Depending on their concentrations, both nitric oxide (NO) and reactive oxygen species (ROS) take part either in myocardial ischemia reperfusion injury or in protection by ischemic and pharmacological preconditioning (Ipre) and postconditioning (Ipost). At the beginning of reperfusion, a transient release of NO is promptly scavenged by ROS to form the highly toxic peroxynitrite, which is responsible for a further increase of ROS through endothelial nitric oxide synthase uncoupling. The protective role of NO has suggested the use of NO donors to mimic Ipre and Ipost. However, NO donors have not always given the expected protection, possibly because they are responsible for the production of different amounts of ROS that depend on the amount of released NO. This review is focused on the role of the balance of NO and ROS in myocardial injury and its prevention by Ipre and Ipost and after the use of NO donors given with or without antioxidant compounds to mimic Ipre and Ipost.
*Department of Clinical and Biological Sciences, University of Turin, S. Luigi Gonzaga Hospital, Orbassano, Italy; and
†Department of Neuroscience, Physiology Division, University of Turin, Turin, Italy.
Reprints: Anna Folino, PhD, Dipartimento di Scienze Cliniche e Biologiche, Università degli Studi di Torino, Regione Gonzole 10, 10043 Orbassano (TO), Italy (e-mail: email@example.com).
Supported by the local Government of Regione Piemonte, the Italian Ministry of Education, University and Research (MIUR), the University of Turin, and the Istituto Nazionale per la Ricerca Cardiovascolare (INRC), Bologna.
The authors have no conflicts of interest to disclose.
Received May 13, 2013
Accepted July 14, 2013