scholarly journals Fluid resuscitation should respect the endothelial glycocalyx layer

Critical Care ◽  
2014 ◽  
Vol 18 (6) ◽  
Author(s):  
Bertrand Guidet ◽  
Hafid Ait-Oufella
Keyword(s):  
Fluid Resuscitation ◽  
Endothelial Glycocalyx ◽  
Endothelial Glycocalyx Layer

scholarly journals The effects of a limited infusion rate of fluid in the early resuscitation of sepsis on glycocalyx shedding measured by plasma syndecan-1: a randomized controlled trial

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Jutamas Saoraya ◽  
Lipda Wongsamita ◽  
Nattachai Srisawat ◽  
Khrongwong Musikatavorn
Keyword(s):  
Adverse Events ◽  
Organ Failure ◽  
Fluid Resuscitation ◽  
Infusion Rate ◽  
Controlled Trial ◽  
Geometric Mean ◽  
Endothelial Glycocalyx ◽  
Open Label ◽  
Randomized Controlled ◽  
Standard Rate

Abstract Background Aggressive fluid administration is recommended in the resuscitation of septic patients. However, the delivery of a rapid fluid bolus might cause harm by inducing degradation of the endothelial glycocalyx. This research aimed to examine the effects of the limited infusion rate of fluid on glycocalyx shedding as measured by syndecan-1 in patients with sepsis-induced hypoperfusion. Methods A prospective, randomized, controlled, open-label trial was conducted between November 2018 and February 2020 in an urban academic emergency department. Patients with sepsis-induced hypoperfusion, defined as hypotension or hyperlactatemia, were randomized to receive either the standard rate (30 ml/kg/h) or limited rate (10 ml/kg/h) of fluid for the first 30 ml/kg fluid resuscitation. Subsequently, the fluid rate was adjusted according to the physician’s discretion but not more than that of the designated fluid rate for the total of 6 h. The primary outcome was differences in change of syndecan-1 levels at 6 h compared to baseline between standard and limited rate groups. Secondary outcomes included adverse events, organ failure, and 90-day mortality. Results We included 96 patients in the intention-to-treat analysis, with 48 assigned to the standard-rate strategy and 48 to the limited-rate strategy. The median fluid volume in 6 h in the limited-rate group was 39 ml/kg (interquartile range [IQR] 35–52 ml/kg) vs. 53 ml/kg (IQR 46–64 ml/kg) in the standard-rate group (p < 0.001). Patients in the limited-rate group were less likely to received vasopressors (17% vs 42%; p = 0.007) and mechanical ventilation (20% vs 41%; p = 0.049) during the first 6 h. There were no significantly different changes in syndecan-1 levels at 6 h between the two groups (geometric mean ratio [GMR] in the limited-rate group, 0.82; 95% confidence interval [CI], 0.66–1.02; p = 0.07). There were no significant differences in adverse events, organ failure outcomes, or mortality between the two groups. Conclusions In sepsis resuscitation, the limited rate of fluid resuscitation compared to the standard rate did not significantly reduce changes in syndecan-1 at 6 h. Trial registration Thai Clinical Trials Registry number: TCTR20181010001. Registered 8 October 2018, http://www.clinicaltrials.in.th/index.php?tp=regtrials&menu=trialsearch&smenu=fulltext&task=search&task2=view1&id=4064

scholarly journals Endothelial Glycocalyx Layer: A Possible Therapeutic Target for Acute Lung Injury during Lung Resection

2017 ◽  
Vol 2017 ◽  
pp. 1-8 ◽  
Author(s):  
JiaWan Wang ◽  
AnShi Wu ◽  
Yan Wu
Keyword(s):  
Serum Albumin ◽  
Lung Resection ◽  
Serum Levels ◽  
Endothelial Glycocalyx ◽  
Major Surgery ◽  
Control Group ◽  
Vats Lobectomy ◽  
Lung Cancer Patients ◽  
Endothelial Glycocalyx Layer ◽  
And Control

Background. Shedding of the endothelial glycocalyx layer (EGL) is known to occur during major surgery, but its degradation associated with minimally invasive video-assisted thoracoscopy (VATS) remains unclear. We investigated if serum biomarkers of EGL disruption were elevated during VATS lobectomy, and whether the urinary trypsin inhibitor (UTI) ulinastatin exerted a protective effect during this procedure.Materials and Methods. Sixty ASA II-III lung cancer patients undergoing elective VATS lobectomy were divided equally into UTI and control groups. UTI group patients received intravenous UTI during surgery. Serum levels of syndecan-1 and heparan sulfate were examined before (T0) and at the end of surgery (T1). Serum albumin and hemoglobin were measured before surgery (BOD) and on the first postoperative day (POD1).Results. In control group, syndecan-1 levels were significantly elevated at T1 compared with T0 (3.77±3.15versus4.28±3.30,P=0.022⁎) and increased even more significantly in patients whose surgery lasted >3 h (3.28±2.84versus4.31±3.39,P=0.003⁎⁎). Serum albumin levels on POD1 were significantly lower in control group compared with UTI group (32.63±4.57versus35.76±2.99,P=0.031⁎).Conclusion. EGL degradation occurs following VATS lobectomy. UTI can alleviate this shedding, thus helping preserve normal vascular permeability.Trail Registration. This trial is registered withChiCTR-IOC-17010416(January 13, 2017).

Effect of endothelial glycocalyx layer redistribution upon microvessel poroelastohydrodynamics

2016 ◽  
Vol 798 ◽  
pp. 812-852 ◽  
Author(s):  
T. C. Lee ◽  
D. S. Long ◽  
R. J. Clarke
Keyword(s):  
Mechanical Stress ◽  
Solid Phase ◽  
Boundary Integral ◽  
Thin Layers ◽  
Cell Junctions ◽  
Endothelial Glycocalyx ◽  
Viscous Effects ◽  
Substantial Impact ◽  
Endothelial Glycocalyx Layer ◽  
The Impact

The endothelial glycocalyx layer (EGL) is a macromolecular layer that lines the inner surface of blood vessels. It is believed to serve a number of physiological functions in the microvasculature, including protection of the vessel walls from potentially harmful levels of fluid shear, as a molecular sieve that acts to regulate transendothelial mass transport, and as a transducer of mechanical stress from the vessel lumen. To best fulfil some of its roles, it has been suggested that the EGL redistributes, so that it is thickest at the cell–cell junctions. It has also been suggested that the majority of mechanotransduction occurs through the solid phase of the EGL, rather than via its fluid phase. The difficulties associated with measuring the distribution of the EGL in vivo make these hypotheses difficult to confirm experimentally. Consequently, to gauge the impact of EGL redistribution from a theoretical standpoint, we compute the flow through a porous-lined microvessel, the endothelial surface of which has been informed by confocal microscopy images of a postcapillary venule. Following earlier studies, we model the poroelastohydrodynamics of the EGL using biphasic mixture theory, taking advantage of a recently developed boundary integral representation of these equations to solve the coupled poroelastohydrodynamics using the boundary element method. However, the low permeabilities of the EGL mean that viscous effects are confined to thin layers, thereby also enabling an asymptotic treatment of the dynamics in this limit. In this asymptotic regime, we also consider a two-layer Stokes flow model for the lumen flow to approximate the effect of red blood cells within the lumen. We demonstrate that redistribution of the EGL can have a substantial impact upon microvessel haemodynamics. We also confirm that the bulk of the mechanical stress is indeed carried through the solid phase of the EGL.

scholarly journals Endothelial Glycocalyx Layer Properties and Its Ability to Limit Leukocyte Adhesion

2020 ◽  
Vol 118 (7) ◽  
pp. 1564-1575 ◽  
Author(s):  
Luis F. Delgadillo ◽  
Graham A. Marsh ◽  
Richard E. Waugh
Keyword(s):  
Leukocyte Adhesion ◽  
Endothelial Glycocalyx ◽  
Endothelial Glycocalyx Layer

scholarly journals Changes in endothelial glycocalyx layer protective ability after inflammatory stimulus

2020 ◽  
Author(s):  
Luis F. Delgadillo ◽  
Elena B. Lomakina ◽  
Julia Kuebel ◽  
Richard E. Waugh
Keyword(s):  
Endothelial Cells ◽  
Fluid Transport ◽  
Leukocyte Adhesion ◽  
Umbilical Vein ◽  
Barrier Properties ◽  
Endothelial Barrier ◽  
Endothelial Glycocalyx ◽  
Neutrophil Adhesion ◽  
Barrier Dysfunction ◽  
Endothelial Glycocalyx Layer

Leukocyte adhesion to the endothelium is an important early step in the initiation and progression of sepsis. The endothelial glycocalyx layer (EGL) has been implicated in neutrophil adhesion and barrier dysfunction, but studies in this area are few. In this report we examine the hypothesis that damage to the structure of the EGL caused by inflammation leads to increased leukocyte adhesion and endothelial barrier dysfunction. We used human umbilical vein endothelial cells (HUVECs) enzymatically treated to remove the EGL components hyaluronic acid (HA) and heparan sulfate (HS) as a model for EGL damage. Using atomic force microscopy, we show reductions in EGL thickness after removal of either HA or HS individually, but the largest decrease, comparable to TNF-a treatment, was observed when both HA and HS were removed. Interestingly, removal of HS or HA individually did not affect neutrophil adhesion significantly, but removal of both constituents resulted in increased neutrophil adhesion. To test EGL contributions to endothelial barrier properties, we measured trans-endothelial electrical resistance (TEER) and diffusion of fluorescently labeled dextran (10 kDa MW) across the monolayer. Removal of EGL components decreased TEER, but had an insignificant effect on dextran diffusion rates. The reduction in TEER suggests that disruption of the EGL may predispose endothelial cells to increased rates of fluid leakage. These data support the view that damage to the EGL during inflammation has significant effects on the accessibility of adhesion molecules, likely facilitates leukocyte adhesion, and may also contribute to increased rates of fluid transport into tissues.

Hypervolemia does not cause degradation of the endothelial glycocalyx layer during open hysterectomy performed under sevoflurane or propofol anesthesia

2019 ◽  
Vol 64 (4) ◽  
pp. 538-545 ◽  
Author(s):  
Janis Nemme ◽  
Camilla Krizhanovskii ◽  
Stelia Ntika ◽  
Olegs Sabelnikovs ◽  
Indulis Vanags ◽  
...  
Keyword(s):  
Endothelial Glycocalyx ◽  
Endothelial Glycocalyx Layer
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