ArticlePloS one2015
Measurement of technetium-99m sestamibi signals in rats administered a mitochondrial uncoupler and in a rat model of heart failure.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 30 citations in OpenAlex.
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- Sarcolemmal and mitochondrial membrane potentials measured ex vivo and in vivo in the heart by pharmacokinetic modelling of [The Journal of physiology · 2026Article
- Rapid mitochondrial repolarization upon reperfusion after cardiac ischemia.Nature cardiovascular research · 2025Article
- A Narrative Review of the Odyssey of Thyroid Cancer Diagnosis: Can 99mTc-SESTAMIBI Molecular Imaging Replace Fine Needle Aspiration Biopsy?Medicina (Kaunas, Lithuania) · 2025Review
- Vascularised and Non-Vascularised Adipofascial Flap Applications in Tissue Trauma with Tendon Injury, Flap Viability and Tendon Healing a Hystological and Scintigraphical Rat Model Study.Medicina (Kaunas, Lithuania) · 2024Article
- Analysis of Cardiac Metabolic Remodeling in Heart Failure Using Nuclear Medicine and Its Application: Japanese Society of Nuclear Cardiology Award.Annals of nuclear cardiology · 2020Review
- Detection of anthracycline-induced cardiotoxicity using perfusion-correctedScientific reports · 2019Article
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- A data sheet for the simultaneous assessment of dual radioactive tracer uptake in the heart.MethodsX · 2016Article
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundMany methods have been used to assess mitochondrial function. Technetium-99m sestamibi ((99m)Tc-MIBI), a lipophilic cation, is rapidly incorporated into myocardial cells by diffusion and mainly localizes to the mitochondria. The purpose of this study was to investigate whether measurement of (99m)Tc-MIBI signals in animal models could be used as a tool to quantify mitochondrial membrane potential at the organ level. METHODS AND
resultsWe analyzed (99m)Tc-MIBI signals in Sprague-Dawley (SD) rat hearts perfused with carbonyl cyanide m-chlorophenylhydrazone (CCCP), a mitochondrial uncoupler known to reduce the mitochondrial membrane potential. (99m)Tc-MIBI signals could be used to detect changes in the mitochondrial membrane potential with sensitivity comparable to that obtained by two-photon laser microscopy with the cationic probe tetramethylrhodamine ethyl ester (TMRE). We also measured (99m)Tc-MIBI signals in the hearts of SD rats administered CCCP (4 mg/kg intraperitoneally) or vehicle. (99m)Tc-MIBI signals decreased in rat hearts administered CCCP, and the ATP content, as measured by (31)P magnetic resonance spectroscopy, decreased simultaneously. Next, we administered (99m)Tc-MIBI to Dahl salt-sensitive rats fed a high-salt diet, which leads to hypertension and heart failure. The (99m)Tc-MIBI signal per heart tissue weight was inversely correlated with heart weight, cardiac function, and the expression of atrial natriuretic factor, a marker of heart failure, and positively correlated with the accumulation of labeled fatty acid analog. The (99m)Tc-MIBI signal per liver tissue weight was lower than that per heart tissue weight.
conclusionMeasurement of (99m)Tc-MIBI signals can be an effective tool for semiquantitative investigation of cardiac mitochondrial membrane potential in the SD rat model by using a chemical to decrease the mitochondrial membrane potential. The (99m)Tc-MIBI signal per heart tissue weight was inversely correlated with the severity of heart failure in the Dahl rat model.
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