Ten patients (56%) were considered as fluid responders. CI, cardiac index EVLWI, extravascular lung water index GEDVI, global end-diastolic volume index HSPG, heparan sulfate proteoglycan MAP, mean arterial pressure PPV, pulse pressure variation PVPI, pulmonary vascular permeability index S1, syndecan 1 SVV, stroke volume variation SVRI, systemic vascular resistance index. 05 compared with baseline, Wilcoxon test. 17 The doses of vasopressors were titrated to maintain mean arterial pressure within 65-85 mm Hg. During the study, the patients received the therapy according to the guidelines of Surviving Sepsis Campaign. Sepsis and septic shock were diagnosed using Sepsis-3 criteria. The exclusion criteria were right heart failure, arrhythmias, and abdominal compartment syndrome. All patients were sedated and received neuromuscular blockers during fluid load test. The inclusion criteria were the presence of informed consent, the diagnosis of septic shock, the age of patients > 18 years, the allocation at the intensive care unit (ICU), and the requirement of mechanical ventilation. Three patients were excluded (2 patients due to progressing refractory shock and death during the screening period and 1 patient due to dysfunction of the thermodilution catheter), thus totally 18 patients were enrolled and underwent further analysis. Twenty-one adult patients with the diagnosis of septic shock were screened for the study entry. Written informed consent was obtained from the patient or next of kin if the patient was unconscious. 02/06-16) of the Northern State Medical University (Arkhangelsk, Russian Federation). The prospective observational study was approved by the Research Ethical Committee (No. The aim of our study was to assess the association of free plasma fraction of key EG components with hemodynamic and metabolic response to fluid therapy, as well as severity of pulmonary edema, in patients with septic shock. However, the relationship between EG and fluid therapy of sepsis is still a subject of debate. 16 Thus, critical remodeling of the endothelial system and EG triggers the mechanism of multiple organ failure. 7, 15, 16 In sepsis, the damaged EG layer becomes thinner resulting in extravasation of proteins and fluid into the interstitial space and causing hypovolemia, hypoalbuminemia, overhydration, and tissue edema. Sepsis and septic shock are associated with severe involvement of the endothelium and EG degradation that leads to dysregulation of homeostasis and permeability of the vascular wall causing damage to the microvasculature. 12, 13 Shedding and flaking of EG result in an instant increase in free plasma concentrations of syndecan 1 (S1) and heparan sulfate proteoglycan (HSPG), which can be determined by enzyme-linked immunosorbent assay. 7- 11 Indeed, glycocalyx plays a key role in the physiology of microcirculation and endothelium integrity and is involved in the regulation of microcirculatory tone and vascular permeability, maintaining the oncotic gradient across the endothelial barrier, leukocyte adhesion, and migration as well as preventing the thrombosis. Nowadays, the effects of fluids on sepsis-induced degradation and shedding of endothelial glycocalyx (EG) and, thereafter, the capillary leakage resulting in the development of interstitial edema are being actively discussed. 5 Moreover, even in the case of fluid responsiveness, increased permeability can lead to progressive tissue edema and organ dysfunction. 1- 4 Thus, before a decision regarding infusion, it is important to determine whether this patient will respond to fluid load with an adequate increase in cardiac output or stroke volume, usually by between 10% and 15% of the initial value. However, it can be accompanied by several potentially dangerous side effects, especially in patients with cardiac comorbidities, acute respiratory distress syndrome (ARDS), and severe “capillary leak”. In patients with septic shock, fluid therapy is one of the key “golden hour” interventions.
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