Triphosphate; D007770:L-Lactate Dehydrogenase; D011683:Purine-Nucleoside Phosphorylase; D003402:Creatine Kinase