Reactive hyperemia correlates with the presence of sepsis and glycocalyx degradation in the intensive care unit: a prospective cohort study

Abstract

Objective To investigate whether reactive hyperemia measured by peripheral arterial tonometry correlates with markers of endothelial dysfunction and may be used to identify sepsis in critical illness. Methods A prospective study was performed using a cohort of critically ill patients. Endothelial dysfunction was assessed on admission by quantifying reactive hyperemia-peripheral arterial tonometry and plasma levels of endothelin-1, soluble E-selectin, endocan and syndecan-1. Septic patients were compared to patients without evidence of infection. Results Fifty-eight septic patients were compared to 28 controls. The natural logarithm of reactive hyperemia-peripheral arterial tonometry was negatively correlated with cardiovascular comorbidities, disease severity and plasma levels of soluble E-selectin (p = 0.024) and syndecan-1 (p < 0.001). The natural logarithm of reactive hyperemia-peripheral arterial tonometry was lower in septic patients than in controls (0.53 ± 0.48 versus 0.69 ± 0.42, respectively). When adjusted for age, the multivariable model predicted that each 0.1-unit decrease in natural logarithm of reactive hyperemia-peripheral arterial tonometry increased the odds for infection by 14.6%. m. Conclusion Reactive hyperemia-peripheral arterial tonometry is closely related to soluble E-selectin and syndecan-1, suggesting an association between endothelial activation, glycocalyx degradation and vascular reactivity. Reactive hyperemia-peripheral arterial tonometry appears to be compromised in critically ill patients, especially those with sepsis.

Heat stress combined with lipopolysaccharide induces pulmonary microvascular endothelial cell glycocalyx inflammatory damage in vitro

“…E-selectin and VCAM-1 were the important symbols to reflect injury of EGCX and endothelium, which also played critical roles in the spread of inflammation via mediating the adhesion between leukocyte and inflammatory cells. 23,39,40 In our results, increased expressions of VCAM-1 and E-selectin were significantly observed in endothelium treated with heat stress and LPS, especially in cells suffering from HPSE. These findings were consistent with those that revealed a significant upregulation of Eselectin in injured vascular EGCX, 41,42 which confirmed a dysfunction of endothelial cells inhibiting inflammation.…”

“…E‐selectin and VCAM‐1 were the important symbols to reflect injury of EGCX and endothelium, which also played critical roles in the spread of inflammation via mediating the adhesion between leukocyte and inflammatory cells 23,39,40 . In our results, increased expressions of VCAM‐1 and E‐selectin were significantly observed in endothelium treated with heat stress and LPS, especially in cells suffering from HPSE.…”

Heat stress combined with lipopolysaccharide induces pulmonary microvascular endothelial cell glycocalyx inflammatory damage in vitro

“…E-selectin and VCAM-1 were the important symbols to reflect injury of endothelial glycocalyx and endothelium, which also played critical roles in the spread of inflammation via mediating the adhesion between leukocyte and inflammatory cells. 24,38,39 In our results, increased expressions of VCAM-1 and E-selectin were significantly observed in endothelium treated with heat stress and LPS, especially in cells suffered from HPSE (Figure 3C ). These findings were consistent with those revealed a significant upregulation of Eselectin in injured vascular endothelial glycocalyx, 40,41 , which confirmed a dysfunction of endothelial cells inhibiting in inflammation.…”

Mortalidade por sepse no Brasil, uma análise de série temporal: 2010-2020

“…Nesta perspectiva em que o quadro clínico do paciente requer tratamento em Unidade de Terapia Intensiva (UTI), a alta disponibilidade de recursos terapêuticos e laboratoriais são evidentemente importantes, detendo potencial de interferir no desfecho clínico. 14 Assim, compreende-se que a apresentação ascendente da mortalidade por sepse em 16 estados brasileiros, entre 2010 e 2020, possivelmente seja uma das consequências da insuficiente disponibilidade de recursos presentes no sistema público de saúde, uma vez que a capilaridade exercida pelo SUS no território nacional não dispõe de tamanha estrutura hospitalar para todas as suas áreas de cobertura, como também as regiões de alta densidade demográfica demonstram sobrecarga em seus serviços hospitalares de alta complexidade. sepse.…”