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(Circulation Research. 2000;87:85.)
© 2000 American Heart Association, Inc.

Editorial

Nitric Oxide and Short-Term Hibernation

Friend or Foe?

John M. Canty, Jr.

From the Veterans Affairs Western New York Health Care System and the Departments of Medicine, Physiology and Biophysics at the University at Buffalo School of Medicine and Biomedical Sciences, Buffalo, NY.

Correspondence to John M. Canty, Jr, MD, University at Buffalo, Division of Cardiology, Biomedical Research Building, Room 345, 3435 Main St, Buffalo, NY 14214. E-mail canty@buffalo.edu

Key Words: nitric oxide • myocardium • ischemia • myocardial stunning

	Introduction

 
Subendocardial blood flow (as a surrogate of regional oxygen consumption) and myocardial function are closely coupled during acute myocardial ischemia.^{1 2} Whereas severe ischemia results in the rapid onset of irreversible injury, viability in the face of moderate levels of acute ischemia can be maintained for several hours.³ A uniform finding during moderate steady-state ischemia is the fact that the myocardium is able to restore a balance between a limited blood supply and demand by exquisite coupling between local flow and metabolism. Thus, the transient increases in myocardial lactate and reductions in creatine phosphate and ATP at the onset of ischemia gradually return toward normal over a period of hours.^{4 5} The intrinsic mechanism by which myocytes are able to metabolically adapt and match function to a reduced level of flow and oxygen delivery has remained elusive, and the phenomenon has become known as "short-term hibernation."³

Nitric oxide (NO) is a potential candidate for such regulation because it is capable of modulating contractile function under a variety of circumstances. It has become increasingly apparent that the biological actions of NO in the heart are quite complex. The effects on contractility vary among experimental preparations, and they are highly concentration-dependent. Part of this variability undoubtedly reflects the complex cellular distribution of nitric oxide synthase (NOS) and the partitioning of isoforms within particular subcellular compartments of the cardiac myocyte. As a result, local cardiac function can be modulated via NO originating from several sources. Coronary flow and shear stress stimulates NOS3 (or endothelial nitric . . . [Full Text of this Article]

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