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(Circulation. 2006;114:1452-1454.)
© 2006 American Heart Association, Inc.

Editorial

Exploring Mitochondria in the Intact Ischemic Heart

Advancing Technologies to Image Intracellular Function

Michael N. Sack, MD, PhD

From the Cardiology Branch, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, Md.

Correspondence to Michael N. Sack, MD, PhD, Cardiology Branch, NHLBI/NIH, Building 10-CRC, Room 5-3150, 10 Center Dr, Bethesda, MD 20892-1454. E-mail sackm@nhlbi.nih.gov

Key Words: Editorials • imaging • ischemia • metabolism

An extract of the first 250 words of the full text is provided, because this article has no abstract.

In describing human nature, the Irish author and satirist Jonathan Swift noted that "vision is the art of seeing what is invisible to others." In the biological sciences, "vision" is transformed into a "science" as progress in imaging technology enables the uncovering of previously "invisible" intracellular programs. This capacity to "see inside cells" is improving in lock-step with advancing technologies that enable fluorophore-labeling of genes, proteins, cells, substrates, and metabolites. Thus, biomedical imaging is expanding our understanding of cellular function and disease pathophysiology. In this issue of Circulation, the practical application of 2-photon scanning laser microscopy is used to directly assess the mitochondrial inner membrane potential in the intact rat heart in response to cardiac ischemia and reperfusion.¹

Article p 1497

Before discussing this study, I will digress for a moment to review the relevance of mitochondrial function and the proposed role of the inner mitochondrial membrane potential on cardiac function and in its response to ischemia and reperfusion. The mitochondrion is central to cardiac function, as it modulates cardiac energetics, reactive radical biology, calcium homeostasis, and apoptosis.² The inner mitochondrial membrane potential in turn reflects a composite of mitochondrial functioning, which means the maintenance of this electrochemical potential requires: (1) the functional integrity of electron transfer redox centers of oxidative phosphorylation; (2) the catalytic integrity of enzymes of ß-oxidation and the Kreb’s cycle; and (3) the appropriate functioning of transport mechanisms linking the cytosol and the mitochondrial matrix.

The mitochondrial inner membrane potential is not static; rather, the . . . [Full Text of this Article]

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