title: Changes in mesenteric vascular reactivity and inflammatory response after cardiopulmonary bypass in a rat model.
abstract: BACKGROUND
  Mesenteric ischemia and acidosis leading to intestinal ischemia has been observed during cardiopulmonary bypass (CPB) despite normal flow in the mesenteric vessels. The aim of this study was to assess mesenteric endothelium-dependent reactivity and vasoconstrictor responses of small mesenteric arteries in a rat model of CPB without aortic cross-clamping.
  
  
  METHODS
  After femoral cannulation a partial 90 minutes CPB was performed with hemodynamics and blood gas parameters monitoring. Blood samples and segments of small mesenteric arteries were obtained in rats sacrificed 2.5 hours (CPBH2.5) or 6 hours (CPBH6) after femoral cannulation. Sham surgery (sham H2.5, sham H6) was performed with femoral cannulation only. Segments of small mesenteric arteries were placed in a myograph in order to assess the contractile response to phenylephrine (with or without NO synthase inhibitor) or the endothelium-dependent relaxation to acetylcholine. Systemic inflammation was evaluated by measuring plasma concentrations of TNFalpha. Pulmonary and intestinal infiltration of activated leukocytes was assessed by immunohistochemistry.
  
  
  RESULTS
  CPB induced increased contractile response to phenylephrine which persisted after blockade of NO synthesis as well as transient impairment of endothelium-dependent relaxations. CPB also led to early and marked release of TNFalpha.
  
  
  CONCLUSIONS
  CPB was responsible for mesenteric endothelial dysfunction and direct increase in the contractile response to alpha1-adrenergic agonist with increased systemic inflammatory response. This phenomenon might contribute to an increase in the risk of mesenteric ischemic events during cardiac surgery especially when vasopressor agents are used.
authors.affiliation: Department of Thoracic and Cardiovascular Surgery, Rouen University Hospital, Rouen, France.
authors.forename: Fabien
authors.initials: F
authors.lastname: Doguet
authors.forename: Pierre-Yves
authors.initials: PY
authors.lastname: Litzler
authors.forename: Fabienne
authors.initials: F
authors.lastname: Tamion
authors.forename: Vincent
authors.initials: V
authors.lastname: Richard
authors.forename: Marie-France
authors.initials: MF
authors.lastname: Hellot
authors.forename: Christian
authors.initials: C
authors.lastname: Thuillez
authors.forename: Alfred
authors.initials: A
authors.lastname: Tabley
authors.forename: François
authors.initials: F
authors.lastname: Bouchart
authors.forename: Jean Paul
authors.initials: JP
authors.lastname: Bessou
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000502:physiology; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D007082:Ileum / Q000098:blood supply; D066298:In Vitro Techniques; D008297:Male; D008638:Mesenteric Arteries / Q000502:physiology; D008641:Mesenteric Vascular Occlusion / Q000175:diagnosis / Q000209:etiology; D019335:Nitroarginine / Q000494:pharmacology; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D051381:Rats; D017208:Rats, Wistar; D013152:Splanchnic Circulation; D018746:Systemic Inflammatory Response Syndrome / Q000175:diagnosis / Q000209:etiology* / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014661:Vasoconstriction / Q000187:drug effects; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014664:Vasodilation / Q000187:drug effects
chemical_list: D014409:Tumor Necrosis Factor-alpha; D014662:Vasoconstrictor Agents; D009599:Nitroprusside; D010656:Phenylephrine; D019335:Nitroarginine; D000109:Acetylcholine