title: Mesenteric endothelial dysfunction in a cardiopulmonary bypass rat model: the effect of diabetes.
abstract: BACKGROUND
  Diabetes is a risk factor for perioperative complications after cardiac surgery. We studied its effects on mesenteric endothelial function in a cardiopulmonary bypass (CPB) model.
  
  
  METHODS
  Forty Wistar rats were divided into four groups: sham (D-CPB-), cardiopulmonary bypass (D-CPB+), diabetic (D+CPB-) and diabetic that have undergone CPB (D+CPB+). Two samples of mesenteric artery were used for nitric oxide synthase (NOS) Western blot analysis, and two others for assessing contractile response and endothelium relaxations. Nitrite products and tumour necrosis factor-alpha (TNF-α) were assessed as markers of inflammatory response.
  
  
  RESULTS
  We observed an enhanced contractile response to the α-adrenergic agonist associated with impairment of mesenteric vasorelaxation in D+CPB+ rats. Western immunoblot analysis of D+CPB+ highlighted an additive effect of hyper-expression of inducible NOS. A significantly increased inflammatory response was observed after CPB in diabetic animals.
  
  
  CONCLUSIONS
  This work confirms the potential deleterious impact of diabetes on the mesenteric endothelium during CPB in cardiac surgery.
authors.affiliation: Department of Thoracic and Cardiovascular Surgery, Rouen University Hospital, France.
authors.forename: Vincent
authors.initials: V
authors.lastname: Le Guillou
authors.forename: Fabienne
authors.initials: F
authors.lastname: Tamion
authors.forename: Isabelle
authors.initials: I
authors.lastname: Jouet
authors.forename: Vincent
authors.initials: V
authors.lastname: Richard
authors.forename: Paul
authors.initials: P
authors.lastname: Mulder
authors.forename: Jean Paul
authors.initials: JP
authors.lastname: Bessou
authors.forename: Fabien
authors.initials: F
authors.lastname: Doguet
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D003921:Diabetes Mellitus, Experimental / Q000097:blood / Q000150:complications* / Q000503:physiopathology; D004305:Dose-Response Relationship, Drug; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology*; D018836:Inflammation Mediators / Q000097:blood; D008297:Male; D008638:Mesenteric Arteries / Q000378:metabolism / Q000503:physiopathology*; D009213:Myography; D052247:Nitric Oxide Synthase Type II / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism; D009573:Nitrites / Q000097:blood; D051381:Rats; D017208:Rats, Wistar; D014409:Tumor Necrosis Factor-alpha / Q000097:blood; D015854:Up-Regulation; D014661:Vasoconstriction; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: D018836:Inflammation Mediators; D009573:Nitrites; D014409:Tumor Necrosis Factor-alpha; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D052247:Nitric Oxide Synthase Type II; D052250:Nitric Oxide Synthase Type III; C496318:Nos2 protein, rat; C496316:Nos3 protein, rat