Occurrence of oxidative stress during myocardial reperfusion

Abstract

Reperfusion, without doubt, is the most effective way to treat the ischaemic myocardium. Late reperfusion may however cause further damage. Myocardial production of oxygen free radicals above the neutralizing capacity of the myocytes is an important cause of this reperfusion damage. There is evidence that prolonged ischaemia reduces the naturally occurring defence mechanisms of the heart against oxygen free radicals, particularly mitochondrial manganese superoxide dismutase, and intracellular pool of reduced glutathione. Consequently, reperfusion results in a severe oxidative damage, as evidenced by tissue accumulation and release of oxidized glutathione. An oxygen free radical-mediated impairment of mechanical function also occurs during reperfusion of human heart. In fact we observed during surgical reperfusion of coronary artery disease (CAD) patients, a prolonged and sustained release of oxidized glutathione; the degree of oxidative stress was inversely correlated with recovery of mechanical and haemodynamic function. These findings represent the rationale for therapeutic interventions which increase the cellular antioxidant capacities and improve the efficacy of myocardial reperfusion.

TRAP1 Provides Protection Against Myocardial Ischemia-Reperfusion Injury by Ameliorating Mitochondrial Dysfunction

“…The mitochondrion is considered to be the primary site of ROS generation in myocardium [27]. Mitochondrial ROS production is increased during I/R through several mechanisms such as nitric oxide inhibition of mitochondrial electron transport complexes [28] and apoptotic cytochrome c release [29].…”

Capillary electrophoresis in the evaluation of ischemic injury: Simultaneous determination of purine compounds and glutathione

“…Adenosine triphosphate degrades rapidly during cold storage, forming end products which permeate freely through the plasma membrane. Depletion of mitochondrial superoxide dismutase (SOD) and glutathione [14] makes the heart vulnerable to oxygen-free radicals. The necessity arises to consider specific metabolites that can be monitored and which reflect the state of myocardial preservation.…”

Diabetic cardiomyopathy-associated dysfunction in spatially distinct mitochondrial subpopulations

“…in the electron transport chain (ETC) are particularly prone to the formation of ROS and include oxidizable electron carriers in the inner mitochondrial membrane (12,32). This has implications for ETC proteins because a major constituent of these structures is their iron-sulphur centers (39), which can react with ROS such as superoxide (O 2…”