Blood plasma levels of progesterone and oestradiol in the dog during the oestrous cycle and pregnancy.

Plasma oestradiol and progesterone levels were studied in German Shepherd and Greyhound bitches during the normal oestrous cycle, pregnancy and at parturition. The mean oestradiol level increased from approximately 7 to 13 pg/ml during the fifth week before onset of oestrus. Oestradiol stayed at this level until pro oestrus which was characterized by a steady increase to a mean peak level of about 30 pg/ml 5-6 days before oestrus. At the start of oestrus the level was approximately 12 pg/ml. A level between 10-15 pg/ml was kept during the following 10 weeks whether or not the bitch was pregnant and no change occurred at parturition. The mean progesterone level was found to be very low, around or under 1 ng/ml, until 1-4 days after the oestradiol peak after which the level gradually increased to around 10 ng/ml at the start of oestrus. During oestrus and metoestrus or pregnancy the pattern was inconsistent. In some bitches the level gradually increased during 3-4 weeks and reached a peak value of 30-50 ng/ml. The level then gradually decreased during 5-6 weeks. During the first 5 weeks of the same period progesterone in other bitches fluctuated between similar maximum levels and extremely low levels. After the fifth week the pattern was the same for all bitches. In the pregnant bitches there was a significant drop of the progesterone level at parturition. The data suggest that the dog is not an ideal test animal for steroids synthetized for use in man.

Metabolism of estradiol in greyhounds and German shepherd dogs. An investigation with special reference to hip dysplasia.

Metabolism of estradiol was investigated in 5 dogs, 3 female Greyhounds with radiographically perfect hip joints and 2 female German Shepherd dogs with hip dysplasia (one pregnant and the other non-pregnant). One of the Greyhounds was studied both when pregnant and non-pregnant. The non-pregnant dogs were injected with C14-labelled estradiol-17beta i.v. and 5 mg estradiol-17beta benzoate i.m. The pregnant dogs were given only radiolabelled estradiol-17beta. Twenty-four-hour-specimens of urine were collected from the dogs for 6--8 days. Determination of urinary estrone, estradiol-17beta, and estriol was made. It was found that most of the injected estradiol was excreted unmetabolized in all dogs. A significant amount of the injected estradiol was converted to estrone and a small amount to estriol. There was no significant difference in the excretion patterns of estrone, estradiol, and estriol between the Greyhounds with perfect hip joints and the German Shepherds with hip dysplasia, regardless whether the dogs were pregnant or not. The conclusion was drawn that the capacity of dogs with hip dysplasia to metabolize estradiol and to eliminate estradiol and metabolites is not impaired.

Plasma levels of estradiol and plasma protein binding of sex steroids in dogs. An investigation with special reference to development of hip dysplasia in growing individuals.

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.

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.

Growth and remodeling of the hip joint and proximal femur in adolescent dogs. A scintimetric investigation with special reference to hip dysplasia and estradiol induced changes.

The uptake of 85Sr was shown to be higher in dysplastic hip joints than in normal joints of adolescent dogs. This was interpreted as a sign of increased remodeling. In contrast, the uptake of 85Sr in the growth plate and metaphysis of the proximal femur was lower in dogs with hip dysplasia than in dogs with normal hip joints. This was interpreted as a sign of retarded growth of the proximal femur (more advanced skeletal maturation). Greyhounds of bitches, which were injected with estradiol during pregnancy, also showed retarded growth of the proximal femur. This was interpreted as a late effect of estradiol.