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(Circulation Research. 2006;99:111.)
© 2006 American Heart Association, Inc.

Editorials

How To Give a Cell a Heart Attack

Michael D. Stern

From the Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, NIH, Baltimore, Md.

Correspondence to Michael D. Stern, Laboratory of Cardiovascular Science, Gerontology Research Center, National Institute on Aging, NIH, 5600 Nathan Shock Blvd, Baltimore, MD 21224. E-mail Sternm@grc.nia.nih.gov

See related article, pages 165–171

Key Words: ischemia • myocyte • hypoxia • reperfusion • mitochondria

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

Cardiac ischemia is the leading killer in the developed world. It is a complex pathology, with myriad factors—electrical, chemical, metabolic, mechanical, and immunological—manifesting on scales ranging from the molecular to the whole organism. So it is not surprising that, despite decades of study, we cannot succinctly identify "the" injury that is central to this disorder. But, ultimately, the fate of millions of people comes down to what happens to a cardiac myocyte when it is deprived of its blood supply. It can die—by necrosis, apoptosis, or mechanical self-destruction. It isn’t always easy to decide when it is "dead." It can lose its contractile function, its relaxation function, and/or its electrical function. It can hibernate and, if provoked by earlier nonlethal episodes of ischemia, it can "learn" to protect itself on time scales from minutes to weeks.

It would make sense, then, to study cardiac ischemia at the single-cell level. This turns out to be surprisingly difficult to do. The isolated cardiac myocyte in the laboratory is normally bathed in an ocean of moving fluid. In contrast, even under the best of conditions, the myocyte in its native habitat is secluded from its sources of nutrition. The pO₂ at the myocyte surface is normally no more than 20 torr. The extracellular space, in which the cell must dispose of its metabolic waste, is tiny. In the heart, it is very easy to make a myocyte ischemic. In a petri dish, it is almost impossible. When studying cardiac myocytes on a patch-clamp . . . [Full Text of this Article]

Related Article:

Dynamic Responses of Single Cardiomyocytes to Graded Ischemia Studied by Oxygen Clamp in On-Chip Picochambers

Vladimir Ganitkevich, Sibylle Reil, Brigitta Schwethelm, Thomas Schroeter, and Klaus Benndorf
Circ. Res. 2006 99: 165-171. [Abstract] [Full Text] [PDF]