title: The effect of ischemia and reperfusion on mitochondrial contact sites in isolated rat hearts.
abstract: Contact sites may be described as energy channels between the mitochondria and the cytosol, created by fusion of the inner and the outer mitochondrial membranes, and their number depends highly on the energy state of the cell. The aim of the present study was to examine the early changes of ischemia and reperfusion on the number of mitochondrial contact sites. Therefore isolated rat hearts were subjected to short periods of ischemia followed by reperfusion. The left ventricular pressure (LVP), the contractility (dP/dtmax) and the heart rate were measured. The number of contact sites was morphometrically evaluated. As the flow was stopped, LVP, dP/dtmax and HR declined rapidly and became undetectable after 2 min of ischemia. The number of contact sites fell to a minimum after 10 min of ischemia after an initial increase (1 min of ischemia). A 15 min ischemic period resulted in a high number of contact sites which decreased again after 20 min of ischemia. Reperfusion after 2 min of ischemia caused an immediate functional recovery and a high presence of contact sites. After 15 min of reperfusion, all values returned to control values. Reperfusion after 10 min of ischemia resulted in a slow recovery of the number of contact sites and after 15 min of ischemia the number of contact sites remained low upon reperfusion. We may conclude that mitochondria lose the ability to form contact sites after more than 15 min of ischemia and this might be a first indication of irreversible injury.
authors.affiliation: Department of Medicine, University of Antwerp, Belgium.
authors.forename: A
authors.initials: A
authors.lastname: Bakker
authors.forename: F
authors.initials: F
authors.lastname: Goossens
authors.forename: M
authors.initials: M
authors.lastname: De Bie
authors.forename: I
authors.initials: I
authors.lastname: Bernaert
authors.forename: H
authors.initials: H
authors.lastname: Van Belle
authors.forename: W
authors.initials: W
authors.lastname: Jacob
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D005260:Female; D006339:Heart Rate / Q000502:physiology; D066298:In Vitro Techniques; D008566:Membranes / Q000502:physiology / Q000648:ultrastructure; D008929:Mitochondria, Heart / Q000648:ultrastructure*; D009200:Myocardial Contraction / Q000502:physiology; D017202:Myocardial Ischemia / Q000473:pathology*; D015428:Myocardial Reperfusion Injury / Q000473:pathology*; D009206:Myocardium / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar; D016277:Ventricular Function, Left / Q000502:physiology