PubMed Health⌕ Search

Biomedical subjects

M J Turnbull

Publications and source records attributed to M J Turnbull.

At least 19 recordsLinked to original sources
PubMed1978

Effect of pretreatment with bronchodilator drugs on in vitro responsiveness of guinea pig lung adenylate cyclase.

Pretreatment of guinea pigs with 5 microgram/kg isoprenaline or 10 microgram/kg salbutamol s.c. thrice daily for 7 days reduced the responsiveness of lung slice and tracheal ring adenylate cyclase to isoprenaline, but not to prostaglandin E1. Pretreatment of guinea pigs with isoprenaline also reduced the sensitivity of tracheal smooth muscle strip adenylate cyclase to isoprenaline. Cross-tolerance developed to noradrenaline in lung slices obtained from guinea pigs pretreated with isoprenaline. Propranolol blocked the response of lung slice adenylate cyclase of control and isoprenaline-pretreated animals to approximately the same degree. The presence of phentolamine in the incubation medium did not affect the reduced sensitivity to isoprenaline. Possible mechanisms of development of tolerance to sympathomimetic bronchodilator drugs are discussed.

Adenylyl Cyclases↗
PubMed1978

In vitro profile of some opioid pentapeptide analogues.

The opiate agonist potency of thirteen synthetic enkephalin pentapeptides has been examined on the electrically stimulated guinea pig ileum and mouse vas deferens preparations in comparison with methionine and leucine enkephalins, beta-endorphin and normorphine. Their antagonism by naloxone (Ke) was also assessed on each preparation. Our findings are compatible with, and are discussed in the context of, the hypothesis that these preparations possess at least two populations of receptors.

Animals↗
PubMed1977

Urinary monoamine metabolite excretion in disorders of movement. Effects of amantadine and levodopa.

We have studied the urinary excretion of 1,4-methylhistamine (1,4-MeHm), 5-hydroxyindole-3-acetic acid (5-HIAA) and homovanillic acid (HVA) in patients with Parkinson's disease, choreiform movements and essential tremor. The effect of amantadine on urinary excretion has been measured in each group of patients as well as the effect of levodopa in patients with Parkinson's disease. In patients with Parkinson's disease, excretion of 1,4-MeHm and HVA was significantly lower than in controls. Patients with choreiform movements had a reduced excretion of HVA but trends toward low levels of 1,4-MeHm and, in patients with Huntington's chorea, elevated excretion of 5-HIAA, were not significant. In patients with essential tremor, urinary excretion of the amine metabolities studied did nof differ significantly from controls. Administration of amantadine to patients with Parkinson's disease was not followed by increased excretion of monoamine metabolites except in those patients who were already receiving anticholinergic drugs. This increase is not significant and there was no effect in other groups of patients. These findings lend no support to the view that amantadine has a general amine-releasing action although there is limited evidence for such an effect in Parkinson's disease. In addition to the expected increase in HVA excretion, administration of levodopa to Parkinsonian patients was followed by significantly reduced excretion of 1,4-MeHm and 5-HIAA. However, if amantadine and levodopa were given together, excretion of 5-HIAA was still reduced, but that of 1,4-MeHm was normal. Levodopa may thus modify the turnover of histamine, which appears to be reduced in Parkinson's disease, and this effect may be modified by amantadine.

Amantadine↗
PubMed1976

Acute tolerance to barbiturate in the rat.

3 experimental approaches to the quantitation of acute barbiturate tolerance have been compared in the rat. There was no difference between the brain hexobarbitone or barbitone concentration found at the time of loss of righting reflex compared with the concentration found on return of the righting reflex following the period of anaesthesia produced by a single i.p. injection of the drug. However, tolerance was induced by a 7 hr infusion of pentobarbitone which kept rats anaesthetized for approximately 8 hr. Such rats awakened with a significantly higher brain pentobarbitone concentration compared with rats awakening after a single i.p. injection. Repeated i.p. injections of pentobarbitone, sufficient to keep animals anaesthetized for 12 hr, also induced a tolerance to pentobarbitone, as indicated by a reduced sleeping time and higher brain barbiturate concentration on awakening following intracerebroventricularly administered pentobarbitone injected 12 hr after the last i.p. injection. The possible relationship between acute cellular tolerance and physical dependence is discussed.

Animals↗
PubMed1976

Determination of halothane-induced sleeping time in the rat: effect of prior administration of centrally active drugs.

A method is described for the determination of halothane-induced sleeping time in the rat. 2 The sleeping time exhibited a diurnal variation which was due, at least in part, to a change in the sensitivity of the central nervous system (CNS) to the anaesthetic. 3 Tolerance to halothane did not develop in rats repeatedly exposed to the anaesthetic over a period of over 48 hours. 4 Repeated sleeping time determinations have been used to follow changes in the sensitivity of the CNS to the anaesthetic occurring with time. 5 A tolerance to halothane was induced by pretreatment of rats with doses of amylobarbitone, pentobarbitone or meprobamate sufficient to keep animals anaesthetized for approximately 12 hours. This tolerance was followed by a period of halothane-hypersensitivity. 6 Halothane-tolerant animals awakened with higher brain halothane concentrations and were also tolerant to intracerebroventricularly administered pentobarbitone. 7 Halothane-hypertensive rats awakened with lower brain halothane concentrations and were also hypersensitivity to intracerebroventricularly administered pentobarbitone. 8 The possibility that the induction of cross-tolerance to halothane may be indicative of a drug's potential to produce dependence is discussed.

Animals↗
PubMed1975

The pharmacology of Avena sativa.

The pharmacology of Avena sativa has been investigated in laboratory animals following a report that tincture of Avena sativa reduced the craying for cigarettes in man. The tincture, evaporated to dryness, craving for cigarettes in man. The tincture, evaporated to dryness, re-constituted in an equal volume of water and administered by stomach tube or intraperitoneal injection, antagonized the antinociceptive effect of morphine in two separate test (hot-plate and tail flick). Compared with animals made depedent on morphine alone, mice pretreated with repeated injections of morphine plus extract passed a smaller number of stools and tended to jump less after administration of nalorphine. The pressor response to intravenously administered nicotine in urethane-anaesthetized rats was also antagonized by prior administration of Avena sativa. However, the aqueous extract prepared from the tincture did not affect the seizure threshold to bemegride or nicotine or the sleeping time induced by barbitone sodium.

Animals↗