Håkan Kasström

Nutrition, weight gain and development of hip dysplasia. An experimental investigation in growing dogs with special reference to the effect of feeding intensity.

Thirty-one dogs from 5 litters with a high parental frequency of hip dysplasia were used in the investigation. Each litter was split in two groups, of which one was put on a high caloric intake, the other one on a low caloric intake. Each member of a group had a paired litter mate in the other group. The litter mates were paired on the basis of the result of a palpatory examination of the hip joints before 12 weeks of age. If possible, paired mates were of the same bodyweight at the time of palpation, and of the same sex. In the groups made up of pups from 3 of the litters, the protein intake was kept at an optimal level, regardless of the amount of calories given. It was found that hip dysplasia was more frequent, occurred earlier, and became more severe in the dogs with a rapid weight gain caused by increased caloric intake than in the dogs which had a low weight gain because of restricted feeding. The final diagnosis was closer correlated with feeding and weight gain than with tightness or laxity of the hip joints before 12 weeks of age.

Growth and Mitotic Rate of the Proximal Tibial Epiphyseal Plate in Hypophysectomized Rats Given Estradiol and Human Growth Hormone

Hypophysectomized female immature albino rats were injected with HGH, HGH and estradiol, or estradiol solely. Some animals were left as controls. All animals were killed on day 3 or 5 of the experiment. One hour before sacrifice, the animals were flash labelled with tritiated thymidine. The following parameters were registered: labelling index, thickness of the growth plate, weight gain, and size of the uterus. The following conclusions were drawn. 1. Estradiol decreases the mitotic rate and retards growth of the epiphyseal cartilage. Its effect on the mitotic rate is more pronounced than its effect on the thickness of the tibial epiphyseal plate. 2. HGH increases the mitotic rate and promotes growth of the epiphyseal cartilage. Its effect on the thickness of the epiphyseal plate is more pronounced than its effect on the mitotic rate. 3. Estradiol decreases the mitotic rate even in the presence of HGH. 4. Estradiol seems to have a direct effect on mitosis of the chondrocytes.

Plasma Levels of Estradiol and Plasma Protein Binding of Sex Steroids in Dogs

Peripheral plasma levels of estradiol were determined in 39 dogs of three breeds (Greyhound, German Shepherd, Golden Retriever). Blood samples were collected weekly from 3 weeks up to 17--21 weeks of age. The pups from all three breeds had mean levels of estradiol varying between 4--8 pg/ml. The lowest levels were found in pups which developed hip dysplasia. There was a significant difference (0.01 less than p less than 0.005) between the estradiol levels of German Shepherd pups with normal and dysplastic hip joints. In female Greyhounds, the peripheral plasma levels of estradiol were examined from 17 weeks of age through the first heat. No increase of the estradiol level was seen with increasing age. The ability of dog plasma to bind dihydrotestosterone (DHT) and estradiol was examined in three dogs. It was found that there are at least three types of binding components for DHT: one with high affinity and extremely low capacity, which is heat labile, another which is also heat labile but has a high capacity and low affinity, and a third which appears to be albumin. Estrogen administration to the three dogs lowered the binding of DHT. It was concluded that it is most unlikely that hyperestrogenism is an etiologic factor in canine hip dysplasia. Unphysiologically high doses of estradiol have been used for experimental induction of hip dysplasia. There is a possibility that the levels of plasma proteins, which bind steroids, could be of importance for the etiology of hip dysplasia. A low plasma level of estradiol could be biologically highly significant if there is a low level of a specific binding protein.