title: Role of cellular energetics in ischemia-reperfusion and ischemic preconditioning of myocardium.
abstract: A short period of ischemia followed by reperfusion produces a state of affairs in which the cells' potential for surviving longer ischemia is enhanced. This is called ischemic preconditioning. The effects of preconditioning are also related to the reperfusion damage which ensues upon tissue oxygenation. The role of the cellular energy state in reperfusion damage remains an enigma, although ischemic preconditioning is known to trigger mechanisms which contribute to the prevention of unnecessary ATP waste. In some species up to 80% of ATP hydrolysis in ischemia can be attributed to mitochondrial F1-F0-ATPase (ATP synthase), and a role for its inhibitor protein (IF1) in ATP preservation has been proposed. Although originally regarded as limited to large animals with a slow heart beat, inhibition by IF1 is probably a universal phenomenon. Coincidentally with ATPase inhibition, the decline in cellular ATP slows down, but even so the difference in ATP concentration between preconditioned and non-conditioned hearts is still small at the final stages of a long ischemia, when the beneficial effect of preconditioning is observable, although the energy state during reperfusion remains low in hearts which do not recover.
authors.affiliation: Department of Medical Biochemistry, University of Oulu, Finland.
authors.forename: I E
authors.initials: IE
authors.lastname: Hassinen
authors.forename: K H
authors.initials: KH
authors.lastname: Vuorinen
authors.forename: K
authors.initials: K
authors.lastname: Ylitalo
authors.forename: A
authors.initials: A
authors.lastname: Ala-Rämi
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D002470:Cell Survival / Q000502:physiology; D004734:Energy Metabolism / Q000502:physiology*; D006863:Hydrogen-Ion Concentration; D007511:Ischemia / Q000503:physiopathology*; D019194:Ischemic Preconditioning; D007700:Kinetics; D008928:Mitochondria / Q000201:enzymology / Q000473:pathology; D009206:Myocardium / Q000473:pathology*; D006180:Proton-Translocating ATPases / Q000378:metabolism; D015427:Reperfusion Injury / Q000503:physiopathology*
chemical_list: D000255:Adenosine Triphosphate; D006180:Proton-Translocating ATPases