Effect of mitochondrial viability and metabolism on technetium-99m-sestamibi myocardial retention

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Abstract
This study investigated the mechanism of myocardial retention of technetium-99m-sestamibi.99mTc-sestamibi was injected intravenously into guinea pigs, and the myocardium was homogenized and fractionated by differential centrifugation. More than 90% of myocardial99mTc-sestamibi was localized within the mitochondrial fraction. Calcium was found to release99mTc-sestamibi from the mitochondrial fraction, with an IC50 of 2.54±0.98 mM. This effect was potentiated by NaCl, and inhibited by the mitochondrial calcium channel blocker ruthenium red. In vitro uptake of99mTc-sestamibi was found to increase from 10.5% ± 3.0% to 61.2% ± 0.2% with the addition of 10 mM succinate, indicating that respiration is involved. Since irreversible ischemia results in cellular and mitochondrial calcium “overload” and loss of mitochondrial metabolic function,99mTc-sestamibi should not be retained in necrotic or irreversibly ischemic myocardium, and could potentially act as a sensitive indicator of myocardial cell viability.