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Biomedical subjects

A Rijnberk

Publications and source records attributed to A Rijnberk.

At least 109 records · Page 6Linked to original sources
PubMed1987

Medroxy-progesterone acetate administration to ovariohysterectomized, oestradiol-primed beagle bitches. Effect on secretion of growth hormone, prolactin and cortisol.

Growth hormone (GH), prolactin (Prl) and cortisol secretion was studied in 5 ovariohysterectomized dogs before and after oestradiol implantation and medroxyprogesterone acetate (MPA) administration. MPA was given at regular intervals during a period of 10 months in a total of 12 injections. Short-term effects of oestradiol were restricted to significantly enhanced Prl responses to thyrotropin-releasing hormone (TRH). MPA treatment after oestradiol implantation resulted in significantly elevated basal GH levels in all dogs, with a continuing increase in one dog. Only in the latter dog was a significant decrease in basal Prl levels seen. MPA administration did not significantly change Prl responses to TRH. The GH responses to clonidine were significantly reduced at 9 and 16 weeks of oestradiol and MPA treatment. In the one dog which exhibited the greatest rise in basal GH levels, GH responses were completely abolished at 9, 16 and 43 weeks of oestradiol and MPA treatment. TRH never evoked significant GH responses. Both basal and lysine-vasopressin (LVP)-stimulated cortisol levels were significantly suppressed during combined oestradiol-MPA treatment. These findings denote that in the dog. Oestradiol rapidly induces an enhanced Prl response to TRH. The oestradiol-MPA induced GH overproduction is associated with a reduced responsiveness of GH to clonidine and is not accompanied by GH responsiveness to TRH. Oestradiol-MPA treatment suppresses both basal and LVP-stimulated cortisol secretion.

Animals↗
PubMed1987

Systemic availability of o,p'-DDD in normal dogs, fasted and fed, and in dogs with hyperadrenocorticism.

The systemic availability of o,p'-DDD was studied in 12 normal dogs and seven dogs with pituitary-dependent hyperadrenocorticism (PDH). The drug was given by mouth at 50 mg kg-1 and plasma o,p'-DDD concentrations were determined by gas-liquid chromatography. First, six normal dogs were given the drug three times at intervals of one week in a Latin square pattern. Systemic drug availability was found to be very poor from intact tablets in fasted dogs, better with pure drug dissolved in maize oil given by stomach tube, and best with ground tablets mixed in oil poured on dog food. Then six normal dogs and five with PDH were given one dose of o,p'-DDD as intact tablets in dog food. Systemic drug availability was good in the normal animals and, for unknown reasons, better in dogs with PDH. The half-time of elimination was shorter in dogs with PDH than in normal ones. There was evidence of a gradual rise in plasma o,p'-DDD concentrations in seven dogs with PDH treated with 25 mg kg-1 every 12 hours for 14 or 20 days. The interaction between food and o,p'-DDD probably contributes to the variation in clinical response of dogs treated with the drug. The efficiency of therapy with o,p'-DDD should be improved considerably by administering the drug with food.

Administration, Oral↗
PubMed1986

Regulation of prolactin secretion in canine pituitary-dependent hyperadrenocorticism.

In 15 dogs with pituitary-dependent hyperadrenocorticism (PDH) the basal prolactin concentrations (means of 6 determinations; range 2.8-24.7 micrograms/l) were significantly higher than those of 23 healthy control dogs (0.9-10.5 micrograms/l). In five dogs with hyperadrenocorticism due to adrenocortical tumour (ATH) the prolactin concentrations were also significantly elevated, but still significantly lower than the values of the dogs with PDH. The prolactin concentrations of the dogs with PDH responded supranormally to TRH-stimulation, whereas in the dogs with ATH the response was not significantly different from the results in the control dogs. Following bromocriptine administration the plasma prolactin concentrations of the dogs with PDH decreased considerably but remained higher than the values obtained in the control dogs and the dogs with ATH. It is concluded that PDH in the dog is associated with a disturbance in the regulation of prolactin secretion, that is not secondary to hypercortisolism per se.

Adrenal Cortex Diseases↗
PubMed1984

Effect of hyposensitization on atopic dermatitis in dogs.

In a double-blind study, 51 dogs with clinically defined atopic dermatitis were injected with either alum-precipitated allergen solutions or a placebo. Comparing the treatment results of both groups on the basis of scores for clinical signs, a significant difference in clinical improvement was established in favor of the allergen-treated dogs (P less than 0.01). The proportional changes of scores for clinical signs in the allergen-treated group ranged between +27.3% and -100% (median, -61.5%) and in the placebo group between +36.4% and -100% (median, 0.0%) with respect to the initial scores. Immediate skin test reactivity disappeared only in the dogs with a good clinical response. Of 27 dogs treated with an allergen solution, 16 (59.3%) had an improvement of 51% or more. In the placebo group, 5 of 24 dogs (20.8%) reacted this way. There was total remission of the clinical signs in 9 and 4 dogs, respectively. In the dogs in which, after 9 months of hyposensitization, any improvement was observed, the chance for final improvement of more than 51% was calculated as 84%. Discriminant analysis revealed that evaluation of the effect of immunotherapy can be restricted to the 9-month follow-up examination.

Adjuvants, Immunologic↗
PubMed1984

[Treatment methods: traditional and alternative].

When choosing a mode of treatment the clinician should consider the basis upon which effectiveness may be expected: (1) unproven clinical experience, (2) rationale based etiology/pathogenesis, or (3) controlled therapeutic experiments. Many therapies are still based on unproven clinical experience, which may be fallacious because of: (1) insufficient insight into the natural course of the condition, (2) statistical variation, (3) placebo effects and (4) the prejudice or bias of the clinician. Against this background the so-called alternative modes of treatment are discussed with special attention to acupuncture and homeopathy. The literature supports the conclusion that from a scientific point of view there is no place for these modes of treatment in (veterinary) medicine. Suggested explanations for the growth of alternative modes of treatment include the changing relation between veterinarians and patients/clients, the shortcomings and limitations of veterinary medicine, and increased interest in what is happening outside the regular culture pattern. Finally, it is proposed that what sets the art of (veterinary) medicine above ordinary (veterinary) medicine is that which can be achieved by good intellectual and emotional contacts between the veterinarian and the patient/client rather than by false therapies.

Acupuncture Therapy↗
PubMed1984

Results of cyproheptadine treatment in dogs with pituitary-dependent hyperadrenocorticism.

Administration of cyproheptadine for 2 months to five dogs with pituitary-dependent hyperadrenocorticism (PDH) at a dose rate of 0.3 mg/kg per 24 h (group 1) and to four dogs with PDH at a dose rate of 1 mg/kg per 24 h (group 2) did not result in any clinical improvement. The hyperadrenocorticoid state, as indicated by the circulating cortisol levels, the urinary corticosteroid excretion and the response of the hypothalamo-pituitary-adrenal axis to lysine-vasopressin, thyrotrophin releasing hormone and dexamethasone did not change consistently, although there was a tendency to normalization of some parameters in the dogs of group 2. However, these changes were not found to be consistent for each individual dog but were limited to one parameter per dog. It is concluded that cyproheptadine is not suitable for the treatment of PDH in the dog.

Adrenal Cortex Hormones↗
PubMed1983

Progesterone-controlled growth hormone overproduction and naturally occurring canine diabetes and acromegaly.

Female pet dogs exhibiting either glucose intolerance alone or glucose intolerance and acromegaly were investigated. Some dogs developed the disorder(s) during dioestrus and some animals developed the disorder(s) after they were given medroxyprogesterone acetate (MPA). Elevated fasting plasma glucose levels (12.3 +/- 1.9 mM, mean +/- SEM) were accompanied by fasting hyperinsulinaemia (144 +/- 21 microU/ml, mean +/- SEM) and drastic elevation of plasma growth hormone (GH) levels (112.6 +/- 45 ng/ml, mean +/- SEM). An iv glucose tolerance test (IVGTT) performed on all dogs revealed non-suppressibility of GH levels and glucose intolerance. Plasma concentrations of glucose, insulin and GH during IVGTT in affected dogs differed significantly from the concentrations measured in normal dogs during the same test. MPA withdrawal and/or ovariohysterectomy (OVx-HYx) in affected animals was followed by reversal of GH levels to normal and improved glucose tolerance. Acromegaly associated soft tissue changes were also reversible after MPA withdrawal and/or OVx-HYx when GH levels had dropped. In 5 dogs which had developed diabetes during dioestrus and in which a spontaneous decrease in plasma progesterone occurred during the investigation a concomittant decrease in GH levels was observed. Plasma GH measured at different stages of pregnancy in 45 dogs was found to be elevated in one animal only. The results show that the development of spontaneous diabetes/acromegaly occurring in some female dogs is related to progestagen (progesterone/MPA) exposure and that reversal of the signs is achieved by progesterone/MPA withdrawal. The results suggest that diabetes/acromegaly in the dogs studied was caused by progesterone/MPA-evoked GH elevation. Finally, the findings also suggest that the GH axis normally not appreciably responsive to progestagen exposure in some dogs becomes and/or is paradoxically controlled by physiologic levels of endogenous progesterone or low doses of MPA.

Acromegaly↗
PubMed1983

Urinary corticoids in the diagnosis of canine hyperadrenocorticism.

In 20 healthy experimental dogs the 24 hour urinary corticoid excretion as measured by cortisol radioimmunoassay on two consecutive days varied from 0.5 to 3.3 nmol/kg/24 hours and from 0.3 to 3.6 nmol/kg/24 hours. In 20 dogs with otherwise proven spontaneous hyperadrenocorticism these values varied from 4.4 to 35.7 nmol/kg/24 hours and from 3.6 to 26.8 nmol/kg/24 hours respectively. Corticoid/creatinine ratios in morning urine samples of 28 healthy pet dogs were 1.2 to 6.9 X 10(-6). In 27 dogs with spontaneous hyperadrenocorticism all ratios exceeded the range observed in the healthy pet dogs.

Animals↗
PubMed1982

Plasma cortisol response to thyrotrophin releasing hormone and luteinizing hormone releasing hormone in healthy kennel dogs and in dogs with pituitary-dependent hyperadrenocorticism.

The change in the plasma concentration of cortisol after the administration of thyrotrophin releasing hormone (TRH) and LH releasing hormone (LH-RH) was studied in normal dogs and in dogs with pituitary-dependent hyperadrenocorticism (PDH). The normal dogs showed a small but significant increase in the plasma concentration of cortisol 15 min after intravenous injection of TRH and LH-RH. In ten of the dogs with PDH the response to TRH was not significantly different from that in the normal dogs, but in 13 the response was significantly greater. In 15 of the dogs with PDH the response to LH-RH administration was within or below the range of responses in the normal dogs and in only one dogs was the response to LH-RH greater than that in the normal dogs. These findings are discussed in relation to the pathogenesis of PDH.

Adrenal Cortex↗
PubMed1981

Hypothalamic catecholamine levels in dogs with spontaneous hyperadrenocorticism.

Hypothalamic norepinephrine (NE) and dopamine content was studied in dogs with spontaneous and iatrogenic hypercortisolism and in untreated normal dogs. The concentration of NE in the hypothalamus was subnormal in 4 of 8 dogs with pituitary-dependent hyperadrenocorticism (PDH), whereas long-term administration of corticotropin or cortisone acetate did not result in low hypothalamic NE content. In dogs with hyperadrenocorticism due to adrenocortical tumor subnormal as well as normal and high hypothalamic NE levels were found. Hypothalamic as well as striatal dopamine content did not differ among groups of dogs with PDH, adrenocortical tumor, corticotropin treatment, cortisone treatment and in untreated normal dogs. The subnormal hypothalamic NE levels in dogs with PDH may be involved in the hypersecretion of ACTH found in this disease. The normal hypothalamic dopamine levels in dogs with PDH are not consistent with a dopaminergic-depletion as the cause of PDH.

Adrenal Gland Neoplasms↗
PubMed1981

Influence of medroxyprogesterone acetate (Provera) on plasma growth hormone levels and on carbohydrate metabolism. I. Studies in the ovariohysterectomized bitch.

Six elderly ovariohysterectomized dogs were given medroxyprogesterone acetate (MPA 10 mg/kg body weight) at 3 week intervals in a total of 5 injections. Mean growth hormone (GH) levels increased significantly after the third injection, continued to increase slightly after the fourth and fifth injections and remained significantly elevated over control levels as late as 16 weeks after the last MPA administration (P less than 0.05). The mean glucose concentrations during iv glucose tolerance tests (IVGTT) were significantly elevated at 30, 45 and 60 min after a glucose load when performed after the third MPA injection. Following the second MPA injection, mean insulin levels were significantly elevated at rest, 30 and 45 min after glucose load. After the fourth and fifth MPA injections, mean insulin levels during IVGTT were significantly elevated at 30 min only. These findings denote that (1) after a lag phase of several weeks MPA induces moderate GH increase in ovariohysterectomized dogs; (2) MPA administration causes moderate disturbance of glucose homoeostasis.

Animals↗
PubMed1980

Studies on the mechanism of polyuria induced by cortisol excess in the dog.

Water balance studies were performed in 7 experimental dogs before and during a period of cortisol-induced polyuria and in one dog with spontaneous hyperadrenocorticism before and after removal of an adrenocortical carcinoma. Measurements of urine and plasma osmolality and plasma arginine vasopressin concentration were made at regular intervals during the water deprivation studies. The results indicate that cortisol does not block the release of vasopressin but interferes with its action in the kidney.

Adrenocortical Hyperfunction↗
PubMed1980

Acromegaly associated with transient overproduction of growth hormone in a dog.

A 6-year-old female crossbred Belgian Shepherd Dog with features of acromegaly was monitored for almost 4 years. The history of frequent and excessive administration of a progestational agent suggested that the progestational drug induced the acromegaly. During the monitoring period. soft tissue changes diminished and there was normalization of several factors: plasma growth hormone concentration, response of plasma insulin and glucose to an oral glucose load, and response of plasma glucose hormone to the injection of insulin.

Acromegaly↗
PubMed1979

Uptake of 131I-19-cholesterol by normal and spontaneously hyperfunctioning canine adrenals.

In six normal dogs the adrenals could be visualized as separate areas of radioactivity at 7--10 days after injection of 20--40 muCi 131I-iodocholesterol per kg of body weight. Image analysis revealed uptake values of 0.15--0.3% of the injected dose. In five dogs with pituitary-dependent hyperadrenocorticism the adrenals became visible at 3--5 days after injection of the radiopharmaceutical, with uptake values of 0.38--2.2%. In six dogs with hyperadrenocorticism due to adrenocortical tumor the scintigraphy contributed to the diagnosis and the presurgical localization. The uptake values were within the normal range; the tumor could be observed at 3--10 days after injection. Additional findings on adrenal asymmetry and a case of fluctuating pituitary-dependent hyperadrenocorticism are discussed.

19-Iodocholesterol↗
PubMed1979

Adrenocortical function tests in dogs with hyperfunctioning adrenocortical tumours.

The response has been studied in nine dogs with hyperadrenocorticism due to adrenocortical tumours to the administration of dexamethasone, insulin, lysine-vasopressin and tetracosactide by measuring the changes in plasma cortisol concentration. Administration of dexamethasone did not produce a decrease in the plasma concentration of cortisol in any of these dogs. Administration of insulin caused slight increases in the plasma concentration of cortisol in four out of eight dogs. Lysine-vasopressin increased the plasma concentration of cortisol in eight out of nine dogs, three responded supranomally. Eight out of the nine dogs responded to tetracosactide administration, three responded supranormally, It is concluded that in the dog, in contrast to man, the lysine-vasopressin test cannot be used to differentiate between pituitary-dependent hyperadrenocorticism and hyperadrenocorticism due to an adenocortical tumour. Apparently pituitary ACTH is not completely depleted in dogs with hyperfunctioning adrenocortical tumours.

Adrenal Cortex Function Tests↗