Cerebral oxygen consumption in experimental hepatic encephalopathy: different responses in astrocytes, neurons, and synaptosomes.
Oxygen consumption was measured polarographically in fractions enriched in astrocytes or neurons, and in synaptosomes derived from rats in which two subsequent stages of acute hepatic encephalopathy were induced by thioacetamide treatment. A 30% decrease of oxygen consumption was noted in astrocytes from animals with coma, well in agreement with the decrease of whole cerebral oxygen consumption and the increase of whole brain ammonia. In contrast, at the same stage the oxygen consumption in neurons was increased by some 35%, whereas synaptosomes remained unaffected. The results are in keeping with the view that astrocytes are the cells whose metabolism is primarily affected during hepatic encephalopathy. On the other hand, they support recent pathophysiologic evidence that ammonia-induced neuronal dysfunction is not a consequence of impaired energy metabolism in the nerve cells.
D000818:Animals; D001253:Astrocytes / Q000378:metabolism*; D001921:Brain / Q000378:metabolism*; D005260:Female; D006501:Hepatic Encephalopathy / Q000378:metabolism*; D009474:Neurons / Q000378:metabolism*; D010100:Oxygen / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D013574:Synaptosomes / Q000378:metabolism*
D010100:Oxygen