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Delayed neuronal death in swine following cardiac arrest and resuscitation (877.12)
Author(s) -
Nguyen Anh,
Cherry Brandon,
Ryou MyoungGwi,
Williams Arthur,
Hollrah Roger,
Baker Charla,
Choudhury Gourav,
OlivenciaYurvati Albert,
Mallet Robert
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.877.12
Subject(s) - ventricular fibrillation , return of spontaneous circulation , resuscitation , medicine , clinical death , anesthesia , cardiology , cardiopulmonary resuscitation , hippocampus
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. 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. 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. Thus, cardiac arrest‐resuscitation produced marked changes in cerebellar neurons evident 7d after acute insult. Grant Funding Source : NINDS 076975