title: Periodic acceleration (pGz) prior to whole body ischemia reperfusion injury provides early cardioprotective preconditioning.
abstract: OBJECTIVE
  Periodic acceleration (pGz) is a method that applies repetitive sinusoidal head-to-foot motion to the horizontally positioned body. pGz adds pulses to the circulation as a function of frequency, thereby increasing shear stress to the endothelium. Pulsatile shear stress increases release of cardioprotective endothelial-derived nitric oxide prostaglandin E-2 and prostacyclin into the circulation. We investigated whether pGz may be effective as an early preconditioning strategy when applied one hour prior to whole body ischemia reperfusion injury induced by ventricular fibrillation (VF).
  
  
  METHODS
  Twenty anesthetized and paralyzed male swine were randomized to one hour of pGz and conventional mechanical ventilation [PC] or solely conventional mechanical ventilation [Control] prior to VF and resuscitation. After eight minutes of unsupported VF, cardiopulmonary resuscitation was carried out followed by defibrillation. Hemodynamics, electrocardiogram, echocardiogram, regional blood flows, and markers of global myocardial injury were measured. Protein expression of endothelial-derived nitric oxide synthase (eNOS), phosphorylated eNOS (p-eNOS), serine/threonine kinase Akt total (t-Akt), and phosphorylated (p-Akt) were determined by immunoblotting.
  
  
  RESULTS
  All animals had spontaneous return of circulation after cardiopulmonary resuscitation (CPR) and defibrillation. Preconditioned animals had less hemodynamically significant arrhythmias, less myocardial stunning, and greater regional blood flows to the brain, heart, kidneys, and ileum than Controls. Troponin I and creatine phosphokinase values in PC were 65% of the values present in Controls. In addition, preconditioned animals had higher protein expression of cardiac eNOS, p-eNOS, t-Akt, and p-Akt than Controls.
  
  
  CONCLUSIONS
  pGz preconditioning confers early cardioprotection in a model of whole body ischemia reperfusion injury.
authors.affiliation: Mt Sinai Medical Center, Division Neonatology, Miami Beach, FL 33140, USA. tony@msmc.com
authors.forename: Jose A
authors.initials: JA
authors.lastname: Adams
authors.forename: Heng
authors.initials: H
authors.lastname: Wu
authors.forename: Jorge A
authors.initials: JA
authors.lastname: Bassuk
authors.forename: Jaqueline
authors.initials: J
authors.lastname: Arias
authors.forename: Arkady
authors.initials: A
authors.lastname: Uryash
authors.forename: Vinod
authors.initials: V
authors.lastname: Jorapur
authors.forename: Gervasio A
authors.initials: GA
authors.lastname: Lamas
authors.forename: Paul
authors.initials: P
authors.lastname: Kurlansky
mesh_terms: D000054:Acceleration; D000818:Animals; D016887:Cardiopulmonary Resuscitation / Q000379:methods; D003402:Creatine Kinase / Q000378:metabolism; D015232:Dinoprostone / Q000378:metabolism; D004554:Electric Countershock; D019157:Ischemic Preconditioning, Myocardial / Q000379:methods*; D008297:Male; D009569:Nitric Oxide / Q000378:metabolism; D052250:Nitric Oxide Synthase Type III / Q000378:metabolism*; D010766:Phosphorylation; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D011897:Random Allocation; D012039:Regional Blood Flow; D015427:Reperfusion Injury / Q000503:physiopathology / Q000517:prevention & control*; D013314:Stress, Mechanical; D013552:Swine; D019210:Troponin I / Q000378:metabolism; D014693:Ventricular Fibrillation / Q000503:physiopathology*
chemical_list: D019210:Troponin I; D009569:Nitric Oxide; D052250:Nitric Oxide Synthase Type III; D051057:Proto-Oncogene Proteins c-akt; D003402:Creatine Kinase; D015232:Dinoprostone