MITOCHONDRIAL FUNCTIONS IN ISCHEMIC MYOCARDIUM I - PROTON ELECTROCHEMICAL GRADIENT, INNER MEMBRANE-PERMEABILITY, CALCIUM-TRANSPORT AND OXIDATIVE-PHOSPHORYLATION IN ISOLATED-MITOCHONDRIA

The effect of temporary coronary artery occlusion for 60 min, on ion transport and oxidative phosphorylation in rabbit heart mitochondria was investigated. Rabbit heart mitochondria, isolated from post-ischemic area, 1 day post-operatively were characterized by decreased ability for respiratory energy-dependent extrusion of H+ and uptake of K+ ions. Proton electrochemical gradient was lowered, as compared with control, by 39% (P < 0.001) with succinate and by 33% (P < 0.001) with glutamate plus malate as a substrate. Proton conductance of the inner mitochondrial membrane and the rate of potassium efflux under anaerobiosis from mitochondria of post-ischemic area were increased by 64% and 44% (P < 0.001) respectively. The rate of Ca2+-dependent H+ ion extrusion from mitochondria and the total Ca2+ uptake capacity were reduced by 46% (P < 0.001) and 40% (P < 0.01), respectively. The rate of oxidative phosphorylation in mitochondria from post-ischemic area 1 day post-operatively was reduced by 55% (P < 0.01). Changes similar in character but of lesser extent were also observed in mitochondria from non-ischemic areas. Most of parameters investigated of mitochondria from post-ischemic and non-ischemic areas recovered to control values in 6 days following a temporary coronary artery occlusion. More pronounced functional differences were observed between mitochondria isolated from infarcted and non-infarcted areas of the human heart. The role of proton electrochemical gradient and mitochondrial inner membrane permeability changes in ischemic cell injury is discussed. © 1979.