Abstract 2502: Cardioprotection via Pretreatment With Periodic Acceleration (pGz )in a Model of Asphyxia Induced Cardiac Arrest in Rats and Activation of Akt/eNOS/NO Pathway
Whole body periodic acceleration (pGz) is a method which moves the body in a repetitive head to foot motion adding pulses to the circulation and increasing pulsatile shear stress to the endothelium. pGz increases endothelial nitric oxide and its enzyme (eNO, eNOS) and releases other endothelial products. pGz as a method of resuscitation in swine decreases post-resuscitation myocardial stunning and blunts rises in indices of tissue injury. Pretreatment with pGz in the same model decreases post- resuscitation arrhythmias, myocardial stunning and suppresses markers of tissue injury. pGz can also be applied in small animal models; its optimal frequency and motion distance have been determined in rats. The rat asphyxia cardiac arrest (ACA) and resuscitation model is a model to assess the effects of whole body ischemia reperfusion injury. We hypothesized that pretreatment with one hour of pGz in rats undergoing ACA could ameliorate post-resuscitation myocardial dysfunction. Male rats (n=10) (320±25 g weight) were anesthetized, tracheally intubated and ventilated with room air, instrumented to measure hemodynamics and randomized to receive 60 min of pGz (pre-pGz) or no treatment (CONT) prior to ACA. Asphyxia was induced by paralysis and discontinuing mechanical ventilation for 5 min. Resuscitation was started by restarting ventilatory support, administering epinephrine and sodium bicarbonate and manual chest compression until return of circulation (ROSC) or 3 min. Four hours after ROSC, myocardial tissue harvested for immunoblotting. ROSC occurred in 3 of 5 (60%) in CONT, and 5 of 5 (100%) pre-pGz. Protein immunoblotting for the Akt/NOS pathway showed 53%, and 6% higher levels of eNOS and phosphorylated-eNOS and 21% and 8% higher Akt and phosphorylated-Akt respectively in pre-pGz compared to CONT. In a rat model ACA, pGz pretreatment ameliorates acute post-resuscitation dysfunction and up-regulates activation of the Akt/NOS pathway.