Balance of nitric oxide and reactive oxygen species in myocardial reperfusion injury and protection.
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.
Anna
A
Folino
Gianni
G
Losano
Raffaella
R
Rastaldo
D000818:Animals; D000975:Antioxidants / Q000009:adverse effects / Q000627:therapeutic use; D003331:Coronary Vessels / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D004347:Drug Interactions; D004730:Endothelium, Vascular / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology; D006321:Heart / Q000187:drug effects / Q000503:physiopathology; D006801:Humans; D057775:Ischemic Postconditioning; D019157:Ischemic Preconditioning, Myocardial; D008929:Mitochondria, Heart / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000503:physiopathology / Q000517:prevention & control / Q000628:therapy; D009206:Myocardium / Q000201:enzymology / Q000378:metabolism; D009569:Nitric Oxide / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*; D020030:Nitric Oxide Donors / Q000009:adverse effects / Q000627:therapeutic use; D017382:Reactive Oxygen Species / Q000819:agonists / Q000037:antagonists & inhibitors / Q000378:metabolism*
D000975:Antioxidants; D020030:Nitric Oxide Donors; D017382:Reactive Oxygen Species; D009569:Nitric Oxide