Search PubMed⌕ Search

Biomedical subjects

W D Reid

Publications and source records attributed to W D Reid.

At least 73 records · Page 4Linked to original sources
PubMed1971

Possible mechanism of liver necrosis caused by aromatic organic compounds.

Treatment of rats with phenobarbital, which stimulates the activity of the drug-metabolizing enzymes in the liver, potentiates hepatic necrosis elicited by bromobenzene and a number of other chemically inert halogenated aromatic hydrocarbons. Radioautographic studies indicate that [(14)C]bromobenzene is covalently bound at the sites of necrosis. From these results, it is inferred that the hepatotoxic effects of the halogenated aromatic hydrocarbons are mediated by chemically active metabolites formed in hepatocytes. In accord with this view, a number of aromatic halogenated hydrocarbons are converted by microsomes in vitro to active intermediates which form covalent complexes with glutathione (GSH).

Animals↗
PubMed1970

Turnover rate of brain 5-hydroxytryptamine increased by D-amphetamine.

1. Administration of two doses of amphetamine HCl (5 mg/kg intraperitoneally) 45 min apart raised body temperature of rats by an average of 3.4 degrees C and increased the turnover rate of brain 5-hydroxytryptamine (5-HT) by almost one-half.2. Both effects were blocked by exposure to 4 degrees C or by pretreatment with the beta-blocker Kö 592 (1-(2-methylphenoxy)-3-isopropylamine-2-propanol), but not by the administration of the ganglionic blocker chlorisondamine combined with atropine.3. Since it has previously been shown that hyperthermia per se increases the turnover rate of brain 5-HT, and that amphetamine does not directly affect the uptake and release of 5-HT in brain slices, it is concluded that the amphetamine-induced increase in 5-HT turnover may be secondary to the rise in temperature produced by the drug.

Adrenergic beta-Antagonists↗
PubMed1969

Tricyclic antidepressants: evidence for an intraneuronal site of action.

Desipramine, a tricyclic antidepressant drug, almost completely prevents the accumulation of tritiated norepinephrine by sympathetic neurons of the rat heart after the injection of a tracer dose of the labeled amine. However, desipramine does not alter the accumulation of norepinephrine after the injection of a large dose of the neurohormone. Despite the failure of desipramine to block the neuronal uptake of norepinephrine, it still prevents exogenous norepinephrine from displacing the endogenous neurohormone (previously labeled with H(3)-norepinephrine) from intraneuronal storage sites.

Animals↗