Open Access Research article

Thoracic epidural anesthesia decreases endotoxin-induced endothelial injury

Fabian Enigk1, Antje Wagner1, Rudi Samapati2, Heike Rittner3, Alexander Brack3, Shaaban A Mousa4, Michael Schäfer4, Helmut Habazettl24 and Jörn Schäper5*

Author Affiliations

1 Department of Anesthesiology and Operative Intensive Care Medicine, Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin, Hindenburgdamm 30, Berlin 12203, Germany

2 Institute of Physiology, Charité–Universitätsmedizin Berlin, Charitéplatz 1, Berlin 10117, Germany

3 Department of Anesthesia and Critical Care, Josef-Schneider-Straße 2, 97080 Würzburg, Germany

4 Department of Anesthesiology and Operative Intensive Care Medicine, Charité–Universitätsmedizin Berlin, Campus Virchow-Klinikum, Augustenburger Platz 1, Berlin 13353, Germany

5 Department of Anesthesiology, Emergency Medicine and Critical Care Medicine, Universitätsmedizin Göttingen, Robert-Koch-Straße 40, Göttingen 37099, Germany

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BMC Anesthesiology 2014, 14:23  doi:10.1186/1471-2253-14-23

Published: 5 April 2014



The sympathetic nervous system is considered to modulate the endotoxin-induced activation of immune cells. Here we investigate whether thoracic epidural anesthesia with its regional symapathetic blocking effect alters endotoxin-induced leukocyte-endothelium activation and interaction with subsequent endothelial injury.


Sprague Dawley rats were anesthetized, cannulated and hemodynamically monitored. E. coli lipopolysaccharide (Serotype 0127:B8, 1.5 mg x kg-1 x h-1) or isotonic saline (controls) was infused for 300 minutes. An epidural catheter was inserted for continuous application of lidocaine or normal saline in endotoxemic animals and saline in controls. After 300 minutes we measured catecholamine and cytokine plasma concentrations, adhesion molecule expression, leukocyte adhesion, and intestinal tissue edema.


In endotoxemic animals with epidural saline, LPS significantly increased the interleukin-1β plasma concentration (48%), the expression of endothelial adhesion molecules E-selectin (34%) and ICAM-1 (42%), and the number of adherent leukocytes (40%) with an increase in intestinal myeloperoxidase activity (26%) and tissue edema (75%) when compared to healthy controls. In endotoxemic animals with epidural infusion of lidocaine the values were similar to those in control animals, while epinephrine plasma concentration was 32% lower compared to endotoxemic animals with epidural saline.


Thoracic epidural anesthesia attenuated the endotoxin-induced increase of IL-1β concentration, adhesion molecule expression and leukocyte-adhesion with subsequent endothelial injury. A potential mechanism is the reduction in the plasma concentration of epinephrine.

Epidural anesthesia; Lidocaine; Endotoxemia; Endothelial injury; Cytokines; Adhesion molecules; Myeloperoxidase