title: Clonidine pre-treatment prevents hemorrhagic shock-induced endotoxemia and oxidative stress in the gut, liver, and lungs of the rat.
abstract: OBJECTIVE
  To study the effect of clonidine pre-treatment on hemorrhagic shock (H/S)-induced endotoxemia and oxidative stress (OS) in three vital organs of the rat.
  
  
  METHODS
  The study protocol consisted of two arms: one for the measurement of organic hydroperoxide  (LOOH) and superoxide radical (O(2)(-·)) production in the gut, liver, and lungs (n = 32 rats) and one for the measurement of endotoxin in portal and systemic circulation (n = 32 rats). Four animal groups (sham, clonidine, H/S,  and clonidine-H/S group) were used in each arm. Three hours after H/S and concominant blood resuscitation, tissues were collected for LOOHs and O(2)(-·) measurement and blood samples were obtained for endotoxin determination.
  
  
  RESULTS
  Clonidine  pre-treatment prior to H/S resulted in a significant reduction of LOOHs and O(2)(-·) production in all vital organs (P < 0.05-0.001), while additionally, clonidine reduced H/S-induced endotoxemia in portal (P < 0.05)  and systemic circulation as well (P < 0.01).
  
  
  CONCLUSIONS
  Clonidine pre-treatment prevents endotoxemia and OS in the gut, liver, and lungs of rats subjected to severe H/S. The improved intestinal barrier function probably stems from the antioxidant effect  of clonidine on the intestinal epithelium, whereas the reduced endotoxemia may contribute to a decreased OS observed in the liver and lungs.
authors: Departments of Anesthesiology and Critical Care Medicine, School of Medicine, University of Patras, Rion - Patras, Greece.
authors: Kriton S
authors: KS
authors: Filos
authors: Eleftheria S
authors: ES
authors: Panteli
authors: Foteini
authors: F
authors: Fligou
authors: Chrysaygi
authors: C
authors: Papamichail
authors: Ioannis
authors: I
authors: Papapostolou
authors: George
authors: G
authors: Zervoudakis
authors: Iris
authors: I
authors: Spiliopoulou
authors: Christos
authors: C
authors: Georgiou
mesh_terms: D000316:Adrenergic alpha-Agonists / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D000818:Animals; D001012:Aorta, Abdominal; D018988:Bacterial Translocation / Q000187:drug effects*; D003000:Clonidine / Q000008:administration & dosage / Q000494:pharmacology / Q000627:therapeutic use*; D019446:Endotoxemia / Q000209:etiology / Q000517:prevention & control*; D004731:Endotoxins / Q000097:blood; D007413:Intestinal Mucosa / Q000187:drug effects / Q000378:metabolism; D007422:Intestines / Q000187:drug effects* / Q000382:microbiology; D015227:Lipid Peroxidation / Q000187:drug effects*; D008054:Lipid Peroxides / Q000032:analysis; D008099:Liver / Q000187:drug effects* / Q000378:metabolism / Q000382:microbiology; D008168:Lung / Q000187:drug effects* / Q000378:metabolism / Q000382:microbiology; D008297:Male; D018384:Oxidative Stress / Q000187:drug effects*; D011169:Portal Vein; D011292:Premedication; D051381:Rats; D017208:Rats, Wistar; D012771:Shock, Hemorrhagic / Q000150:complications / Q000188:drug therapy* / Q000503:physiopathology; D013481:Superoxides / Q000032:analysis
chemical_list: D000316:Adrenergic alpha-Agonists; D004731:Endotoxins; D008054:Lipid Peroxides; D013481:Superoxides; D003000:Clonidine