Literature DB >> 1480452

Changes in piglet auditory brainstem response amplitudes without increases in serum or cerebrospinal fluid neuron-specific enolase.

T W Hansen1, W J Cashore, W Oh.   

Abstract

We studied the relationship between changes in auditory brainstem responses (ABR) and serum and cerebrospinal fluid levels of neuron-specific enolase (NSE) in hyperbilirubinemic 2- to 8-d-old piglets. Infusion of a stabilized solution of bilirubin resulted in serum bilirubin levels of 571.1 +/- 48.8 mumol/L (mean +/- SEM) after 6 h. ABR were obtained at baseline and then hourly until the piglets were killed. We measured peak amplitudes and latencies for waves I-V, as well as latency for the post-V trough. Changes in amplitudes and latencies were analyzed as slopes because of heterogeneous variances. Over time, a significant reduction was observed in peak II-V amplitudes of bilirubin-infused piglets, but not in those of corresponding controls. No change was observed in latencies. NSE was analyzed by RIA. Serum NSE remained stable throughout the experiment (means 5.1-6.6 micrograms/L) and did not differ between the groups. Cerebrospinal fluid NSE values also remained stable, and no differences that could be ascribed to hyperbilirubinemia were detected. We conclude that hyperbilirubinemia induced significant changes in piglet ABR amplitudes without concomitant evidence of severe neuronal compromise, as might have been indicated by significant increases in serum and/or cerebrospinal fluid NSE levels. This provides further support to the clinical impression that early ABR changes during hyperbilirubinemia may be reversible.

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Year:  1992        PMID: 1480452     DOI: 10.1203/00006450-199211000-00005

Source DB:  PubMed          Journal:  Pediatr Res        ISSN: 0031-3998            Impact factor:   3.756


  5 in total

1.  Neuron-specific enolase, but not S100B or myelin basic protein, increases in peripheral blood corresponding to lesion volume after cortical impact in piglets.

Authors:  Beth A Costine; Patricia B Quebeda-Clerkin; Carter P Dodge; Brent T Harris; Simon C Hillier; Ann-Christine Duhaime
Journal:  J Neurotrauma       Date:  2012-09-27       Impact factor: 5.269

2.  Bilirubin inhibits Ca2+-dependent release of norepinephrine from permeabilized nerve terminals.

Authors:  T W Hansen; S B Mathiesen; I Sefland; S I Walaas
Journal:  Neurochem Res       Date:  1999-06       Impact factor: 3.996

3.  Ex vivo (1)H nuclear magnetic resonance spectroscopy reveals systematic alterations in cerebral metabolites as the key pathogenetic mechanism of bilirubin encephalopathy.

Authors:  Wenyi Hu; Xiaojie Cheng; Xinjian Ye; Liangcai Zhao; Yanan Huang; Huanle Zhu; Zhihan Yan; Xuebao Wang; Xiaojie Wang; Guanghui Bai; Hongchang Gao
Journal:  Mol Brain       Date:  2014-11-26       Impact factor: 4.041

4.  Impairment of enzymatic antioxidant defenses is associated with bilirubin-induced neuronal cell death in the cerebellum of Ugt1 KO mice.

Authors:  G Bortolussi; E Codarin; G Antoniali; C Vascotto; S Vodret; S Arena; L Cesaratto; A Scaloni; G Tell; A F Muro
Journal:  Cell Death Dis       Date:  2015-05-07       Impact factor: 8.469

5.  Moderate Hyperbilirubinemia Alters Neonatal Cardiorespiratory Control and Induces Inflammation in the Nucleus Tractus Solitarius.

Authors:  Marie-Laure Specq; Mélisande Bourgoin-Heck; Nathalie Samson; François Corbin; Christian Gestreau; Maxime Richer; Hazim Kadhim; Jean-Paul Praud
Journal:  Front Physiol       Date:  2016-09-30       Impact factor: 4.566

  5 in total

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