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Biomedical subjects

E MacDonald

Publications and source records attributed to E MacDonald.

118 records · Page 7Linked to original sources
PubMed1976

Effect of pyrazole, 4-methylpyrazole, 4-bromopyrazole and 4-iodopyrazole on brain noradrenaline levels of mice and rats.

Four daily doses of pyrazole (50 mg/kg), caused a reduction in rat brain noradrenaline (NA) of over 20% when determined 24 hrs after the final injection. Neither 4-methylpyrazole (10-50 mg/kg), nor 4-iodopyrazole (10-50 mg/kg) had any effect. In mice treated similarly, pyrazole (50-400 mg/kg) caused a dose-dependent decrease in brain NA. Neither 4-methylpyrazole, 4-bromopyrazole nor 4-iodopyrazole caused any significant change in the levels. However if the brain NA levels were examined 6 hrs after a single dose, then in addition to pyrazole, 4-methylpyrazole showed a dose-dependent ability to lower brain NA. 4-bromopyrazole and 4-iodopyrazole, given acutely, caused a dose-dependent decrease in rectal temperature and exploratory behaviour. 4-methylpyrazole in high doses (200-400 mg/kg) showed similar properties but they did not correlate with the decrease in brain NA. Pyrazole, after acute treatment, showed little ability to change rectal temperature of exploratory behaviour. It is concluded that the NA-depleting effect of pyrazole is not related to inhibition of alcohol dehydrogenase, since other 4-substituted pyrazoles which are more potent inhibitors of the enzyme have little or no effect on brain NA levels.

Animals↗
PubMed1972

Lead and zinc poisoning and the interaction between Pb and Zn poisoning in the foal.

Groups of young growing horses were fed toxic amounts of lead only, zinc only and the same amounts of lead and zinc together. Those fed Pb only developed pharyngeal and laryngeal paralysis ("roaring") whereas those fed Zn only and Pb and Zn together developed the same clinical syndrome which included swelling at the epiphyseal region of the long bones, stiffness and lameness. Anemia and decreased weight gains were most pronounced in animals fed Zn for the longest periods. Animals fed Pb only did not become anemic and weight loss did not occur until after there was an interference in swallowing. The clinical signs and tissue Pb values from animals fed toxic amounts of both Pb and Zn continuously, differed markedly from those present in animals fed comparable amounts of Pb only. Th clinical signs were similar to those caused by Zn poisoning. The hepatic and renal tissue Pb values were approximately twice as high and the epiphyseal and cancellous bone sample results were one half as high as the comparable Pb values from animals fed toxic amounts of Pb only. It appeared that toxic amounts of Zn prevented the development of clinical signs of Pb poisoning in the young growing horse.

Animal Feed↗
PubMedDate not supplied

Effect of a single lethal dose of TCDD on the levels of monoamines, their metabolites and tryptophan in discrete brain nuclei and peripheral tissues of Long-Evans rats.

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is one of the most potent anorexigens in rats with a yet unidentified mechanism of action. Since biogenic amines are known to essentially participate in the control of body weight and food intake, their levels were determined in various hypothalamic and other brain sites together with selected peripheral tissues after TCDD administration to adult male Long-Evans rats. Rats were given a single lethal dose of TCDD (1000 micrograms/kg intraperitoneally, in dimethylsulphoxide) or vehicle alone and they were decapitated at 1, 5, 25 hr or 8 days after TCDD administration. The samples were analyzed for concentrations of biogenic amines and their metabolites by HPLC-EC. Administration of TCDD increased the concentration of tryptophan at 8 days after exposure by about 20% in almost all nuclei examined, with the change reaching statistical significance in the lateral hypothalamic area and in lateral and medial accumbens nuclei. Importantly, this elevation was not seen in pair-fed control animals. Although not statistically significant, there was a tendency to 5-10% diminished dopamine, serotonin and/or 5-hydroxyindoleacetic acid levels in most brain sites during the first day postexposure. The present results argue against a crucial role for catecholamines as mediators of TCDD toxicity. However, the delayed changes in brain tryptophan do not appear to be secondary to TCDD hypophagia.

Adrenal Glands↗
PubMedDate not supplied

AHIMA reengineers FORE.

Explore the source record for details and available documents.

Information Services↗
PubMedDate not supplied

Metoprine, an inhibitor of histamine N-methyltransferase but not catechol-O-methyltransferase, suppresses feeding in sated and in food deprived rats.

Metoprine is a histamine N-methyltransferase (HMT) inhibitor often used to elevate endogenous histamine (HA) levels when studying the role of brain HA. Since central histaminergic systems may be involved in the regulation of feeding, the effect of metoprine on food intake was studied in sated and in food deprived rats. The treatment caused a dose-dependent decrease in food intake in sated rats. It also suppressed deprivation-induced feeding. To clarify the specificity of the treatment, the effect of metoprine on another methylating enzyme, catechol-O-methyltransferase (COMT), was examined indirectly by examining the ratio of the non-methylated dopamine metabolite, dihydroxyphenylacetic acid (DOPAC) to that of its methylated product homovanillic acid (HVA). The dopamine metabolites did not change in a manner consistent with COMT inhibition, but instead a transient decrease in DOPAC levels was observed. However, the suppression of feeding is considered to be related to the metoprine-induced inhibition of brain HA catabolism and not with the changes in dopaminergic systems. Metoprine had no effect on brain concentration of serotonin (5-HT) or its metabolite 5-hydroxyindoleacetic acid (5-HIAA). The results provide further support for the role of brain HA in the control of feeding behavior.

3,4-Dihydroxyphenylacetic Acid↗
PubMedDate not supplied

Functional bracing of tibial shaft fractures.

This paper examines the reduced risk of non-union in tibial fractures by allowing controlled motion at the fracture site. It argues that this can also stimulate healing and can be achieved by using functional bracing, which holds the position of the limb, allows weight-bearing and mobilisation of neighbouring joints. It also describes how to apply such a brace.

Casts, Surgical↗