DOI
https://doi.org/10.25772/PE1H-JF64
Defense Date
2009
Document Type
Thesis
Degree Name
Master of Science
Department
Physiology
First Advisor
Steven Shapiro
Second Advisor
Ann Rice
Third Advisor
George Ford
Abstract
In newborns, unconjugated bilirubin (UCB) is not readily excreted, and when bilirubin levels exceed the serum albumin binding capacity, pathological levels of UCB exist. Hyperbilirubinemia may lead to auditory damage and ultimately cause a hearing disorder called auditory neuropathy/dys-synchrony, characterized by absent or abnormal brainstem auditory evoked potentials (BAEPs) with evidence of normal inner ear function assessed by either otoacoustic emissions or cochlear microphonic responses. Phototherapy and double volume exchange transfusion are used as treatment methods for neonatal hyperbilirubinemia. Spontaneously jaundiced Gunn rat pups given sulfadimethoxine to displace bilirubin from serum albumin develop bilirubin encephalopathy and have abnormal BAEPs comparable to human neonates. BAEPs are a noninvasive electrophysiological measure of neural function of the auditory system. High levels of calcineurin activity are believed to be involved in the mechanism of this bilirubin induced auditory neuropathy. FK506, a calcineurin inhibitor, was administered 3 hours prior to sulfa in concentrations of 0.1mg/kg, 1.0mg/kg, and 10.0mg/kg body weight. Due to the observation that all animals had abnormal BAEPs after treatment with FK506 and sulfa, it can be concluded that none of the treatment doses protected against bilirubin induced auditory impairment.
Rights
© The Author
Is Part Of
VCU University Archives
Is Part Of
VCU Theses and Dissertations
Date of Submission
May 2009