title: Neurohistological abnormalities during early porcine endotoxemia.
abstract: BACKGROUND
  Brain dysfunction is common in sepsis. We aimed to assess whether cerebral perfusion, oxygenation, and/or metabolism are abnormal during early endotoxemia, and how they may relate to potential neurohistological changes.
  
  
  METHODS
  In this prospective animal study, we included 12 pigs (weight: 42 ± 4 kg; mean ± SD) that were exposed to Escherichia coli lipopolysaccharide (E. coli LPS B0111 : B4, 0.4 μg/kg/h) or saline infusion (n = 6, each) for 10 h. Systemic hemodynamics, cerebral blood flow, intracranial pressure, and brain tissue oxygen tension were continuously measured. At the end of the experiment, formalin-fixed brains were cut in coronal sections and embedded in paraffin. Afterwards, the sections were cut at 5 microns and stained with hematoxylin and eosin.
  
  
  RESULTS
  Stable systemic hemodynamics in both groups were associated with higher carotid arterial blood flow after 10 h of endotoxemia (9.0 ± 2.2 ml/kg/min) compared to controls (6.6 ± 1.2 ml/kg/min; time-group interaction: P = 0.014). Intracranial pressure, cerebral perfusion pressure, brain oxygen consumption, and brain tissue oxygen tension were similar in both groups. In four of the six endotoxemic animals but in none of the controls, cerebral tissue lesions were found (encephalomalacia with spongy degeneration of white matter, axonal swelling, and ischemic neuronal thalamic necrosis), including significant venous vascular alterations, predominantly in the brainstem, in three of the four animals.
  
  
  CONCLUSIONS
  Early endotoxemia seems to be associated with histological signs of brain damage unrelated to systemic or cerebral hemodynamics or oxygenation.
authors.affiliation: Department of Anesthesiology and Pain Therapy, Bern University Hospital, University of Bern, Bern, Switzerland.
authors.forename: B
authors.initials: B
authors.lastname: Bänziger
authors.forename: T
authors.initials: T
authors.lastname: Regueira
authors.forename: R
authors.initials: R
authors.lastname: Vogt
authors.forename: S
authors.initials: S
authors.lastname: Brandt
authors.forename: M
authors.initials: M
authors.lastname: Vandevelde
authors.forename: S M
authors.initials: SM
authors.lastname: Jakob
mesh_terms: D000818:Animals; D001921:Brain / Q000473:pathology; D002560:Cerebrovascular Circulation; D019446:Endotoxemia / Q000139:chemically induced / Q000150:complications* / Q000473:pathology*; D005260:Female; D006439:Hemodynamics; D007427:Intracranial Pressure; D008070:Lipopolysaccharides; D008297:Male; D009422:Nervous System Diseases / Q000209:etiology* / Q000473:pathology*; D010101:Oxygen Consumption; D011446:Prospective Studies; D015656:Respiratory Mechanics; D013552:Swine
chemical_list: D008070:Lipopolysaccharides