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Right arrow Cerebral protection

Ann Thorac Surg 2002;74:632
© 2002 The Society of Thoracic Surgeons

Correspondence

Diazoxide for cerebral protection during deep hypothermic circulatory arrest: is it really safe?

Loïc Lang-Lazdunski, MD, PhDa, Catherine Heurteaux, PhDb, Michel Lazdunski, PhD, DSb

a Department of Thoracic Surgery, Percy Military Hospital, 101 Ave Henri Barbusse B.P. 406, 92141 Clamart Cedex, France
b Institut de Pharmacologie Moléculaire et Cellulaire du CNRS, Valbonne, France

e-mail: loic.lang@wanadoo.fr

The first 20% of the full text of this article appears below.

To the Editor

We read with interest the study by Shake and collaborators on the protective effect of diazoxide during hypothermic circulatory arrest (HCA) [1]. Ischemic preconditioning is an endogenous protective mechanism in which brief periods of ischemia and reperfusion render the brain more resistant to a subsequent more sustained ischemic insult [2]. Our group has demonstrated that the mechanism of ischemic preconditioning in the brain involved the liberation of adenosine, stimulation of adenosine A1 receptors, and, via those receptors, opening of the sulfonylurea-sensitive K+ATP channels [2]. We showed that pretreatment with the K+ATP channels openers cromakalim, nicorandil, and pinacidil mimicked the effect of a brief . . . [Full Text of this Article]






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