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Biomedical subjects

A Barnett

Publications and source records attributed to A Barnett.

At least 145 records · Page 8Linked to original sources
PubMed1980

The economics of pharmaceutical policy in Ghana.

Pharmaceutical expenditure in Ghana accounts for about one-third of the total recurrent costs of the Ministry of Health, but in isolation this figure is a misleading indicator of economic importance. In the primary care sector up to 75-80 percent of the running cost of a health center may be accounted for by pharmaceuticals, and because the Ghanaian currency is heavily overvalued, even these proportions understate the true value of resources used on important drugs. An apparent lack of central control of drugs expenditure led to a study of the existing allocation procedures and prescribing practices. The results suggest large-scale wastage through overprescribing, often in response to patients' preferences for more costly medication. Approaches to improved planning of drug use, including the setting of expenditure norms based on recommended prescribing routines, are detailed, and it is concluded that the resultant savings could allow a sizable extension of the coverage given to rural populations by the primary health care system.

Drug Utilization↗
PubMed1980

Blockade by l-lysine of non-narcotic analgesics.

The antinociceptive effects of the non-narcotic analgesics clonixin, flunixin, acetylsalicylic acid, aminopyrine and phenylbutazone in the yeast paw test were blocked by l-lysine. Blockade occurred at doses of l-lysine which did not affect pain threshold. The site(s) or mechanism of action of blockade could not be determined with certainty. It appears unlikely that l-lysine prevented the analgesics from getting to active sites since plasma or brain levels of flunixin were not altered for up to 2 hr after drug administration and binding of flunixin to plasma protein was not affected. Blockade by l-lysine appears to occur at least in part at a peripheral site since it was not blockade by l-arginine or l-ornithine which compete for a common transport system with l-lysine and, hence, would have reduced the effect of l-lysine if its actions were central. However, blockade within the central nervous system cannot be ruled out. Antagonism by l-lysine does not seem to involve endogenous serotonin since it was not reversed by the serotonin precursor, 5-hydroxytryptophan, or by fluoxetine, a specific blocker of serotonin uptake. In contrast to the block of non-narcotic analgesics, l-lysine potentiated the antinociceptive effects of morphine.

Aminopyrine↗
PubMed1977

Quipazine-induced head-twitch in mice.

Quipazine has been reported to be a direct serotonin receptor agonist. In this laboratory, quipazine produced head-twitch in mice similar to that produced by the serotonin precursor, 5-hydroxytryptophan (5-HTP). Three antiserotonergic drugs (methiothepin, methysergide, and cinanserin) antagonized both the 5-HTP and quipazine-induced head-twitch responses. In addition, the quipazine response was significantly potentiated by a monoamine oxidase (MAO) inhibitor, pargyline. Since it is not likely that quipazine itself is metabolized by MAO, these results suggested that quipazine might cause release of endogenous serotonin. Parachlorophenylalanine, a serotonin depletor, significantly antagonized the potentiation of quipazine by the MAO inhibitor but failed to antagonize the head-twitch produced by quipazine itself. The present studies suggest that quipazine influences serotonin receptors in the brain to produce head-twitch by two mechanisms of action: (1) by direct serotonin receptor activation, and (2) indirectly by causing a release of endogenous serotonin.

5-Hydroxytryptophan↗
PubMed1976

The role of serotonergic pathways in isolation-induced aggression in mice.

Male mice that became aggressive following four weeks of social isolation were treated with seven known serotonin receptor antagonists. All of the antiserotonergic drugs selectively antagonized the fighting behavior of the isolated mice; the antiaggressive activity was selective since, at antifighting doses, none of the drugs either significantly altered spontaneous motor activity or impaired inclined-screen performance. Antagonism of 5-HTP-induced head-twitch was used as an in vivo measure of antiserotonergic activity and a statistically significant correlation existed between potency as an antiserotonergic and potency as an antiaggressive. PCPA, a serotonin depletor, also significantly antagonized isolation-induced aggression for at least 24 hr postdrug administration. The interrelationship between cholinergic and serotonergic mechanisms in the mediation of isolation aggression was investigated. The involvement of serotonergic systems in isolation-induced aggression is discussed.

5-Hydroxytryptophan↗
PubMed1975

Central versus peripheral anticholinergic activity as assessed by two in vivo procedures in mice.

The activity of tertiary and quaternary anticholinergic drugs was compared in two different test procedures designed to measure cholinolytic activity in mice. The four drugs utilized were atropine sulfate, atropine methylnitrate, scopolamine hydrobromide, and scopolamine methylnitrate. The results led to the conclusion that one of these test procedures, the induction of mydriasis (increase in pupil size), primarily measures peripheral anticholinergic activity whereas the other procedure, inhibition of physostigmine lethality, primarily measures anticholinergic activity in the CNS. These two test procedures can be utilized to characterize the nature of the cholinolytic properties of prospective therapeutic drug candidates.

Animals↗
PubMed1975

The evaluation of anti-parkinson drugs on reserpine-induced rigidity in rats.

The effect of anti-parkinson drugs on reserpine-induced rigidity was examined using a technique which measured rigidity by hind limb palpation. Centrally acting dopaminergic and anti-cholinergic drugs were able to antagonize reserpine-induced rigidity, whereas peripherally acting drugs had no effect. Results are discussed in terms of possible modes of action. Relative potencies of the drugs studied in this model were well correlated with the dose ranges of clinically established anti-parkinson drugs. It is concluded that measurement of reserpine-induced rigidity by hind limb palpation is a rapid and sensitive technique to evaluate potential anti-parkinson drugs.

Amantadine↗
PubMed1975

Etonitazine-induced rigidity and its antagonism by centrally acting muscle relaxants.

Some narcotic drugs have been reported to produce increases in muscle tone in rats. In our laboratory we have found that etonitazine produces a 'lead-pipe' rigidity of the trunk and limb musculature. The reported studies were conducted to characterize etonitazine-induced rigidity more fully, to compare the degree of rigidity with that produced by morphine, codeine and methadone, and to assess the sensitivity of this rigidity to centrally acting muscle relaxants. Of the 4 narcotics tested, etonitazine was far more potent than methadone or morphine for producing rigidity; codeine did not produce peak rigidity comparable to the other 3 narcotics. Etonitazine-induced rigidity occurs at a supraspinal level since the effect was prevented by spinal transsection. Etonitazine-induced rigidity was prevented by the narcotic antagonists cyclazocine, pentazocine and naloxone but not by the serotonin depletor, p-chlorophenylalanine. Etonitazine-induced rigidity was antagonized by centrally acting muscle relaxants, including diazepam, methocarbamol, carisoprodol and zoxazolamine; in agreement with their relative clinical muscle relaxant potencies, diazepam is the most potent antagonist of etonitazine-induced rigidity.

Analgesics, Opioid↗
PubMed1975

Ribosomal RNA metabolism in cucumber leaf mesophyll protoplasts.

Aspects of the metabolism of RNA have been studied in enzymatically isolated protoplasts from cotyledon and first leaf mesophyll tissue of two cultivars of cucumber. The first leaf mesophyll protoplasts incorporated (3H)-uridine into ribosomal RNA at a constant rate for up to 25 hr in a simple salts medium and for up to 45 hr in a growth medium. Pulse-chase labelling experiments on such preparations showed a rapid dilution of the intracellular (3H)-uridine pool(s) and a high metabolic rate in the cells in one cultivar but not in another. Gel electrophoretic analysis of the RNA from both cotyledon and first leaf protoplasts showed that both protoplast types incorporated either (14C)- or (3H)-uridine into ribosomal RNA species. Incorporation of (3H)-uridine into chloroplasts RNA was minimal in cotyledon protoplasts, but significant in leaf protoplasts. Greater incorporation into the chloroplast RNA species could be achieved by longer pulses. Synthesis of all of the ribosomal RNA species was sensitive to actinomycin D at 10 and 25 mug/ml concentrations in all protoplasts tested.

Cells, Cultured↗
PubMed1975

Head-turning induced by electrical stimulation of the caudate nucleus and its antagonism by anti-parkinson drugs.

Intermittent high-frequency electrical stimulation of the caudate nucleus induces contralateralhead-turning in rats. The anti-Parkinson drugs, L-dopa, amantadine and apomorphine, raise the threshold for or completely inhibit head-turning. There was a high correlation between the predicted clinical potency and these drugs based on inhibition of head-turning and their respective clinical anti-Parkinson potency. The centrally acting anticholinergic drugs also antagonized head-turning but there was not a good correlation between the predicted and acutal anti-Parkinson doses used in man. In order to determine if these drugs blocked head-turning by acting on the caudate nucleus, a combination cannula and stimulating electrode was used to administer drugs directly into the same area of the caudate nucleus being stimulated electrically. Dopamine, amantadine and apomorphine each antagonized head-turning when infused into the same site, at doses which did not produce concurrent overt sterotyped behavior. Time- and dose-response data with all three drugs suggest a direct inhibitory action on the caudate nucleus consistent with their proposed mechanism for treatment of Parkinson symptomatology. Head-turning appears to be a useful animal model for the development of new, specific anti-Parkinson drugs and for the study of possible mechanism(s) of action of existing drugs.

Amantadine↗