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We discovered that the original branching and creation of the rudimentary duct happened normally in


div>We have previously demonstrated associations between- and negative predictive values of high circulating catecholamines and endothelial damage in trauma, sepsis and ST segment elevation myocardial infarction patients. However, no studies have previously investigated the association between circulating catecholamines, endothelial damage and outcome in cardiac arrest patients. The objective of the present study was to investigate the association between sympathoadrenal activation, endothelial damage and outcome in OHCA patients, hypothesizing that excessive sympathoadrenal activation and endothelial damage would be associated and linked to poor outcome. We had access to previously collected plasma samples from OHCA patients included at a single site in The Targeted Temperature Management at 33 degrees C versus 36 degrees C after Cardiac Arrest trial. The main TTM study reported similar outcomes with targeting 33 versus 36 degrees. The TTM protocol was approved by the ethics committees in each participating country and institution and the Danish Data 8-PIP-cAMP Protection Agency) and conducted in accordance with the Declaration of Helsinki. Written informed consent was obtained from a legal surrogate and from all patients who regained mental capacity. Participant consent was documented as a signed consent form that was kept according to Danish Legislation. The procedure for obtaining written informed consent was approved by the ethics committee. The TTM inclusion criteria were patients _18 years of age who were unconscious <8) on admission to the hospital after OHCA of presumed cardiac cause, irrespective of the initial rhythm. Eligible patients had more than 20 consecutive minutes of spontaneous circulation after resuscitation. The main exclusion criteria were an interval from the ROSC to screening of more than 240 minutes, unwitnessed arrest with asystole as the initial rhythm, suspected or known acute intracranial hemorrhage or stroke and a body temperature of less than 30°C. Eligible patients for the present study were patients included at Rigshospitalet, Copenhagen University Hospital, Denmark. Furthermore, to be included, an adequate volume of stored plasma and serum should be available from the pre-intervention admission blood sample to allow for investigation of the planned biomarkers. The present study is based on these 163 patients. We had access to the following data as part of the TTM trial protocol: Demography, medical history, characteristics of the cardiac arrest, patient characteristics at admission and outcome and modified Rankin scale ; all surviving patients were followed until 180 days after the enrollment of the last patient). In the present study, OHCA patients presented with high and inter-correlated levels of circulating catecholamines and biomarkers of excessive endothelial damage. Increased time from OHCA to ROSC, lower pH and STEMI were independently associated with higher syndecan-1 levels, a marker of glycocalyx damage, whereas lower pH, higher age and higher sVE-cadherin were independently associated with higher thrombomodulin levels, a marker of endothelial cell injury. By Cox proportional-hazards analyses, high thrombomodulin levels independently predicted 30-day and 180-day mortality. Acute critical illness is accompanied by excessive sympathoadrenal activation that induces widespread, dose-dependent effects on the vascular system, including the endothelium. We have proposed that endogenously released catecholamines ensure oxygen supply to vital organs in acute critical illness by balancing the clotting ability of the circulating blood according to the degree of endothelial anti-/procoagulation in the microcirculation. Hereby, progressive endothelial damage in the microcirculation is balanced by increasing hypocoagulability in the circulating blood. Given this, the evolutionary rational for the coagulopathy observed in many acute critically ill patients, may be that evolution has prioritized tissue oxygenation above hemostasis. We have reported of associations between- and negative predictive values of high circulating catecholamines and endothelial damage in trauma, sepsis and STEMI patients. In line with this, the present study found that circulating levels of adrenaline and noradrenaline correlated positively with syndecan-1 and thrombomodulin levels, biomarkers of endothelial glycocalyx and cell damage, respectively. F

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