© 2001 by European Society of Cardiology
Copyright © 2000, European Society of Cardiology
Diazoxide induced cardioprotection: what comes first, KATP channels or reactive oxygen species?
Department of Pharmacology and Toxicology, Medical College of Wisconsin, 8701 Watertown Plank Road, Milwaukee, WI 53226, USA
* Corresponding author
Received 14 June 2001; accepted 15 June 2001
| The first 150 words of the full text of this article appear below. |
See article by Carroll et al. [32] (pages 691–700) in this issue.
Ischemic preconditioning (IPC) is a phenomenon in which a sublethal stress of short duration has proved to be protective against a subsequent lethal stress [1]. The protection is biphasic in that there is an immediate phase of protection that is transient and disappears a few hours after the conditioning stimulus [2], and a late phase that occurs 24 h after the conditioning stimulus and can last up to 72 h [3,4]. The conditioning stimuli can be variable and include ischemia, stimulation of adenosine receptors [5–7], opioid receptors [8–11], physical manipulation such as heat stress [12–15], or activation of the mitochondrial ATP-dependent K-channel (mitoKATP) [16,17]. Early events appear to be linked to protein modification and translocation through activation of signal transduction pathways that are already in place. Late events are most
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