Njury modelJOURNAL OF EXTRACELLULAR VESICLESallows EV profiles from uninjured, injured and repairing/regenerating cardiac tissue to be determined and compared. Results: Live imaging of transgenic zebrafish with endothelial cell-derived EVs labelled with mCherry reveals huge numbers of EVs in the peripheral circulation, interactions with downstream endothelial cells and release in to the blood flow from filopodia-like protrusions. Cardiomyocyte-derived EVs are observed within the pericardial fluid surrounding the heart and are frequently observed interacting with cells from the pericardial wall. Also, a modified FACS protocol reveals how cardiomyocyte-derived EV numbers fluctuate in response to cardiac injury. Summary/Conclusion: This information present exciting opportunities to additional dissect the cargo being carried by these EVs inside a vertebrate model of human disease. Funding: British Heart Foundation.OT01.Enhanced fibrinolysis and altered extracellular vesicles soon after remote ischaemic preconditioning in non-diabetic coronary artery illness individuals Caroline J. Reddela, Jerrett Laub, Gabrielle Penningc, Vivien Chend and Leonard Kritharidesea ANZAC Investigation Institute, University of Sydney, Concord Repatriation General Hospital, Concord, Australia; bDepartment of Cardiology, Concord Repatriation General Hospital, Concord, Australia; cANZAC Study Institute, University of Sydney, Concord Repatriation General Hospital, Concord, Australia; dANZAC Analysis Institute and Department of Haematology, Concord Repatriation Common Hospital, Concord, Australia; e ANZAC Analysis Institute and Department of Cardiology, Concord Repatriation Basic Hospital, Concord, Australiaassessed by flow cytometry (Reddel et al. Thromb Haemost. 2018; 118(4): 72333) utilizing fluorescent surface markers for phosphatidylserine and cell origin such as platelets (CD41a), leukocytes (CD45) and MAC-1 (CD11b). Good events have been 5-HT4 Receptor Antagonist Source defined with supernatant of ultracentrifuged pooled normal plasma as negative manage. Adjustments pre ost RIPC were assessed by paired t-test. The study was approved by the regional ethics committee. Benefits: Inside the whole population, there was no effect of RIPC on fibrinolytic elements but a decrease in plateletderived EV. Nevertheless, in non-diabetic patients and not in diabetic patients, RIPC elevated general fibrinolytic potential and CD45+ and CD11b+ EV. These effects were not noticed following sham treatment. Summary/Conclusion: There is a international increase in fibrinolytic prospective immediately after RIPC therapy in CAD patients with no diabetes mellitus, which could be contributed to by increased leukocyte-derived EV and/or decreased AMPK Activator custom synthesis platelet-derived EV. Ongoing function aims to straight identify this contribution in patients who undergo RIPC.OTO1.Urinary extracellular vesicle concentration, microRNA-155 expression and inflammatory surface marker expression are altered in patients with symptomatic coronary artery disease Stephen Fitzsimonsa, Silvia Oggerob, Niall Mahonc, Nicola Ryanc, Mauro Perrettid and Orina BeltonaaIntroduction: Short non-harmful ischaemia, remote ischaemic preconditioning (RIPC) has been shown to confer advantage to sufferers with coronary artery illness (CAD). Some research indicate lesser benefit in sufferers with diabetes. RIPC might improve fibrinolysis. Hypothesis: RIPC causes an increase in fibrinolytic potential through release of fibrinolytic aspects from the endothelium or fibrinolysis-supporting extracellular vesicles (EVs) and this impact is much less evident in pa.