Experimental Bilirubin Encephalopathy: Importance of Total Bilirubin, Protein Binding, and Blood-Brain Barrier View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

1986-08

AUTHORS

Richard P Wennberg, A J Hance

ABSTRACT

The cause of bilirubin encephalopathy has been variously ascribed to elevated total serum bilirubin concentration, high free bilirubin levels (or impaired albumin binding), and disruption of the blood-brain barrier. An experimental rat model for acute bilirubin encephalopathy was developed in which these three factors could be varied independently. Osmotic opening of the blood-brain barrier in the right hemisphere was produced by infusing a hypertonic arabinose solution into the right carotid artery. The total bilirubin level and bilirubin binding state were varied by adjusting the amount of bilirubin infused intravenously and/or by infusing human serum albumin. Brain electrical activity (EEG) served as an indicator of developing encephalopathy. Neither staining nor EEG changes occurred if the blood-brain barrier remained intact. Bilirubin staining without EEG evidence of encephalopathy sometimes occurred when the blood-brain barrier was open. Discriminant analysis showed that EEG changes were best predicted by the degree of blood-brain barrier opening (as indicated by brain bilirubin content) and by the quality of serum bilirubin binding. Serum total bilirubin concentration was not an important discriminator of encephalopathy. More... »

PAGES

pr1986260

Identifiers

URI

http://scigraph.springernature.com/pub.10.1203/00006450-198608000-00018

DOI

http://dx.doi.org/10.1203/00006450-198608000-00018

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1031658655

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/3737293


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