In our experiments, 20 Slovak Merino sheep 36.5 +/- 4.0 kg b.w., aged 3.5 y
ears were used. They were starved 12 h before the experiment and for 6 h af
ter the initial administrations of the agents. Sheep had free access to wat
er throughout the period. Control sheep received in addition to urea (0.5 g
/kg b.w.), an equimolar quantity of 15% nonbuffered glutamic acid solution
and the experimental sheep received the same quantity of sodium hydroxide b
uffered glutamic acid solution. The laboratory indices demonstrated that no
nbuffered glutamic acid in contrast to sodium hydroxide buffered glutamic a
cid was able to protect sheep from ammonia intoxication induced via p.o. ad
ministration of urea (see Tab. I). The experiments demontrated a significan
t trend towards higher concentrations of ammonia (P < 0.01) and lower value
s of pH (P < 0.01) in the rumen fluid and lower concentrations of ammonia i
n the blood (P < 0.01) of sheep with nonbuffered glutamic acid in contrast
to sodium hydroxide buffered glutamic acid, especially 60 min and more afte
r the administration of agents. We did not however register any significant
differences in the dynamics of urea concentrations between both groups of
sheep in blood plasma throughout the period of experiments (P < 0.05). Clin
ical observations of animals demonstrated that sodium hydroxide buffered gl
utamic acid was not able to protect sheep satisfactorily against ammonia in
toxication. Sheep in this group showed some intoxication symptoms and one d
ied, in contrast to sheep in the control group with nonbuffered glutamic ac
id.