Cardiac surgery is one of the highest-risk procedures, usually involving cardiopulmonary bypass and commonly inducing endothelial injury that contributes to the development of perioperative and postoperative organ dysfunction. Substantial scientific efforts are being made to unravel the complex interaction of biomolecules involved in endothelial dysfunction to find new therapeutic targets and biomarkers and to develop therapeutic strategies to protect and restore the endothelium. This review highlights the current state-of-the-art knowledge on the structure and function of the endothelial glycocalyx and mechanisms of endothelial glycocalyx shedding in cardiac surgery. Particular emphasis is placed on potential strategies to protect and restore the endothelial glycocalyx in cardiac surgery. In addition, we have summarized and elaborated the latest evidence on conventional and potential biomarkers of endothelial dysfunction to provide a comprehensive synthesis of crucial mechanisms of endothelial dysfunction in patients undergoing cardiac surgery, and to highlight their clinical implications.

We aimed to analyse granulysin (GNLY)‐mediated cytotoxicity in the peripheral blood of patients with non‐ST‐segment elevation myocardial infarction (NSTEMI) treated with anti‐ischaemic drug therapy. Thirty‐nine NSTEMI patients with a median age of 70 years and 28 age‐matched healthy subjects were enrolled in this study. On day 7 after MI, the number of GNLY⁺ lymphocytes in the peripheral blood increased approximately six‐fold of that in the healthy subjects, measured by flow cytometry. On day 14, the number of GNLY⁺ cells significantly decreased in T, NKT, and both CD56^+dim and CD56^+bright NK subsets. GNLY⁺CD3⁺ and GNLY⁺CD56⁺ cells infiltrated central zone of myocardial infarction (MI). In persons who died in the first week after MI, GNLY⁺ cells were found within accumulation of apoptotic leucocytes and reached the apoptotic cardiomyocytes in border MI zones probably due to the influence of interleukin‐15 in peri‐necrotic cardiomyocytes, as it is was shown by immunohistology. By day 28, the percentage of GNLY⁺ lymphocytes in peripheral blood returned to the levels similar to that of the healthy subjects. Anti‐GNLY mAb decreased apoptosis of K562 targets using peripheral blood NK cells from days 7 and 28 after MI, while in assays using cells from days 1 and 21, both anti‐GNLY and anti‐perforin mAbs were required to significantly decrease apoptosis. Using NK cells from day 14, K562 apoptosis was nearly absent. In conclusion, it seems that GNLY⁺ lymphocytes, probably attracted by IL‐15, not only participate partially in myocardial cell apoptosis, but also hasten resolution of cardiac leucocyte infiltration in patients with NSTEMI.