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Biomedical subjects

R W Fuller

Publications and source records attributed to R W Fuller.

At least 325 records · Page 18Linked to original sources
PubMed1983

The effect of sodium cromoglycate on the development of exercise-induced angina pectoris.

The effect of inhaling sodium cromoglycate on the development of chest pain in 8 patients with exercise-induced angina pectoris was studied in a double-blind cross-over placebo controlled trial. Blood levels of sodium cromoglycate of 24-136 ng/ml did not affect either the time to develop pain on exercise or the rate-pressure product at the time of pain. In view of the original observation that Khellin reduces angina, it is suggested that further studies should be performed to assess the effect of SCG at higher concentrations in the plasma.

Angina Pectoris↗
PubMed1983

Antagonism by tomoxetine of the depletion of norepinephrine and epinephrine in rat brain by alpha-methyl-m-tyrosine.

Tomoxetine hydrochloride, a potential antidepressant drug, antagonized the alpha-methyl-m-tyrosine-induced depletion of hypothalamic epinephrine and norepinephrine in rats. The findings suggest that tomoxetine, like several uptake-inhibiting antidepressant drugs that have been examined, inhibits uptake into epinephrine neurons as well as norepinephrine neurons in brain.

Animals↗
PubMed1983

Evidence for inhibition of monoamine oxidase in vivo in rat brain by 7,8-dichloro-1,2,3,4-tetrahydroisoquinoline.

7,8-Dichloro-1,2,3,4-tetrahydroisoquinoline (DCTQ) (50 mg/kg i.p.) antagonized the inactivation of MAO by pargyline as measured by direct enzyme assays in brain homogenates and by accumulation of hypothalamic catecholamines. These findings lend credence to the earlier interpretation that changes in brain concentrations of biogenic amines and their metabolites in DCTQ-treated rats were due at least in part to MAO inhibition.

Animals↗
PubMed1982

Dopamine accumulation after dopamine beta-hydroxylase inhibition in rat heart as an index of norepinephrine turnover.

Dopamine concentration in rat heart is normally very low, only a few percent of the concentration of norepinephrine. After treatment of rats with a dopamine beta-hydroxylase inhibitor, 1-cyclohexyl-2-mercapto-imidazole (CHMI), there was a rapid increase in dopamine concentration even before norepinephrine concentration had decreased perceptibility. This accumulation of dopamine was readily measured by liquid chromatography with electrochemical detection. Since the percentage change in dopamine was much greater than the percentage change in norepinephrine, especially at early times, measurement of dopamine accumulation rather than norepinephrine decline was considered as a useful measure of norepinephrine turnover. Drugs that act on noradrenergic receptors and are known to alter norepinephrine turnover were found to alter the rate of dopamine accumulation. Clonidine and guanabenz decreased dopamine accumulation after CHMI, whereas piperoxan (but not prazosin) increased dopamine accumulation after CHMI. Pergolide, a dopamine agonist whose lowering of blood pressure and cardiac rate has been suggested to be due to suppression of neurogenic release or norepinephrine, also decreased dopamine accumulation after CHMI. The results suggest that measuring dopamine accumulation may have advantages over measuring norepinephrine disappearance after dopamine beta-hydroxylase inhibition as an indicator of norepinephrine turnover in heart.

Animals↗
PubMed1982

Depletion of epinephrine in rat hypothalamus by a dopamine agonist, pergolide.

The i.p. injection of pergolide mesylate, a dopamine agonist, at doses of 0.3-0.6 mg/kg led to a decrease in epinephrine concentration in rat hypothalamus. After a 0.6 mg/kg dose of pergolide mesylate, epinephrine concentration in hypothalamus decreased within 2 hr, reached a minimum concentration at about 8 hrs, and then returned toward control values. Norepinephrine N-methyltransferase activity was not decreased after pergolide injection in vivo nor was it inhibited by pergolide added in vitro at concentrations as high as 10(-3) M. Higher i.p. doses of less potent dopamine agonists, apomorphine (10 mg/kg) and lergotrile (3 mg/kg), also decreased epinephrine concentration in hypothalamus. The pergolide-induced decrease in hypothalamic epinephrine concentration was prevented by pretreatment with haloperidol or spiperone, antagonists of dopamine receptors. Activation of dopamine receptors appears to result in a decrease in epinephrine concentration in rat brain, possibly due to enhanced release of epinephrine.

Animals↗
PubMed1982

Further studies on the long-term depletion of striatal dopamine in iprindole-treated rats by amphetamine.

(+) Amphetamine was more potent (-) amphetamine in causing persistent depletion of striatal dopamine in iprindole-treated rats. This effect of amphetamine was not mimicked by EXP561, a structurally related compound that is more potent than amphetamine as an inhibitor of dopamine uptake. The depletion of striatal dopamine at 1 week after amphetamine injection in iprindole-treated rats was prevented by amfonelic acid, an inhibitor of uptake into dopamine neurons. The depletion of dopamine by amphetamine was prevented when amfonelic acid was given at the same time as amphetamine or as long as 4 hr after amphetamine but not when amfonelic acid was given 24-48 hr after amphetamine. Amfonelic acid antagonized the depletion of dopamine by amphetamine but not the depletion of serotonin by p-chloroamphetamine; fluoxetine antagonized the depletion of serotonin by p-chloroamphetamine but not the depletion of dopamine by amphetamine. Pretreatment with alpha-methyl-tyrosine to block dopamine synthesis antagonized the persistent depletion of dopamine by amphetamine, but pretreatment with an inhibitor of monoamine oxidase to increase that dopamine concentration had no effect. The possibility that prolonged release of dopamine from intraneuronal storage granules leads to deleterious effects on dopamine neurons is discussed.

Amphetamines↗
PubMed1982

Pharmacology of brain epinephrine neurons.

Neurons that contain PNMT, the epinephrine-forming enzyme, have their cell bodies in brain stem regions in rat brain and send projections mainly into other brain stem areas, hypothalamus, and spinal cord. These neurons can be affected pharmacologically by various kinds of drugs. Epinephrine neuronal systems might play a part in some pharmacologic actions of MAO inhibitors and uptake inhibitors as well as alpha and beta agonists and antagonists. PNMT inhibitors currently represent the only means of modifying epinephrine neurons pharmacologically without also altering norepinephrine or dopamine neurons in brain. The continued study of drugs affecting epinephrine neurons should be useful in elucidating functions of these neurons. Drugs that affect epinephrine neurons may be of use in the treatment of hypertension, psychiatric disorders, neuroendocrine dysfunction, and possibly other diseases.

Animals↗
PubMed1982

Effect of cis and trans isomers of 1-amino-2-(p-chlorophenyl)cyclohexane, conformationally restricted analogs of p-chloroamphetamine, on 5-hydroxyindoles in rat brain.

Cis and trans isomers of 1-amino-2-(p-chlorophenyl)cyclohexane, conformationally restricted analogs of p-chloroamphetamine, did not decrease brain serotonin and 5-hydroxyindoleacetic acid concentrations at i.p. doses of .05 and .1 mmole/kg in rats, doses at which p-chloroamphetamine itself decreased the concentrations of these 5-hydroxyindoles to half or less of their initial values. These analogs of p-chloroamphetamine, unlike several others studied previously, apparently lack the ability of the parent compound to inhibit serotonin uptake or synthesis or to release serotonin from intraneuronal granular stores.

Animals↗
PubMed1982

Functional consequences of inhibiting serotonin uptake with fluoxetine in rats.

Fluoxetine alone enhances central serotonin function as measured by a variety of test systems and potentiates the effects of serotonin precursors. Table 1 lists various effects of tryptophan or 5HTP that have been potentiated by fluoxetine. This potentiation or synergistic interactions between fluoxetine and L-5HTP constitute excellent evidence that any given effect is influenced by a serotonin synaptic connection.

Analgesics↗