Hepatic encephalopathy: An approach to its multiple pathophysiological features

Figure 1 Changes induced by hyperammonemia (modified)[183]. NMDA: N-methyl-D-aspartate; LTP: Long term potentials.

Figure 2 Interaction of oxidative stress, astrocyte swelling and cerebral ammonia toxicity. PTN: Protein tyrosine nitration (reproduced with permission)[64]. NMDA: N-methyl-D-aspartate; ROS: Reactive oxygen species.

Figure 3 Proposed sequences that finally induce changes in the long term potentials, which is down regulated in hyperammonemia (modified from Lynch[182]). AMPA: α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor; NMDA: N-metil D-aspartato; mGlu: Metabotropic glutamate receptors; PI-3K: Phosphatidylinositol 3-kinases; PKA and PKC: Protein kinase A and C; CaMKII: Ca²⁺/calmodulin-dependent protein kinases II.