Abstract
Aims Cardiac arrest (CA) and resuscitation are models of whole body ischemia reperfusion injury. Interventions performed prior to (pre-treatment) or after (post-treatment) can result in cardioprotection. Myocardial stunning, characterized by microcirculatory and contractile dysfunction after CA, is an important component of the post-cardiac arrest syndrome. Periodic acceleration (pGz), produced by the cyclical motion of the supine body headward to footward, increases microcirculatory blood flow to vital organs and elicits production of endothelial derived cytoprotective factors in normal animals. We tested the hypothesis that application of pGz 30 min after return of circulation from CA, as a delayed post-treatment strategy, would improve regional microcirculatory blood flow to vital organs and functional indices of myocardial stunning in pigs. Methods 8 min of unsupported VF followed by cardiopulmonary resuscitation and defibrillation was carried out in twenty anesthetized and paralyzed male swine who were randomized to delayed post-treatment with pGz (dPost) or none (CONT). pGz was begun 30 min after return of circulation along with conventional mechanical ventilation. Hemodynamics, echocardiogram, and regional blood flows were measured as well as biochemical index of cardiac tissue injury. Results All animals had spontaneous return of circulation after cardiopulmonary resuscitation (CPR) and defibrillation. dPost animals had less myocardial stunning and greater regional blood flows to the heart, brain, kidneys, ileum and stomach than CONT. Post-treatment with pGz blunted the increase in Troponin I produced by CA and resuscitation, and, induced a greater rise in endothelial derived nitric oxide synthase (eNOS) and its phosphorylation (p-eNOS). Conclusions Delayed post-treatment with pGz as a therapeutic strategy, protects against early myocardial stunning in VF cardiac arrest by improving microcirculatory blood flow to the heart and also protects other vital organs by this mechanism.
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