Improvement of Mitochondrial Energy Production in Ischemic Myocardium by in Vivo Infusion of Ruthenium Reb

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Abstract
Reperfusion of acutely ischemic myocardium results in deficient energy production and abnormal Ca2+ deposition. This study evaluates mitochondrial energy production in ishemic reperfused myocardium following an in vivo infusion of a Ca2+ antagonist, ruthenium red. Results are summarized as follows: (1) In vivo infusion of ruthenium red increases adenosine diphosphate-induced respiration threefold and adenosine triphosphate (ATP) production fivefold compared with those mitochondria derived from myocardium which had been occluded 2 hr and reperfused 2 hr without ruthenium red. (2) Infusion of ruthenium red improves state 3 respiration and ATP production to nearly normal levels by mitochondria isolated from myocardium which had been occluded 30 min and reperfused 2 hr. However, mitochondrial respiration and ATP production from nonischemic myocardium are not altered by in vivo ruthenium red infusion. (3) Ruthenium red infusion decreases both tissue and mitochondrial Ca2+ content in ischemic-reperfused myocardium. (4) The partial improvement in energy production in ischemic-reperfused myocardium by ruthenium red is probably related to a decrease in intracellular Ca2+ concentration.

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