Changes in energy transduction efficiency in mitochondria isolated from ischemic myocardium.

The effects of temporary coronary artery occlusion (TCAO) in vivo and ischemia in situ (autolysis) on mitochondrial functions and inner membrane permeability were investigated. It was found that one day after TCAO the permeability of inner membrane to H+ was increased 64% and the maximal activity of the glutamate plus malate oxidase system was reduced 35% with respect to control. The proton-electrochemical gradient and the rate of oxidative phosphorylation were decreased 35% and 55%, respectively. The most significant alterations during autolysis were observed in respiratory control ratio, state IV respiration and in H+ permeability of inner membrane. The H+ permeability of inner membrane increased progressively with time, and after 4 hr of autolysis it was 378% higher than the control. The data suggest that the alterations in energy transduction efficiency of mitochondria isolated from ischemic myocardium depend largely on the increase of inner membrane permeability to H+.