Objectives: Hyperglycaemia is implicated in microvascular inflammatory injury and subsequent cardiac injury/dysfunction. Leucocyte adhesion to the endothelium, migration into tissue and toxic metabolite release are early critical steps. Taurine is a semi-essential amino acid that is endothelial protective and restrains excess leucocyte activity by the formation of less toxic inflammatory mediators. The aim was to establish if taurine reduces acute hyperglycaemia-induced endothelial cell apoptosis and leucocyte interactions and associated cardiac abnormalities. Methods: Male Sprague-Dawley rats (190–250 g) were randomised to control, hyperglycaemia, and hyperglycaemia plus taurine pre-treated groups. Taurine was gavaged (200 mg/kg body weight) for 5 days. Intravenous hyperglycaemia was established which was 4 times that of baseline for the 3-hour experiment. Using intravital microscopy, mesenteric post-capillary venules were examined for leucocyte rolling, adhesion and migration every 30 min from baseline. Endothelial cell apoptosis and intracellular adhesion molecule (ICAM-1) expression were assessed. In a separate experiment, blood pressure, pulse rate, cardiac injury marker (troponin T), cardiac tissue injury and oedema were also assessed. Results: Hyperglycaemia significantly increased leucocyte adhesion and migration. Blood pressure and troponin T were also elevated significantly. Taurine prevented these cardiac changes, endothelial cell apoptosis and ICAM-1 expression. Conclusions: Taurine may have a therapeutic role in reducing diabetic microvascular inflammatory injury and concomitant cardiac dysfunction.