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Inflammation

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Endocarditis can present various clinical features depending on the causative organism and the patient's underlying health conditions. Initially, the clinical features of infective endocarditis develop gradually, presenting with nonspecific symptoms that can be easily mistaken for other illnesses.General SymptomsEarly symptoms of infective endocarditis are fever, chills, weakness, malaise, fatigue, and weight loss. These symptoms reflect the systemic nature of the infection and the body's...

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Updated: Mar 25, 2026

In vivo Measurement of the Mouse Pulmonary Endothelial Surface Layer

In vivo Measurement of the Mouse Pulmonary Endothelial Surface Layer

Published on: February 22, 2013

THE ENDOTHELIUM IN SEPSIS.

Can Ince¹, Philip R Mayeux, Trung Nguyen

¹*Department of Intensive Care, Erasmus MC, University Medical Center, Rotterdam, the Netherlands †Department of Pharmacology and Toxicology University of Arkansas for Medical Sciences, Little Rock, Arkansas ‡Pediatric Critical Care Medicine, Department of Pediatrics, Baylor College of Medicine, Texas Children's Hospital, Houston, Texas §The Center for Critical Care Nephrology Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania ||Department of Intensive Care, Fundación Valle del Lili, Universidad ICESI, Cali, Columbia ¶Department of Intensive Care Medicine, Pontificia Universidad Católica De Chile, Santiago, Chile **University College Dublin, Dublin, Ireland ††CHIREC Hospitals and Université Libre de Bruxelles, Brussels, Belgium.

Shock (Augusta, Ga.)

|February 13, 2016

Summary

Sepsis severely impacts endothelial cell (EC) functions, including vasoregulation and barrier integrity, contributing to organ failure. This review examines EC responses in sepsis, focusing on hemostasis and inflammation across different organs.

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Area of Science:

Cell Biology
Pathophysiology
Medical Science

Background:

Sepsis profoundly disrupts endothelial cell (EC) function, a critical factor in sepsis-induced organ failure.
Key EC functions compromised by sepsis include vasoregulation, barrier integrity, inflammation, and hemostasis.
Mechanisms involve glycocalyx shedding, altered nitric oxide metabolism, oxidative stress, and coagulation pathway activation.

Purpose of the Study:

To review current understanding of endothelial cell-associated hemostatic and inflammatory responses to sepsis.
To explore the heterogeneity of EC responses to sepsis across different organ systems (kidney, liver, lung).
To evaluate whether EC responses to sepsis are adaptive or maladaptive.

Main Methods:

Literature review of endothelial cell function in sepsis.
Analysis of sepsis-induced changes in EC vasoregulation, barrier function, inflammation, and hemostasis.
Comparative discussion of EC responses in kidney, liver, and lung tissues.

Main Results:

Sepsis triggers widespread EC dysfunction, impacting multiple physiological processes.
Endothelial responses vary significantly depending on the organ system.
Mechanisms include glycocalyx degradation, altered redox balance, and pro-coagulant shifts.

Conclusions:

Endothelial cell dysfunction is central to sepsis progression and organ failure.
Understanding organ-specific EC responses is crucial for targeted therapies.
The adaptive or maladaptive nature of EC responses requires further investigation.