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   <subfield code="a">10.1007/s10620-011-1625-y</subfield>
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   <subfield code="a">Gut-Brain Chemokine Changes in Portal Hypertensive Rats</subfield>
   <subfield code="h">[Elektronische Daten]</subfield>
   <subfield code="c">[Joaquin Merino, Maria-Angeles Aller, Sandra Rubio, Natalia Arias, Maria-Paz Nava, Maria Loscertales, Jaime Arias, Jorge-Luis Arias]</subfield>
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   <subfield code="a">Background: Hepatic encephalopathy is a syndrome whose physiopathology is poorly understood; therefore, current diagnostic tests are imperfect and modern therapy is nonspecific. Particularly, it has been suggested that inflammation plays an important role in the pathogenesis of portal hypertensive encephalopathy in the rat. Aim: We have studied an experimental model of portal hypertension based on a triple partial portal vein ligation in the rat to verify this hypothesis. Methods: One month after portal hypertension we assayed in the splanchnic area (liver, small bowel and mesenteric lymph nodes) and in the central nervous system (hippocampus and cerebellum) fractalkine (CX3CL1) and stromal cell-derived factor alpha (SDF1-α) as well as their respective receptors (CX3CR1 and CXCR4) because of their key role in inflammatory processes. Results: The significant increase of fractalkine in mesenteric lymph nodes (P&lt;0.05) and its receptor (CX3CR1) in the small bowel (P&lt;0.05) and hippocampus (P&lt;0.01), associated with the increased expression of SDF1-α in the hippocampus (P&lt;0.01) and the cerebellum (P&lt;0.01) suggest that prehepatic portal hypertension in the rat induces important alterations in the expression of chemokines in the gut-brain axis. Conclusion: The present study revealed that portal hypertension is associated with splanchnic-brain inflammatory alterations mediated by chemokines.</subfield>
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   <subfield code="a">Springer Science+Business Media, LLC, 2011</subfield>
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   <subfield code="a">Chemokines</subfield>
   <subfield code="2">nationallicence</subfield>
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   <subfield code="a">Hepatic encephalopathy</subfield>
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   <subfield code="a">Neuroinflammation</subfield>
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   <subfield code="a">CXCR4/SDF1-alpha</subfield>
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   <subfield code="a">CXCR1/Fractalkine</subfield>
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   <subfield code="a">Merino</subfield>
   <subfield code="D">Joaquin</subfield>
   <subfield code="u">Department of Surgery I, School of Medicine, Complutense University of Madrid, Plaza de Ramón y Cajal s.n, 28040, Madrid, Spain</subfield>
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   <subfield code="a">Aller</subfield>
   <subfield code="D">Maria-Angeles</subfield>
   <subfield code="u">Department of Surgery I, School of Medicine, Complutense University of Madrid, Plaza de Ramón y Cajal s.n, 28040, Madrid, Spain</subfield>
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   <subfield code="a">Rubio</subfield>
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   <subfield code="u">Department of Psychobiology, School of Psychology, Autonomous University of Madrid, 28049, Cantoblanco, Madrid, Spain</subfield>
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   <subfield code="a">Arias</subfield>
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   <subfield code="u">Neurosciences Laboratory, School of Psychology, University of Oviedo, Pza. de Feijoo s/n, 33003, Oviedo, Asturias, Spain</subfield>
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   <subfield code="u">Department of Physiology (Animal Physiology II), School of Biology, Complutense University of Madrid, J. A. Novais 2, 28040, Madrid, Spain</subfield>
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   <subfield code="a">Loscertales</subfield>
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   <subfield code="u">Department of Surgery, Massachusetts General Hospital, 1055 Fruit St., 02114, Boston, MA, USA</subfield>
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   <subfield code="u">Department of Surgery I, School of Medicine, Complutense University of Madrid, Plaza de Ramón y Cajal s.n, 28040, Madrid, Spain</subfield>
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   <subfield code="t">Digestive Diseases and Sciences</subfield>
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   <subfield code="g">56/8(2011-08-01), 2309-2317</subfield>
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