title: Hemodynamic and mitochondrial parameters during hypoxia and reoxygenation in working rat hearts.
abstract: Hypoxia and reoxygenation in working rat hearts were investigated in this study. Cardiac hemodynamic parameters which decline immediately under hypoxic conditions, recover during reoxygenation. Biochemical and ultrastructural alterations exhibit a more complicated pattern. There is a primary phase in hypoxic perfusion up to 15 min with a steep increase of ADP contents and ATPase activities, and a severe fall of ATP/ADP ratios in mitochondria, as well as in tissue. High CAT (carboxyatractyloside) sensitivity of the ATPase is observed at 5 min of hypoxia. Furthermore, the number of ATPase particles visible at the inner mitochondrial membrane decreases. During the ensuing second phase of hypoxic perfusion (from 30 min on) the damage of mitochondrial ultrastructure becomes more evident. The amount of ATPase particles visible at the inner mitochondrial membrane further decreases. ATPase activities fluctuate, however, they remain connected with the membrane during hypoxia. ATP/ADP ratios attain values of almost 1. During reoxygenation (after 30 min of hypoxia) the levels of mitochondrial adenine nucleotides, oxidative phosphorylation rate and respiratory control index increase within 20 min and then slightly decline again. The ATP/ADP ratio is diminished in the course of reoxygenation. ATPase activity also decreases within 20 min of reoxygenation and the ADP/O ratio reaches control values. The ATPase activity gains its highest sensitivity towards CAT at 10 min of reoxygenation attaining a value similar to that of 5 min of hypoxic perfusion. It is suggested that hypoxia and reoxygenation under our conditions result in reversible derangement of ATPase and mitochondrial membrane structure.
authors.affiliation: Gustav-Embden-Zentrum der Biologischen Chemie, Universität Frankfurt, Main, Fed. Rep. of Germany.
authors.forename: H J
authors.initials: HJ
authors.lastname: Freisleben
authors.forename: H
authors.initials: H
authors.lastname: Kriege
authors.forename: C
authors.initials: C
authors.lastname: Clarke
authors.forename: F
authors.initials: F
authors.lastname: Beyersdorf
authors.forename: G
authors.initials: G
authors.lastname: Zimmer
mesh_terms: D000227:Adenine Nucleotides / Q000378:metabolism; D000244:Adenosine Diphosphate / Q000378:metabolism; D000251:Adenosine Triphosphatases / Q000378:metabolism; D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D006339:Heart Rate / Q000502:physiology; D006439:Hemodynamics / Q000502:physiology*; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D008929:Mitochondria, Heart / Q000378:metabolism*; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism / Q000648:ultrastructure; D010101:Oxygen Consumption; D010477:Perfusion; D011506:Proteins / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D013194:Staining and Labeling
chemical_list: D000227:Adenine Nucleotides; D011506:Proteins; D000244:Adenosine Diphosphate; D000255:Adenosine Triphosphate; D000251:Adenosine Triphosphatases