In acute myocardial infarction early restoration of coronary blood flow is the most effective
strategy to limit infarct-size. Paradoxically, reperfusion itself also aggravates myocardial
injury and contributes to final infarct size, a process termed 'reperfusion injury'. Ischemia
and reperfusion (IR)-induced endothelial dysfunction seems to play a pivotal role in this
process, resulting in vasoconstriction and reduced blood flow to the already ischemic tissue.
Recently, it has been shown that the glucose-lowering drug metformin is able to limit
IR-injury in murine models of myocardial infarction, probably by increased formation of the
endogenous nucleoside adenosine. In the current research proposal, the investigators aim to
translate this finding to the human in vivo situation, using flow-mediated dilation (FMD) of
the brachial artery as a well-validated model of (endothelial) IR-injury.