title: Jejunal luminal nitric oxide during severe hypovolemia and sepsis in anesthetized pigs.
abstract: OBJECTIVE
  Lowered gut blood perfusion and the associated intestinal mucosal barrier dysfunction is considered important in the pathophysiology leading to critical illness. Intestinal mucosal nitric oxide formation has been attributed a key role in the regulation of epithelial permeability and other properties of the intestinal mucosal barrier. This study was performed to delineate intestinal mucosal NO formation during hypovolemia or sepsis, both of which are associated with intestinal hypoperfusion.
  
  
  METHODS
  Seventeen pigs were subjected to 2 h of severe hypovolemia (bleeding induced) or sepsis (systemic infusion of live Escherichia coli) or no treatment (controls). Jejunal mucosal NO production was monitored by a tonometer. Mesenteric blood flow was measured as portal venous blood flow by an ultrasonic transit time flowmeter probe, and oxygen delivery and consumption were calculated from regional blood samples.
  
  
  RESULTS
  Intestinal perfusion and oxygen delivery were reduced by the same order of magnitude in both groups. Jejunal mucosal NO production and oxygen consumption decreased markedly in the hypovolemia group but remained stable in the group subjected to septic shock.
  
  
  CONCLUSIONS
  These data suggest that blood loss inhibits jejunal mucosal NO production as part of a general downregulation of nonvital organs. Sepsis represents a more complex stress condition with activation/maintenance of host defense mechanisms as reflected by maintained jejunal mucosal NO production despite reduced gut blood perfusion.
authors.affiliation: Department of Anaesthesiology and Intensive Care, Sahlgrens University Hospital/Eastern Hospital, 41685 Gothenburg, Sweden. johan.snygg@vgregion.se
authors.forename: J
authors.initials: J
authors.lastname: Snygg
authors.forename: L
authors.initials: L
authors.lastname: Fändriks
authors.forename: J
authors.initials: J
authors.lastname: Bengtsson
authors.forename: M
authors.initials: M
authors.lastname: Holm
authors.forename: A
authors.initials: A
authors.lastname: Pettersson
authors.forename: A
authors.initials: A
authors.lastname: Aneman
mesh_terms: D000704:Analysis of Variance; D000818:Animals; D004731:Endotoxins; D005753:Gastric Mucosa / Q000378:metabolism; D020896:Hypovolemia / Q000503:physiopathology*; D007583:Jejunum / Q000378:metabolism*; D009569:Nitric Oxide / Q000096:biosynthesis*; D010101:Oxygen Consumption; D012039:Regional Blood Flow; D018805:Sepsis / Q000503:physiopathology*; D013152:Splanchnic Circulation; D013552:Swine
chemical_list: D004731:Endotoxins; D009569:Nitric Oxide