Cellular mechanisms against ischemia reperfusion injury induced by the use of anesthetic pharmacological agents.
Ischemia-reperfusion (IR) cycle in the myocardium is associated with activation of an injurious cascade, thus leading to new myocardial challenges, which account for up to 50% of infarct size. Some evidence implicates reactive oxygen species (ROS) as a probable cause of myocardial injury in prooxidant clinical settings. Damage occurs during both ischemia and post-ischemic reperfusion in animal and human models. The mechanisms that contribute to this damage include the increase in cellular calcium (Ca(2+)) concentration and induction of ROS sources during reperfusion. Pharmacological preconditioning, which includes pharmacological strategies that counteract the ROS burst and Ca(2+) overload followed to IR cycle in the myocardium, could be effective in limiting injury. Currently widespread evidence supports the use of anesthetics agents as an important cardioprotective strategy that act at various levels such as metabotropic receptors, ion channels or mitochondrial level. Their administration before a prolonged ischemic episode is known as anesthetic preconditioning, whereas when given at the very onset of reperfusion, is termed anesthetic postconditioning. Both types of anesthetic conditioning reduce, albeit not to the same degree, the extent of myocardial injury. This review focuses on cellular and pathophysiological concepts on the myocardial damage induced by IR and how anesthetic pharmacological agents commonly used could attenuate the functional and structural effects induced by oxidative stress in cardiac tissue.
Critical Care Unit, Hospital Clínico Metropolitano La Florida, Santiago, Chile; Faculty of Medicine, University Finis Terrae, Chile; Pathophysiology Program, Faculty of Medicine, University of Chile, Chile.
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P
Álvarez
Pathophysiology Program, Faculty of Medicine, University of Chile, Chile; Emergency Unit, Clínica Dávila, Santiago, Chile.
L
L
Tapia
Pathophysiology Program, Faculty of Medicine, University of Chile, Chile.
L A
LA
Mardones
Anesthesia Unit, Pontificia Universidad Católica de Chile, Santiago, Chile.
J C
JC
Pedemonte
Departamento de Ingeniería Química, Facultad de Ingeniería y Ciencias, Universidad de la Frontera, Casilla 54-D, Temuco, Chile.
J G
JG
Farías
Pathophysiology Program, Faculty of Medicine, University of Chile, Chile. Electronic address: rcastillo@med.uchile.cl.
R L
RL
Castillo
D000777:Anesthetics; D000818:Animals; D002468:Cell Physiological Phenomena; D006801:Humans; D019157:Ischemic Preconditioning, Myocardial; D018384:Oxidative Stress; D015427:Reperfusion Injury / Q000139:chemically induced* / Q000503:physiopathology*
D000777:Anesthetics
Anesthetics drugs; Ischemia–reperfusion; Oxidative stress