title: Glycine selectively reduces intestinal injury during endotoxemia.
abstract: BACKGROUND
  Glycine is well known to protect the intestine against ischemia-reperfusion injury and during mechanical manipulation. Here, we studied whether glycine protects the small intestine during endotoxemia, even without being the site of the infection.
  
  
  METHODS
  Lipopolysaccharide (LPS) was infused at a rate of 1 mg/kg × h over a period of 7 h (subacute endotoxemia) in male Wistar rats. Glycine (single dose: 50 mg/kg × 15 min) was applied intravenously at 180 and 270 min after the beginning of the LPS infusion. Systemic parameters were periodically determined. The small intestine was analyzed for macroscopic (hemorrhages) and histopathologic changes (hematoxylin and eosin staining), and markers of inflammation (myeloperoxidase activity).
  
  
  RESULTS
  Glycine neither decreased mortality nor beneficially affected vital parameters (e.g., mean arterial blood pressure and breathing rate), electrolytes, blood gases including pH and base excess, and plasma parameters of tissue injury such as lactate concentration, hemolysis, and aminotransferases activities during experimental endotoxemia. It, however, specifically diminished the LPS-induced small intestinal injury, as indicated by less intestinal accumulation of blood, less intestinal hemorrhages, and reduced intestinal hemoglobin content.
  
  
  CONCLUSIONS
  The present results demonstrate that glycine selectively protects the small intestine during subacute endotoxemia, even after manifestation of a severe systemic impairment. Because glycine is non-toxic at low doses, an administration of a moderate glycine dose (50-100 mg/kg) may be suitable to protect from intestinal damage during sepsis. Its true clinical potential, however, needs to be verified in further experimental studies and clinical trials.
authors.affiliation: Institute of Physiological Chemistry, University Hospital Essen, Germany. Electronic address: katharina.effenberger-neidnicht@uni-due.de.
authors.forename: Katharina
authors.initials: K
authors.lastname: Effenberger-Neidnicht
authors.affiliation: Institute of Physiological Chemistry, University Hospital Essen, Germany.
authors.forename: Johannes
authors.initials: J
authors.lastname: Jägers
authors.affiliation: Institute of Physiological Chemistry, University Hospital Essen, Germany.
authors.forename: Rabea
authors.initials: R
authors.lastname: Verhaegh
authors.affiliation: Institute of Physiological Chemistry, University Hospital Essen, Germany.
authors.forename: Herbert
authors.initials: H
authors.lastname: de Groot
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D019446:Endotoxemia / Q000150:complications / Q000188:drug therapy*; D004751:Enteritis / Q000188:drug therapy* / Q000209:etiology; D006471:Gastrointestinal Hemorrhage / Q000188:drug therapy / Q000209:etiology; D005998:Glycine / Q000494:pharmacology*; D018684:Glycine Agents / Q000494:pharmacology*; D006454:Hemoglobins / Q000378:metabolism; D007421:Intestine, Small / Q000187:drug effects; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D009102:Multiple Organ Failure / Q000188:drug therapy / Q000209:etiology; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000150:complications / Q000188:drug therapy*; D015996:Survival Rate
chemical_list: D018684:Glycine Agents; D006454:Hemoglobins; D008070:Lipopolysaccharides; D005998:Glycine
keywords: Gut hypothesis; Hemoglobin content; Intestinal hemorrhage; Intestinal inflammation; Ischemia-reperfusion injury; Lipopolysaccharide; Multiple organ failure; Sepsis