THE EFFECT OF ISCHEMIA AND REPERFUSION ON MITOCHONDRIAL CONTACT SITESIN ISOLATED RAT HEARTS

Contact sites may be described as energy channels between the mitochon dria and the cytosol, created by fusion of the inner and the outer mit ochondrial membranes, and their number depends highly on the energy st ate of the cell. The aim of the present study was to examine the early changes of ischemia and reperfusion on the number of mitochondrial co ntact sites. Therefore isolated rat hearts were subjected to short per iods of ischemia followed by reperfusion. The left ventricular pressur e (LVP), the contractility (dP/dt(max)) and the heart rate were measur ed. The number of contact sites was morphometrically evaluated. As the flow was stopped, LVP, dP/dt(max) 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 mi n of ischemia). A 15 min ischemic period resulted in a high number of contact sites which decreased again after 20 min of ischemia. Reperfus ion after 2 min of ischemia caused an immediate functional recovery an d a high presence of contact sites. After 15 min of reperfusion, all v alues 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 reper fusion. We may conclude that mitochondria lose the ability to form con tact sites after more than 15 min of ischemia and this might be a firs t indication of irreversible injury.