A light and electron microscopic study of experimental portal-systemic (ammonia) encephalopathy. Progression and reversal of the disorder.
A sequential light and electron microscopic study of cerebral cortex was performed in a rat model of portal-systemic encephalopathy produced by creating a portacaval shunt and followed by ammoniate resin feedings. Prior to coma, astrocytes were characterized ultrastructurally by marked cytoplasmic enlargement, proliferation of mitochondria and endoplasmic reticulum, and an accumulation of cytoplasmic glycogen. The Alzheimer type II astrocyte change was seen only in coma and was characterized ultrastructurally by additional hydropic and degenerative mitochondrial and nuclear changes. Attempts at reversal of the encephalopathy were successful only if ammoniated resin feedings were discontinued prior to coma. Results suggest (1) that the astrocyte response initially reflects an ammonia-induced increased metabolic activity in that cell; (2) that subsequently a gliopathy develops having the light microscopic appearance of the Alzheimer type II change; and (3) that the Alzheimer type II astrocyte change may be responsible for an irreversible clinical course in this experimental condition.
D000544:Alzheimer Disease / Q000473:pathology; D000641:Ammonia; D000818:Animals; D001253:Astrocytes / Q000648:ultrastructure; D002540:Cerebral Cortex / Q000473:pathology; D003593:Cytoplasm / Q000648:ultrastructure; D004721:Endoplasmic Reticulum / Q000648:ultrastructure; D006501:Hepatic Encephalopathy / Q000139:chemically induced / Q000473:pathology*; D006801:Humans; D008928:Mitochondria / Q000648:ultrastructure; D011167:Portacaval Shunt, Surgical; D011168:Portal System / Q000473:pathology; D051381:Rats
D000641:Ammonia