TY  - JOUR
A1  - Enigk, Fabian
A1  - Wagner, Antje
A1  - Samapati, Rudi
A1  - Rittner, Heike
A1  - Brack, Alexander
A1  - Mousa, Shaaban A.
A1  - Schäfer, Michael
A1  - Habazettl, Helmut
A1  - Schäper, Jörn
T1  - Thoracic epidural anesthesia decreases endotoxin-induced endothelial injury
JF  - BMC Anesthesiology
N2  - Background: 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. Methods: 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. Results: In endotoxemic animals with epidural saline, LPS significantly increased the interleukin-1 beta 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. Conclusions: Thoracic epidural anesthesia attenuated the endotoxin-induced increase of IL-1 beta concentration, adhesion molecule expression and leukocyte-adhesion with subsequent endothelial injury. A potential mechanism is the reduction in the plasma concentration of epinephrine.
KW  - endotoxemia
KW  - myeloperoxidase
KW  - endothelial injury
KW  - adhesion molecules
KW  - inflammatory response
KW  - intestinal microvascular perfusion
KW  - cell-adhesion
KW  - induced impairment
KW  - reperfusion injury
KW  - sepsis
KW  - neutrophil
KW  - lidocaine
KW  - lung injury
KW  - cytokines
KW  - epidural anesthesia
Y1  - 2014
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-116787
VL  - 14
IS  - 23
ER  - 
TY  - JOUR
A1  - Schmitz, Tobias
A1  - Jannasch, Maren
A1  - Weigel, Tobias
A1  - Moseke, Claus
A1  - Gbureck, Uwe
A1  - Groll, Jürgen
A1  - Walles, Heike
A1  - Hansmann, Jan
T1  - Nanotopographical Coatings Induce an Early Phenotype-Specific Response of Primary Material-Resident M1 and M2 Macrophages
JF  - Materials
N2  - Implants elicit an immunological response after implantation that results in the worst case in a complete implant rejection. This biomaterial-induced inflammation is modulated by macrophages and can be influenced by nanotopographical surface structures such as titania nanotubes or fractal titanium nitride (TiN) surfaces. However, their specific impact on a distinct macrophage phenotype has not been identified. By using two different levels of nanostructures and smooth samples as controls, the influence of tubular TiO2 and fractal TiN nanostructures on primary human macrophages with M1 or M2-phenotype was investigated. Therefore, nanotopographical coatings were either, directly generated by physical vapor deposition (PVD) or by electrochemical anodization of titanium PVD coatings. The cellular response of macrophages was quantitatively assessed to demonstrate a difference in biocompatibility of nanotubes in respect to human M1 and M2-macrophages. Depending on the tube diameter of the nanotubular surfaces, low cell numbers and impaired cellular activity, was detected for M2-macrophages, whereas the impact of nanotubes on M1-polarized macrophages was negligible. Importantly, we could confirm this phenotypic response on the fractal TiN surfaces. The results indicate that the investigated topographies specifically impact the macrophage M2-subtype that modulates the formation of the fibrotic capsule and the long-term response to an implant.
KW  - nanotopographical surfaces
KW  - combination of physical vapor deposition and electrochemical etching
KW  - defined humanized test system
KW  - inflammatory response
Y1  - 2020
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-203378
SN  - 1996-1944
VL  - 13
IS  - 5
ER  -