Role of Toxins and Synergism in Hepatic Encephalopathy

摘要: The foremost hypothesis of pathogenesis hepatic encephalopathy recognizes that in failure, toxins with coma-inducing potential accumulate and depress neuronal function by affecting fundamental neurophysiologic processes such as postsynaptic inhibition excitation, metabolic mitochondrial electron transfer microsomal Na+, K+-ATPase activity. While accumulating, the interact synergistically each other various augmenting endogenous abnormalities to intensify their cellular effects. Specific both failure induce coma experimental animals are ammonia, methanethiol, fatty acids, phenols (Figure 1). By interacting synergistically, they have neurological effects out proportion individual abnormalities. Of these toxins, ammonia is most important has cumulative evidence for its role an etiologic factor. However, relative importance toxin may vary pathologic process.