title: Cerebrovascular relaxation responses to endothelium-dependent and -independent vasodilators after normothermic and hypothermic cardiopulmonary bypass in the rabbit.
abstract: BACKGROUND
  Cardiopulmonary bypass causes activation of leukocytes and increased concentrations of proinflammatory mediators, which may result in endothelial dysfunction. Because hypothermia attenuates many inflammatory processes, the authors hypothesized that hypothermic cardiopulmonary bypass would be associated with better endothelial function than normothermic cardiopulmonary bypass.
  
  
  METHODS
  Isoflurane-anesthetized New Zealand White rabbits were randomized to undergo 90 min of either normothermic (37 degrees C, n=9) or hypothermic (27 degrees C, n=9) cardiopulmonary bypass with terminal rewarming. A third group served as anesthetized normothermic non-cardiopulmonary bypass surgical controls (n=8). Basilar artery and descending thoracic aorta were isolated from each animal. In vitro vessel relaxation responses to increasing concentrations of acetylcholine (which induces endothelial release of nitric oxide) and nitroprusside (which provides exogenous nitric oxide) were measured in phenylephrine-precontracted vessel rings.
  
  
  RESULTS
  There were no differences in vessel relaxation responses between normothermic and hypothermic cardiopulmonary bypass groups in basilar artery or aorta. In contrast, basilar arteries from non-cardiopulmonary bypass controls had increased relaxation responses to both acetylcholine (P=0.004) and nitroprusside (P=0.031) compared with the pooled cardiopulmonary bypass animal data.
  
  
  CONCLUSIONS
  The authors observed no differences in endothelial or vascular smooth muscle function between normothermic and hypothermic cardiopulmonary bypass groups. Compared with non-cardiopulmonary bypass controls, cardiopulmonary bypass appeared to decrease basilar artery smooth muscle relaxation in response to endogenous and exogenous nitric oxide.
authors.affiliation: Department of Anesthesia, University of Iowa, College of Medicine, Iowa City, USA. Brad_Hindman@uiowa.edu
authors.forename: B J
authors.initials: BJ
authors.lastname: Hindman
authors.forename: S
authors.initials: S
authors.lastname: Enomoto
authors.forename: F
authors.initials: F
authors.lastname: Dexter
authors.forename: J N
authors.initials: JN
authors.lastname: Bates
authors.forename: G
authors.initials: G
authors.lastname: Aldape
authors.forename: J
authors.initials: J
authors.lastname: Cutkomp
authors.forename: T
authors.initials: T
authors.lastname: Smith
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D001013:Aorta, Thoracic / Q000187:drug effects / Q000502:physiology; D001488:Basilar Artery / Q000187:drug effects / Q000502:physiology; D002315:Cardiopulmonary Bypass / Q000379:methods*; D004730:Endothelium, Vascular / Q000187:drug effects / Q000502:physiology*; D006979:Hyperthermia, Induced; D066298:In Vitro Techniques; D009126:Muscle Relaxation / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011817:Rabbits; D014665:Vasodilator Agents / Q000494:pharmacology*
chemical_list: D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine; D000109:Acetylcholine