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Biomedical subjects

J W Oliver

Publications and source records attributed to J W Oliver.

15 recordsLinked to original sources
PubMed1992

Effects of phenothiazine and thiabendazole on bovine dorsal pedal vein contractility induced by ergonovine and serotonin; potential for alleviation of fescue toxicity.

Phenothiazine and thiabendazole were studied for their ability to antagonize venoconstriction induced by ergonovine, and the biogenic amine serotonin, in the isolated dorsal pedal vein of cattle. The two compounds are commercially available, approved for usage in cattle and have been reported to reverse some of the toxic effects associated with the intake of Acremonium coenophialum-infested fescue forage by cattle. Neither compound had any antagonistic activity against venoconstriction induced by ergonovine. However, thiabendazole did have some activity against venoconstriction induced by serotonin. Ergot alkaloids are known to cause venoconstriction through effects on biogenic amine receptors, including serotonergic receptors, and since thiabendazole has anti-serotonin activity, part of the reported beneficial effects of thiabendazole in alleviating fescue toxicity may be due to the anti-serotonin activity of the drug. Further work is needed to determine if phenothiazine and thiabendazole have any effect on other types of alkaloids that are present in A. coenophialum-infested fescue.

Acremonium↗
PubMed1989

Reactivity of dorsal pedal vein of cattle to selected alkaloids associated with Acremonium coenophialum-infected fescue grass.

We determined the vasoconstrictive effects of selected ergot alkaloids, and a sample containing loline and its derivative alkaloids, on the isolated dorsal pedal vein of cattle, as a model system to study one of the toxic effects that result from cattle ingesting fescue forage infected with the endophytic fungus Acremonium coenophilalum. The ergot compounds ergotamine, ergosine, and agroclavine constricted this peripheral vein of cattle, but much less so than did the alpha-adrenergic agonist norepinephrine, which supports the ergots acting as partial agonists for these receptors. However, the sample of loline and loline-derivative alkaloids did not affect the dorsal pedal vein when given at concentrations similar to those of the ergot compounds. Loline and loline-derivative alkaloid sample at high concentrations partially inhibited norepinephrine-elicited vascular contraction, an effect that appeared to be unrelated to alpha-adrenoceptor activity. Thus, in the dorsal pedal vein model in cattle, the ergopeptide alkaloids were more venoconstrictive than were loline and its derivative alkaloids.

Acremonium↗
PubMed1987

Effects of zinc deficiency on thyroid function.

Interactive combinations of altered zinc and thyroid states were studied in rats to assess pathophysiologic effects. Clinical signs of zinc deficiency or thyroid alteration were limited to effects on growth rate. Changes in organ and glandular weights and serum thyrotropin levels reflected changes in serum thyroid hormone concentrations. Significantly (probability less than .001), zinc-deficient rats had enhanced hepatic thyroxine-5'-monodeiodinase activity. In addition, the zinc-deficient state was found to be protective against thiouracil-induced suppression of the microsomal-monooxygenase and thyroxine-5'-monodeiodinase enzyme complex. This protective effect was evident by greater thyroxine-5'-monodeiodinase and reduced nicotinamide-adenine dinucleotide phosphate cytochrome c reductase activities, as well as cytochrome P-450 content, in zinc-deficient/thiouracil-treated animals. Thus, the enzyme complex had increased triiodothyronine-generating capacity in conditions of zinc deficiency, which may be important because of the greater biological reactivity of triiodothyronine. Primary zinc deficiency conditions of the magnitude seen in this study and in this-age rat did not appear to alter serum thyroid hormone levels or organ/glandular function. However, concurrent zinc deficiency and altered thyroid status did change thyroid hormone response and disposition, which may be important to populations at risk because of thyroid dysfunctional states.

Animals↗
PubMed1985

Thyrotropin stimulation test--new perspective on value of monitoring triiodothyronine.

Thyrotropin (thyroid stimulating hormone; TSH) stimulus to thyroid cells of horses and dogs resulted in increased serum triiodothyronine (T3) concentrations that were detected earlier than those of thyroxine (T4). Doubling of the base-line T3 values in horses was detected 0.5 hours after injection of 5 IU of TSH IV, with peak response of 5 times base-line value detected 2 hours after injection. Doubling of T4 values in horses was noticed between 2 and 3 hours, with the peak response of 2.4 times base-line value at 4 hours after injection of TSH. Doubling of base-line T3 values in dogs in response to 0.2 IU TSH/kg of body weight (IV-5 IU maximum dose) was noticed at 1 hour, whereas T4 response doubled between 1.5 and 2 hours. Peak release of T3 and T4 in response to TSH in dogs had not developed by 4 hours; however, the percentage increase over base-line values was greater for T3 than T4 at early sampling time points, and this response has resulted in an increased T3/T4 ratio in hypothyroid dogs. Thus, in both dogs and horses, these studies indicated that T3 response to TSH could be used as a measure of thyroid function at earlier time intervals after TSH administration than one measures T4 response.

Animals↗
PubMed1984

Stages of hyperadrenocorticism: response of hyperadrenocorticoid dogs to the combined dexamethasone suppression/ACTH stimulation test.

A study was designed to evaluate the response of blood cortisol content in dogs tentatively diagnosed as having hyperadrenocorticism by using the combined dexamethasone suppression/ACTH stimulation test procedure. Four groups of abnormal responses were identified in 54 dogs. In group I (14.8% of the dogs with abnormal responses), the only abnormality was partial suppression with dexamethasone (clinically normal dogs suppressed to less than 10 ng/ml). In group II (29.6%), 2 abnormalities were found: partial suppression with dexamethasone and hyperreactivity to the ACTH stimulation test. In group III (typical pituitary-dependent hypercortisolism, 48.1%), 3 abnormalities were found: base-line hypercortisolemia, partial suppression with dexamethasone, and hyperreactivity to the ACTH stimulation test. In group IV (7.4%), 2 abnormalities were found: base-line hypercortisolemia and partial suppression with dexamethasone. Base-line blood cortisol content was normal in 44.4% of the adrenopathic dogs. A normal response to ACTH stimulation was seen in 25.9% of the dogs, and 74.1% of the dogs hyperreacted to the ACTH stimulation test. All of the adrenopathic dogs were found to suppress partially with dexamethasone. Failure to suppress the adrenal gland completely (less than 10 ng/ml) with dexamethasone was the most consistent finding in adrenopathic dogs when using the combined dexamethasone suppression/ACTH stimulation test procedure. It was concluded that the test procedure is feasible, flexible, and convenient for clinical situations. Also, these results suggested that there may be several stages in the negative feedback failure associated with hyperadrenocorticism in dogs.

Adrenal Cortex Function Tests↗
PubMed1984

A sampling protocol for the thyrotropin-stimulation test in the horse.

A study was designed to assess the secretory response of thyroid glands in horses to an economically feasible dose (5 IU) of thyrotropin injected IV, and to establish valid blood sampling periods in cases in which thyroxine concentrations were different from base-line values. Significant (P less than 0.001) response (doubling or near-doubling of base line) occurred as early as 3 hours after thyrotropin administration, with peak response at 4 to 5 hours. It was concluded that administration of 5 IU of thyrotropin is economical and effective in the horse, with collection of a second blood sample possible as early as 3 hours after administration.

Animals↗
PubMed1984

Diagnosis of canine Cushing's syndrome based on multiple steroid analysis and dexamethasone turnover kinetics.

A comparison of cortisol concentrations, determined by high-performance liquid chromatography (HPLC) and radioimmunoassay, was made in healthy, mixed-breed dogs and in dogs with clinical signs of Cushing's syndrome. Absolute concentration of cortisol was less in resting, dexamethasone-suppressed, and ACTH-stimulated plasma samples, when measured by HPLC relative to cortisol concentrations determined by radioimmunoassay. Diagnosis of Cushing's syndrome could be made using either method. Plasma concentrations of cortisone and corticosterone were determined by HPLC. Cortisone and corticosterone concentrations alone were not diagnostic of Cushing's syndrome; but when used in conjunction with cortisol determinations, they provided additional criteria for laboratory confirmation of the clinical diagnosis of Cushing's syndrome. The clearance of exogenous dexamethasone used in the dexamethasone-suppression test was examined in the normal and cushingoid dogs. Plasma concentrations of exogenous dexamethasone were constant during the 3-hour test in the normal dogs. However, in 75% of the dogs with Cushing's syndrome, exogenous dexamethasone was cleared completely in the 3-hour test. Thus, dexamethasone clearance rates were excessively fast in most dogs with Cushing's syndrome.

Adrenal Cortex Function Tests↗
PubMed1983

Sampling protocol for thyrotropin stimulation test in the dog.

A study was designed to assess the secretory response of thyroid glands in dogs to small doses of thyrotropin (thyroid-stimulating hormone, TSH; 2.5 and 5.0 units, total IV dose), and to establish valid blood-sampling periods in cases in which thyroxine concentrations were different from base-line values. Significant (P less than 0.001) response occurred as early as 3 hours after TSH administration, with peak response at 5 to 7 hours. Fasting dogs for 12 hours had no effect on test results. Because base-line thyroxine concentrations in dogs are equivocal and base-line triiodothyronine concentrations are influenced by many factors, thyrotropin stimulation testing is one of the best methods at present to evaluate thyroid function. Administration of a total dose of 2.5 to 5.0 units of TSH is economical, and collection of the 2nd blood sample as early as 3 hours for response may be advantageous in terms of scheduling for the client and practicing veterinarian.

Animals↗
PubMed1978

Effect of thyroid state on magnesium concentration of rat tissues.

The effect of alteration of thyroid status by thiouracil (0.1% concentration in drinking water for 60 days) or exogenous thyroxine (25 mg/dg of body weight administered SC from days 30 to 60) on magnesium content of rat tissues following exogenous magnesium was evaluated. Treatment of rats with magnesium solution (25 mg of magnesium sulfate/dg of body weight) resulted in increased magnesium concentration in most tissues of hypothyroid and hyperthyroid rats, with the mesenchymal-derived tissues (aorta, trachea, and ear cartilage) exhibiting the greatest increases (respectively, 154, 130, and 133% of control group values for hypothyroid rats, and 115, 108, and 107% of control group values for the hyperthyroid group). Magnesium concentration in skeletal and cardiac muscle was similar for hyperthyroid and control rats, but magnesium concentration in these same tissues of hypothyroid rats was decreased. Magnesium distribution and retention in rat tissues is altered considerably, depending on the functional status of thyroid gland.

Animals↗
PubMed1976

Interrelationships between athyreotic and manganese-deficient states in rats.

Possible interrelationships of manganese-deficient and hypothyroid (thiouracil treatment) states in rats were examined. Clinical signs, necropsy changes, and plasma thyroxine concentrations were determined in control rats (group A), thiouracil-treated (hypothyroid) rats (group B), rats given manganese-deficient feed (group C), and rats given thiouracil and manganese-deficient feed (group D). Clinical signs observed included a hyperemic condition of the ears in group C and D rats that was considerably more severe in the latter group. One rat from group D also had middle ear changes, as reflected by a tilting of the head. Fluid intake was severely reduced in group D rats near the end of the 60-day experimental period and resulted in marked dehydration. Pathologic change (fatty liver) was observed at necropsy in only 1 rat from group D. Thiouracil treatment of rats reduced plasma thyroxine concentration to 48 to 68% of base line from experimental days 20 to 60. The same thiouracil treatment combined with feeding a manganese-deficient ration significantly reduced plasma thyroxine concentrations to 37% of base line at day 20 and 5% of base line at day 40; the concentration at day 60 was 76% of base line, apparently approaching normal because of concentration of the plasma (and thyroxine) in the dehydrated rats. Mean adrenal gland weight was significantly less than normal in group D rats, whereas mean thyroid gland weight in this group was increased, although less than that of group B rats treated with thiouracil only. Thus, clinical signs of deficiency were enhanced when athyreotic and manganese-deficient states were combined, and plasma thyroxine concentrations were markedly decreased, giving added meaning to the need for awareness of hormonal and trace mineral status of animals.

Animals↗
PubMed1975

Interrelationships between athyroetic and copper-deficient states in rats.

Possible interrelationships of copper-deficient (copper-deficient ration) and hypothyroid (thiouracil treatment) states in rats were examined. Clinical signs, necropsy changes, and thyroxine concentrations were determined in 6 groups of rats treated as follows: group A--nontreated control; group B--thiouracil treated; group C--fed copper-deficient ration; group D--thiouracil treated and fed copper-deficient ration; group E--thyroid-stimulating hormone (TSH) treated; and group F--TSH treated and fed copper-deficient ration. Clinical signs occurred first and were most severe in the thiouracil-treated rats fed copper-deficient ration and included conformational changes and slower maturation, weakening of ear cartilage, middle ear changes (reflected by tilting of heads), and alopecia. Fatty infiltration of hepatic tissue was found in all rats fed copper-deficient rations, and considerable fluid retention occurred in rats fed copper-deficient ration and subjected to daily TSH treatment. Adrenal gland weights were 81% of control values (adjusted for body weight) in thiouracil-treated rats fed copper-deficient ration, and hypophysis weights were 114 and 154% of control values in thiouracil-treated rats and thiouracil-treated rats fed copper-deficient ration, respectively. Thyroid gland weights were 281% of control values in both thiouracil-treated rats and thiouracil-treated rats fed copper-deficient ration. Plasma thyroxine concentrations were markedly reduced (9% of control value) in thiouracil-treated rats fed copper-deficient ration. Thus, copper-deficient and hypothyroid states were considerably enhanced when the 2 existed concurrently, giving added meaning and necessity to close surveillance of trace mineral concentrations and thyroid gland status.

Adipose Tissue↗