Effect of ammonia intoxication on cerebral blood flow, its autoregulation and responsiveness to carbon dioxide and papaverine.

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Abstract
Cerebral blood flow (CBF) was measured in anaesthetised cats with 133Xe clearance method under normal conditions and with hyperammonaemia. Elevation of blood ammonia concentration by an intravenous infusion of ammonium acetate caused an increase in CBF and a parallel decrease in cerebrovascular resistance (CVR). These parameters reached, however, plateau at an arterial blood ammonia level exceeding 500 mumol/l. Cerebrovascular reactivity to CO2 diminished following elevation of blood ammonia concentration and at arterial blood ammonia level exceeding 500 mumol/l it was virtually abolished. In contrast, hyperammonaemia influenced neither cerebrovascular responsiveness to papaverine nor autoregulatory properties of the cerebral circulation. It is concluded, therefore, that hyperammonaemia exerts some dilatatory effect on cerebral vessels and severely impairs chemical regulation of CBF but does not elicit cerebral vasomotor paralysis.