title: Effects of reduction of contractile work on mechanical function in post-hypoxic guinea pig papillary muscles and on myocardial energy metabolism in post-ischemic rat hearts.
abstract: This study was designed to investigate effects of quiescence by cessation of electrical stimulation during the first stage of reoxygenation on recovery of mechanical function from hypoxia-induced contractile dysfunction in papillary muscles and effects of the absence of cardiac output on myocardial energetic metabolism of post-ischemic hearts. (1) Regular contractions and postextrasystolic contraction were evoked. After 120 min hypoxia, muscles were reoxygenated. In muscles of quiescence during the first 30 min reoxygenation, the recovery of regular contractions was better than that in muscles in which programmed stimulation was continued. However, the quiescence had no effect on the recovery of post-extrasystolic contractions from hypoxia-induced contractile dysfunction. (2) Isolated hearts were perfused either according to Langendorff technique or as working heart preparations. After 40 min ischemia, hearts were reperfused for 25 min. Although there was no difference in energy charge of myocardium between 2 modes of reperfusion, % incidence of sustained ventricular fibrillation in muscles in which non-working mode was maintained for the first step of reperfusion was lower than that in which working mode was continued. We presume that the reduction of contractile work during the initial step of reperfusion is of value for cardio-protection.
authors.affiliation: Second Department of Medicine, Kyoto Prefectural University of Medicine, Japan.
authors.forename: J
authors.initials: J
authors.lastname: Asayama
authors.forename: Y
authors.initials: Y
authors.lastname: Yamahara
authors.forename: T
authors.initials: T
authors.lastname: Tatsumi
authors.forename: T
authors.initials: T
authors.lastname: Matsumoto
authors.forename: H
authors.initials: H
authors.lastname: Miyazaki
authors.forename: R
authors.initials: R
authors.lastname: Sakai
authors.forename: M
authors.initials: M
authors.lastname: Inoue
authors.forename: I
authors.initials: I
authors.lastname: Omori
authors.forename: D
authors.initials: D
authors.lastname: Inoue
authors.forename: M
authors.initials: M
authors.lastname: Nakagawa
mesh_terms: D000818:Animals; D002302:Cardiac Output; D003327:Coronary Disease / Q000503:physiopathology*; D004562:Electrocardiography; D004734:Energy Metabolism; D006168:Guinea Pigs; D000860:Hypoxia / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D009200:Myocardial Contraction; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D009206:Myocardium / Q000378:metabolism*; D010100:Oxygen / Q000502:physiology; D010210:Papillary Muscles / Q000503:physiopathology; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D010100:Oxygen