The effect of ischemia and reperfusion on mitochondrial contact sites in isolated rat hearts
-
Bakker, A. [1] ; Goossens, F. [2] ; De Bie, M. [1] ; Bernaert, I. [2] ; Van Belle, H. [2] ; Jacob, W. [1]
-
[1] University of Antwerp
University of Antwerp
Arrondissement Antwerpen, Bélgica
-
[2] Janssen pharrnaceutica, Beerse, Belgiurn
-
- Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 10, Nº. 2, 1995, págs. 405-416
- Idioma: inglés
- Enlaces
-
Resumen
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 (dPIdt,, ) and the heart rate were measured. The number o? contact sites was morphometrically evaluated. As the flow was stopped, LVP, dP/dt and HR declined rapidly and became undetectable a P2 min of ischemia. The number of contact sites fe11 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 rnin of ischemia caused an immediate functional recovery and a high presence of contact sites. After 15 rnin of reperfusion, al1 values returned to control values. Reperfusion after 10 rnin of ischemia resulted in a slow recovery of the number of contact sites and after 15 rnin 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.
