PubMed1985
The relations between an effect of ammonia on postsynaptic inhibition, the amount of ammonium acetate i.v. to obtain this effect, and the tissue concentrations of NH4+ and glutamine were investigated in the cerebral cortex of cats without and with portacaval shunts. Normal cats required 2.43 mmol/kg ammonium acetate to affect postsynaptic inhibition. Cerebral NH4+ and glutamine increased from 0.21 mumol/g to 0.77 mumol/g and from 2.92 mumol/g to 5.54 mumol/g, respectively. In portacaval shunted cats, postsynaptic inhibition was normal in spite of increases of NH4+ and glutamine to 1.37 mumol/g and 14.28 mumol/g, respectively. Only 0.7 mmol/kg of ammonium acetate were sufficient to affect postsynaptic inhibition. This was associated with a statistically insignificant increase of NH4+ to 1.61 mumol/g and no change of glutamine. A chronic portasystemic shunt markedly increases the tolerance of postsynaptic inhibition to NH4+. However, postsynaptic inhibition becomes very sensitive to an acute systemic ammonia load and the associated increase of tissue NH4+ in the cerebral cortex. These observations help to understand the pathogenesis of the encephalopathy precipitated in patients with portasystemic shunts by an acute systemic ammonia load such as resulting from a gastrointestinal hemorrhage.