EXPERIMENTAL STUDIES ON THE PATHOGENESIS OF KERNICTERUS

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Abstract
The effect of bilirubin on cellular energy metabolism has been studied in vitro. Bilirubin inhibits oxidative phosphorylation in isolated rat-liver and brain mitochondria, with a depression of the underlying respiration as a concomitant phenomenon. The latter effect can be prevented by the addition to the mitochondrial suspensions of diphosphopyridine nucleotide and cytochrome C. In experiments with rabbits in vivo it has been shown that the penetration of bilirubin from blood into central nervous system is greatly enhanced by intracisternal treatment with p-chloromercuribenzoate, an agent which inhibits the function of the blood-brain barrier system. The increase of the concentration of bilirubin in the cerebrospinal fluid upon treatment with p-chloromercuribenzoate is parallelled by an equal increase of the total protein content. The bearing of these findings on the pathogenesis of kernicterus, and some of the clinical implications are discussed.

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