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(Circulation. 2008;118:1915-1919.)
© 2008 American Heart Association, Inc.

Editorial

Cardioprotection

Nitric Oxide, Protein Kinases, and Mitochondria

Gerd Heusch, MD; Kerstin Boengler, PhD; Rainer Schulz, MD

From the Institut für Pathophysiologie, Universitätsklinikum Essen, Essen, Germany.

Correspondence to Prof Dr med Dr hc Gerd Heusch, FRCP, Direktor des Instituts für Pathophysiologie, Universitätsklinikum Essen, Hufelandstr 55, 45122 Essen, Germany. E-mail gerd.heusch@uk-essen.de

Key Words: Editorials • ischemia • nitric oxide • nitric oxide synthase • reperfusion • signal transduction

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

	Introduction

 
Over the past 2 to 3 decades, several phenomena have been identified that provide powerful protection against myocardial infarction and other sequelae of ischemia/reperfusion¹: myocardial hibernation that is related to stunning,² ischemic preconditioning,³ delayed or second-window ischemic preconditioning,⁴ ischemic postconditioning,⁵ and their pharmacological recruitment. Stunning and hibernation share contractile function as an end point. In stunning, reduced postischemic contractile function is viewed as reversible injury, whereas in hibernation dysfunction is viewed as an adaptive response. Ischemic preconditioning is characterized by infarct size reduction as its most robust end point but shares with hibernation the underlying idea of a regulated protective response. These phenomena have been confirmed in patients with coronary artery disease.^2,6–8 Nitric oxide (NO) and mitochondria also are important in patients with coronary artery disease. Nitroglycerin induces delayed protection against periinterventional ischemic ECG alterations, contractile dysfunction, and pain sensation,⁷ and cyclosporin A, which inhibits opening of the mitochondrial permeability transition pore (MPTP), attenuates reperfusion injury in patients with acute myocardial infarction.⁹

Articles pp 1961 and 1970

	Stunning Versus Hibernation Versus Preconditioning: What Is the Difference?

 
The "new ischemic syndromes" have intrigued scientists and clinicians trying to understand their underlying pathophysiology and to recruit their cardioprotective potential. This initial enthusiasm has not materialized into translational medicine.¹⁰ Why is that? There has been a long but ultimately fruitless debate as to whether the phenotype of hibernating myocardium is the result of ongoing ischemia with reduced baseline coronary blood flow or repetitive cycles of ischemia/reperfusion and consequent stunning without reduced baseline flow. Clearly, perfusion-contraction matching cannot be maintained for >12 . . . [Full Text of this Article]

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