Elevated glucose at presentation with an acute coronary syndrome is associated with a poor outcome. However, clinical intervention trials have shown that normalization of glucose in the post-infarct period does not improve outcomes and may actually increase cardiovascular mortality particularly when associated with hypoglycaemia.. This studentship examines the hypothesis that hypoglycaemia in the post-infarct period induces cellular oxidative stress, and in vulnerable ischaemic tissue exacerbates myocardial damage. This hypothesis will be explored in an ex vivo model of myocardial infarction in control & diabetic rats: Langendorff perfusion followed by global ischemia and reperfusion. We will assess the effect of varying glucose concentration at reperfusion on reperfusion-induced arrhythmias, markers of oxidative stress & myocardial damage in the coronary effluent, oxidative modification of cardiac proteins, and infarct development . Thereafter quantitative proteomics & metabolomics will define diabetes-induced changes in myocyte subcellular compartments that might account for differences in ischemic tolerance.