Inherited portosystemic shunts occur in 2 to 3 per cent of Irish wolfh
ounds and are associated with high venous ammonia concentrations and s
igns of hepatic encephalopathy. Moreover, the vast majority of Irish w
olfhound pups without signs of hepatic encephalopathy have moderate hy
perammonaemia. The aim of this study was to investigate whether the in
creased ammonia levels in these clinically healthy dogs are caused by
low-grade portosystemic shunting, and whether the hyperammonaemia pers
ists in adulthood. The fasting venous ammonia concentration and the fr
action of portal blood by-passing the liver, expressed as the shunt in
dex (SI) were measured in 42 Irish wolfhound pups, and the dogs with h
igh SI values were examined post mortem. The ammonia concentration was
also measured in 25 adult Irish wolfhounds in which it had been measu
red when they were seven to eight weeks old. Eleven of the 42 pups had
a portosystemic shunt, as evidenced by a high SI (mean 0.82, range 0.
12 to 1.00, normal range 0.01 to 0.05) and by post mortem examination.
Their mean ammonia concentration was 249 mu mol/litre (range 121 to 3
50). The 31 pups with a normal SI (mean 0.025, range 0.00 to 0.05) had
a mean ammonia concentration of 93 mu mol/litre (range 51 to 125). In
the 25 dogs in which the ammonia concentration was measured twice, th
e mean concentration at seven to eight weeks of age was 77 mu mol/litr
e (range 47 to 115) and in the adults it was 17 mu mol/litre (range 6
to 27) at a mean age of 3.1 years (range 1.0 to 8.9). These results sh
ow that Irish wolfhounds with ammonia concentrations >125 mu mol/litre
had a portosystemic shunt, whereas the hyperammonaemia in dogs with a
mmonia concentrations <120 mu mol/litre was transient and of metabolic
origin.