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(Circulation. 1998;98:378-379.)
© 1998 American Heart Association, Inc.

Correspondence

Phentolamine and Preconditioning During Coronary Angioplasty

Ali Dana, BSc, MRCP; Jun-ichi Imagawa, PhD; ; Derek M Yellon, PhD, DSc, FESC, FACC

The Hatter Institute of Cardiology, UCL Hospitals & Medical School, London, UK

To the Editor:

We read with great interest the article by Tomai et al¹ on the role of -adrenergic receptors in ischemic preconditioning during coronary angioplasty. They provide evidence that pretreatment with phentolamine, a nonselective -adrenoceptor blocking agent, abolishes the adaptation to myocardial ischemia during sequential coronary balloon inflations. The authors conclude a role for -adrenergic receptors in mediating ischemic preconditioning in this model. This work extends previous work by the same group implicating a role for adenosine A₁ receptors² and the ATP-sensitive potassium channels (K_ATP)³ in ischemic preconditioning using the same model.

What the authors fail to mention in their discussion is the fact that phentolamine, independent of its -blocking properties, has been shown to block K_ATP channels in insulin-producing cells,⁴ in vascular⁵ and nonvascular smooth muscle cells,⁶ and more recently, in cardiac ventricular myocytes.⁷ The involvement of K_ATP channels in the mechanism of ischemic preconditioning has been demonstrated in a number of animal models,⁸ as well as in isolated human atrial trabeculae.^{9 10} Furthermore, Tomai et al³ have previously shown that blockade of K_ATP channels abolishes the myocardial adaptation observed during sequential coronary balloon inflations. It is therefore not possible to draw any conclusions about the exact mode of action of phentolamine and consequently about the mechanisms of ischemic preconditioning during coronary angioplasty from the presented data.¹ Although, as the authors suggest, the -blocking properties of phentolamine may be responsible for the loss of adaptation to ischemia, their observations can also be explained by blockade of K_ATP channels . . . [Full Text of this Article]

Fabrizio Tomai, MD, FESC; Filippo Crea, MD, FACC, FESC; Achille Gaspardone, MD, FESC; ; Pier A. Gioffrè, MD, FESC

Divisione di Cardiochirurgia, Università di Roma Tor Vergata, European Hospital, Rome, Italy

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