2019-08-222019-08-222014-032014-02-03https://hdl.handle.net/20.500.12503/26970Research Appreciation Day Award Winner - 2014 Texas College of Osteopathic Medicine Awards - 3rd Place Student Research AwardPurpose (a): Cardiac arrest, a leading cause of death in the U.S., kills >90% of its victims, and survivors often are disabled by permanent brain injury inflicted by ischemia-reperfusion. Purkinje cells of the cerebellum and CA1 neurons of the hippocampus are especially vulnerable to post-ischemic neuronal death. We tested the hypothesis that cardiac arrest in a swine model caused delayed neuronal death. Methods (b): Yorkshire swine (25-35 kg) were subjected to cardiac arrest-resuscitation (n = 9) or non-arrest sham (n = 5) protocols. Ventricular fibrillation was induced by electrical pacing. Precordial compressions (100/min) were given at 6-10 min arrest, and then sinus rhythm was restored with transthoracic countershocks. NaCl was infused iv at 0.1 mmol/kg/min during CPR and the first 60 min after return of spontaneous circulation (ROSC). At 7 d ROSC, brain regions were fixed in 4% paraformaldehyde and H&E stained. Results (c): More than 70% of the Purkinje cells were shrunken, lacked dendrites and displayed condensed cytoplasm at 7 d ROSC; in contrast, in shams the majority of Purkinje cells retained the characteristic thick dendrites and well-defined nuclei. Conclusions (d): Thus, cardiac arrest-resuscitation produced marked changes in cerebellar neurons evident 7d after acute insult.encardiac arrestneuroprotectionischemia-reperfusionposter