Following the hypothesis that metabolic screens may be useful tools in the diagnosis of canine aggression we have investigated the blood plasma amino acid levels of dogs which have been found aggressive (N = 10) against dogs or men in comparison to non-aggressive dogs (N = 10). In summary, the aggressive dogs showed elevated plasma concentrations of the neurophysiological active aromatic amino acids tryptophan (46/171 micromol/l, p < 0,001), tyrosine (38/67 micromol/l, p < 0.01) and histidine (74/91 micromol/l, p < 0.01) and lower lysine concentrations (175/151 micromol/l, p < 0.05), which seems to point to a stress situation of these dogs. The nitrogen metabolism is impaired in the urea-cycle in the conversion of ornithine (17/34 micromol/l, p < 0.01) to citrulline (64/47 micromol/l). Higher levels of branched chain amino acids, especially leucine (122/150 micromol/l, p < 0.01), mainly metabolized in muscles, and isoleucin (60/71 micromol/l, p < 0.05) show a high energy potential. The acidose-stimulator methionine (48/78 micromol/l, p < 0.01) proved elevated. The results show that the changed behavior in the aggressive dogs is also reflected in their free amino acid plasma concentrations, independent of the question whether these data are the cause or the result of the aggressivity.
In order to test the hypothesis of zinc-deficiency as a factor in canine aggression, we examinated sera of dangerously aggressive dogs and of behaviourally normal (nonaggressive) dogs for their zinc-contents. The results showed distinctly higher zinc-concentrations (mean +/- SD) in aggressive dogs (1,69 +/- 0,49 mug/ml) than in normal non aggressive dogs (0,76 +/- 0,16 mug/ml).
The determination of the fate of a compound following administration can be performed using the disposition method with 14C-labeled substances, which also allow the measurement of metabolism with CO2 as an expired end product. To substitute the laborious CO2-collection in washing bottles as carbonate a simple instrumentation was built for continuous 14CO2-measurement. The air from the metabolic cage is led in thin layer through a chamber fitted to a foot-monitor, the output of which is online for computation. The instrument is sensitive and calibration is easy.
In the present investigation experiments have been made on the modification of the teratogenesis by a Mycoplasma pulmonis infection in rats. Substances with known teratogenic effects (Actinomycin D, Cyclophosphamide) were used. Groups of artificially infected pregnant rats were compared with pregnant rats from the SPF unit. The present study has shown that in the group of artificially infected animals no significant increase of the teratogenic effects by Actinomycin was found. In the Cyclophosphamide-treated groups more and more serious malformations have been observed in relation to dose and day of treatment.
Transfer of laboratory animals from the breeder to the experimental unit includes in most cases a change of the microbial environment even under SPF-conditions. Many experimental treatments may also disturb the balance between host and microbial load and provoke infections. With the aim to detect such undesired effects in the course of the experiment the suitability of the leukergy test was investigated. SPF-rats, endotoxin-treated rats, and conventionalized germ-free rats were checked for leukocyte agglomeration, and the findings were compared with total leukocyte number, blood picture, endotoxin content in the blood and body temperature. A rise of leukergy from 10 to more than 20% was recorded in endotoxin-treated and conventionalized rats.