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Evidence for the role of oxidative stress in acute ischemic heart disease: a brief review.

BACKGROUND
Although contractile performance of the acutely damaged ischemic heart is invariably depressed on reperfusion (myocardial stunning), the mechanisms of cardiac dysfunction in stunned myocardium are poorly understood.


OBJECTIVES
To review briefly the current state of knowledge and to provide further experimental evidence of whether oxidative stress plays a crucial role in cardiac dysfunction and membrane abnormalities due to ischemia-reperfusion.


MATERIALS AND METHODS
Isolated rat hearts perfused in the absence or presence of superoxide dismutase (SOD) plus catalase, a well known oxyradical scavenger system, were subjected to 30 mins of global ischemia and 60 mins of reperfusion. Cardiac performance, hydrogen peroxide and calcium contents, lipid peroxidation and membrane activities associated with calcium transport were measured in the control, ischemic and ischemic- reperfused hearts.


RESULTS
Cardiac dysfunction, as reflected by depressed left ventricular developed pressure, +dP/dt and -dP/dt as well as elevated left ventricular end-diastolic pressure, in the ischemic-reperfused heart was associated with increased hydrogen peroxide, calcium and malondialdehyde contents as well as increased formation of conjugated dienes. These changes due to ischemia-reperfusion were attenuated in hearts treated with SOD plus catalase. Both ischemia and ischemic-reperfused hearts showed depressions in sarcolemmal Na+/K+-ATPase and sodium-calcium exchange, as well as sarcoplasmic reticular calcium uptake and calcium release activities; these membrane abnormalities were also partially prevented by the presence of SOD plus catalase.


CONCLUSIONS
Oxidative stress due to the formation of hydrogen peroxide leading to lipid peroxidation and sulfhydryl group oxidation during ischemia-reperfusion seems to be one of the mechanisms that may produce membrane defects and result in intracellular calcium overload and cardiac contractile dysfunction in the stunned myocardium.