Acute effects of "delayed postconditioning" with periodic acceleration after asphyxia induced shock in pigs

Asphyxia cardiac arrest and shock are models for whole body ischemia reperfusion injury. Periodic acceleration (pGz) achieved by moving the body on a platform is a novel method for inducing pulsatile vascular shear stress and endogenous production of endothelial nitric oxide, prostaglandin E2, tissue plasminogen activator, and adrenomedullin. The aforementioned are cardioprotective during and after ischemia reperfusion injury. We investigated whether pGz, applied 15 min after return of spontaneous circulation (ROSC) would serve as an effective "delayed" post conditioning tactic to lessen acute reperfusion injury markers in a pediatric swine model of asphyxia induced shock. Asphyxia shock was induced in 20 swine weight 3.9 +/- 0.6 kg. Fifteen minutes after ROSC, the animals were randomized to receive conventional mechanical ventilation (CMV, [Control]) or CMV with pGz. All animals had ROSC and no significant differences in blood gases or hemodynamics after ROSC. pGz treated had significantly less myocardial dysfunction post resuscitation, (i.e. better % ejection fraction (EF), % fractional shortening (FS), and wall motion score index) and lower biochemical indices of reperfusion injury (lower TNF-alpha, IL-6, and Troponin I, and myeloperoxidase activity). Delayed postconditioning with pGz ameliorates acute post resuscitation reperfusion injury and improves myocardial dysfunction after asphyxia-induced shock.