Cardiac arrest (CA) affects over 300,000 Americans annually and results in severe brain injury (impaired motility, memory loss, or death) due to poor recovery. Over stimulation of glutamatergic N-methyl-D-aspartate receptor (NMDAR) channel activation, allows Ca² ions to enter cells, triggers a cascade of excitotoxic events and eventual neuronal death, but down-regulation of NMDAR post arrest may contribute to progressive injury. Previous studies have indicated that NMDARs are down-regulated within hours to days after resuscitation, therefore re-stimulation of NMDARs after CA should improve neurological outcome. The purpose of this thesis was to: 1.) Implement an in vivo asphyxial CA (ACA) rat model at UAF to reproduce CA seen clinically in prenatal/pediatric populations, and 2.) Test the hypothesis that partial NMDAR agonist (D-cycloserine, DCS) would improve recovery from neuronal injury. Male Sprague Dawley rats (250-330g) were administered a low dose of DCS (10mg/kg, IP) 24 and 48hr after resuscitation from either 6 or 8-min ACA. Behavioral Neurological Deficit Scores (NDS) were taken at 2hr and daily for 7 days after ACA to assess injury. Histopathology assessed CA1 hippocampal neuronal injury. DCS had no effect on neurological improvement but the ACA model produced significant brain injury in rats regardless of CA duration.
Thesis (M.S.) University of Alaska Fairbanks, 2013
Table of Contents
Chapter 1. General introduction to excitotoxic effects resulting from cerebral ischemia -- Chapter 2. Health implications and technique assessment of an asphyxial cardiac arrest (ACA) rat model transferred to the University of Alaska, Fairbanks (UAF) from the University of Miami School of Medicine -- Chapter 3. D-Cycloserine (DCS) activiation of N-methyl-D-aspartate receptors (NMDAR) 24 & 48hr after asphyxial cardiac arrest (ACA) has no effect on hippocampal CA1 neurological deficits -- Chapter 4. General conclusion -- Appendices.
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