title: Inhibition of NF-κB activation by β-glucan is not associated with protection from global ischemia-reperfusion injury in pigs.
abstract: BACKGROUND
  Pretreatment with β-glucan has been shown to protect against regional ischemia-reperfusion injury, through inhibition of myocardial NF-κB activation. The aim was to examine whether β-glucan pretreatment could protect against the global ischemia-reperfusion injury, which is encountered in the clinical setting during open heart surgery.
  
  
  METHODS
  Twenty-one pigs were randomized to pretreatment with oral β-glucan (SBGo, n = 7), pretreatment with i.p. β-glucan (SBGip, n = 7), and untreated controls (n = 7). The pigs were subjected to cardiopulmonary bypass (CPB) with 1 h of global cardioplegic ischemia followed by wean from CPB and reperfusion for 4 h. Cardiac function was determined by a conductance catheter, and troponin T was sampled from the coronary sinus. Atrial biopsies obtained at baseline, following 30 min, and 3 h of reperfusion were analyzed for phosphorylated NF-κB by Western blot.
  
  
  RESULTS
  Following reperfusion, phosphorylated NF-κB increased by 210% in the control group, 197% in the SBGo group, but was reduced by 5% in the SBGip group (P < 0.01 versus control). After 4 h of reperfusion, preload recruitable stroke work dropped by 19% in the control group and 25% in the SBGo group compared with 60% in the SBGip group (P < 0.01 versus control). The area under the curve for troponin T was larger in the SBGip group compared with the control group (P < 0.05) and the SBGo group (P < 0.01).
  
  
  CONCLUSIONS
  Inhibition of NF-κB activation by i.p. β-glucan does not protect against ischemia-reperfusion injury in pigs subjected to global ischemia and reperfusion, and may be associated with aggravation of ischemia-reperfusion injury.
authors.affiliation: Department of Cardiothoracic and Vascular Surgery, University Hospital of North Norway, Tromsø, Norway. erling.johan.aarsaether@unn.no
authors.forename: Erling
authors.initials: E
authors.lastname: Aarsaether
authors.forename: Thor Allan
authors.initials: TA
authors.lastname: Stenberg
authors.forename: Ugo
authors.initials: U
authors.lastname: Moens
authors.forename: Mona
authors.initials: M
authors.lastname: Johannessen
authors.forename: Øyvind
authors.initials: Ø
authors.lastname: Jakobsen
authors.forename: Rolf
authors.initials: R
authors.lastname: Busund
mesh_terms: D000818:Animals; D002315:Cardiopulmonary Bypass / Q000009:adverse effects*; D054326:Coronary Sinus / Q000378:metabolism; D004195:Disease Models, Animal; D006324:Heart Arrest, Induced / Q000009:adverse effects; D015428:Myocardial Reperfusion Injury / Q000378:metabolism* / Q000517:prevention & control*; D016328:NF-kappa B / Q000037:antagonists & inhibitors* / Q000378:metabolism; D010766:Phosphorylation / Q000502:physiology; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D034421:Sus scrofa; D017211:Treatment Failure; D020107:Troponin T / Q000378:metabolism; D016277:Ventricular Function, Left / Q000502:physiology; D047071:beta-Glucans / Q000494:pharmacology*
chemical_list: D016328:NF-kappa B; D020107:Troponin T; D047071:beta-Glucans; D051057:Proto-Oncogene Proteins c-akt