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Biomedical subjects

H R Bürki

Publications and source records attributed to H R Bürki.

At least 19 recordsLinked to original sources
PubMed1983

Measurement of cholecystokinin octapeptide-induced motility of rat antrum, pylorus, and duodenum in vitro.

Motor effects of cholecystokinin octapeptide (CCK-OP) on rat antrum, pylorus, and duodenum have been studied in vitro under standard conditions. Intraluminal pressure changes were simultaneously measured at the three locations using a perfusion manometric system with a novel intraluminal pressure-sensor device. This device comprised an acrylic cast of the rat gastroduodenal tract containing the perfusion catheters that reached the surface of the cast with their outlets in the antrum, pylorus, and duodenum. A selective and sensitive intraluminal local pressure measurement was achieved with this pressure sensor due to its shape. CCK-OP increased base-line pressure in the antrum, pylorus, and duodenum; frequencies of phasic contractions in the antrum and pylorus; and amplitudes in the duodenum. The peptide also decreased contraction amplitudes in the antrum and pylorus and frequency of phasic contractions in the duodenum. It is concluded that the novel intraluminal pressure sensor is a useful tool for measuring local pressure changes in the gastroduodenal tract of the rat. In this experimental model, effects of CCK-OP on antral, pyloric, and duodenal base-line pressure are comparable with those observed in isolated muscle strips and in the intact organ of humans, dogs, and opossums. A different behavior, however, was observed in the force of antral and frequency of duodenal phasic contractions.

Animals↗
PubMed1983

Mechanism of action of cholecystokinin octapeptide on rat antrum, pylorus, and duodenum.

The mechanism of action of cholecystokinin octapeptide (CCK-OP) on tonic and phasic contraction of antral, pyloric, and duodenal smooth muscles was studied with a novel perfusion manometric system in isolated esophagogastroduodenal preparations of the rat. CCK-OP increased baseline pressure at each site, frequencies of phasic contractions in the antrum and pylorus, and amplitudes in the duodenum. It decreased antral and pyloric amplitudes and frequency of duodenal phasic contractions. CCK-OP action on tonic contraction was tetradotoxin (TTX) susceptible and its action on phasic contractions was TTX resistant. Phentolamine, phenoxybenzamine, propranolol, catecholamine depletion of preparations by reserpine-tetrabenazine, and the block of catecholamine synthesis at different levels significantly inhibited CCK-OP-induced tonic contraction, whereas atropine had no influence. Adrenergic and cholinergic neural actions on phasic contractions altered the level of amplitudes and frequencies on which CCK-OP action occurred. It is concluded that CCK-OP action on tonic contraction of the rat gastroduodenal junction is mediated by a neural noncholinergic pathway, whereas its effect on muscles responsible for phasic contractions is a direct one.

Animals↗
PubMed1981

Receptor dynamics: effect of repeated administration of desmethylimipramine on the noradrenergic systems in rat brain.

The effects of a single and of repeated administration of desmethylimipramine (DMI) on the densities of various receptors and on the metabolism of noradrenaline (NA) were determined in rat brain. Inhibition of the uptake of NA into cortex slices, measured in vitro, was not diminished after repeated administration of DMI. The turnover of NA was inhibited only after the single administration of the drug. After repeated administration the turnover of NA was again within the normal range, but now the density of beta-receptors was significantly reduced. Repeated administration of DMI had no significant effect on the densities of alpha-adrenergic, dopaminergic, cholinergic, histaminergic, opiate and serotoninergic receptors. These results indicate that the continued blockade of NA-reuptake caused a selective desensitization of beta-receptor-regulated systems in the brain.

Animals↗
PubMed1980

The pharmacology of 5-chloro-4-(2-imidazolin-2-yl-amino)-2,1,3-benzothiadiazole (DS 103-282), a novel myotonolytic agent.

5-Chloro-4-(2-imidazolin-2-yl-amino)-2,1,3-benzothiadiazole (DS 103-282) is a centrally acting agent with a novel chemical structure and a pharmacological profile different from that of myotonolytic drugs in current use such as diazepam, baclofen and dantrolene. It inhibits alpha- and gamma-rigidity in rats, reflex muscle tone in rabbits and the linguomandibular reflex in cats at low doses, but has little or no effect on gross spinal reflexes or electrically-induced segmental reflexes in cats. The mechanism underlying the muscle relaxation is unknown. Effects on convulsions induced by impaired GABA-transmission and by strychnine suggest a possible influence on glycine-mediated neurotransmission. In muscle-relaxing doses, DS 103-282 is without appreciable sedative, haemodynamic or neurochemical effects. Clinical investigations have confirmed the pharmacological predictions with regard to both the myotonolytic activity and the low propensity to produce side-effects.

Analgesics↗
PubMed1979

Two novel prolactin release-inhibiting 8 alpha-amino-ergolines.

Prolactin secretion inhibition and changes in striatal dopamine metabolism in rats were compared after the administration of 8 alpha-amino-ergoline CH 29-717 and 2 derivates. CQ 32-084 was similar to but less potent than CH 29-717, while 32-085, the l-methyl derivative, showed delayed dopaminomimetic effects.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1978

Neurochemical and neuropharmacological investigations with four ergot derivatives: bromocriptine, dihydroergotoxine, CF 25-397 and CM 29-712.

Neurochemical and neuropharmacological investigations with four ergot derivatives reveal differential pharmacodynamic effects of these compounds. Bromocriptine and CM 29-712 showed actions typical of postsynaptic dopamine receptor stimulants, in particular in the extrapyramidal system. CM 29-712 proved to be more potent than bromocriptine, with an early onset of action. CF 25-397 and dihydroergotoxine, while not showing all actions typical of central dopamine agonists, appeared to exert some of their effects by means of a stimulation of central serotoninergic sites. In the rat sleep-wakefulness cycles and in reserpine-induced ponto-geniculooccipital waves in the cat, they mimicked the effects of 5-hydroxytryptophan. In the latter test, CF 25-397 proved to be particularly potent. In addition, bromocriptine, dihydroergotoxine and CM 29-712 showed neurochemical effects consistent with central alpha-adrenergic blockade or an enhanced impulse flow in central noradrenergic neurons.

Animals↗
PubMed1977

Animal models for tardive dyskinesia: effects of thioridazine.

After repeated administration of classical neuroloptics to the rat, supersensitivity of striatal dopamine (DA) receptors towards DA-receptor agonists can be demonstrated. This effect can be quantified (a) by measuring the turning response to apomorphine in rats with unilateral striatal lesions or (b) by measuring the changes induced by neuroleptics in the DA metabolism in the striatum of intact rats. In these test systems, thioridazine induces an increase in DA-receptor sensitivity which is significantly less intense and of shorter duration than that induced by haloperidol. The tendency of a drug to increase DA-receptor sensitivity has been related to its propensity to induce tardive dyskinesia in man, and on this basis it may be expected that tardive dyskinesias following treatment with thioridazine will be rare and less intense than those seen after classical neuroleptics.

Animals↗
PubMed1977

Effects of clozapine and other dibenzo-epines on central dopaminergic and cholinergic systems. Structure-activity relationships.

Structure-activity relationships of 16 dibenzoepines, including clozapine, loxapine, clothiapine and perlapine, have been investigated with regard to locomotor inhibition, cataleptogenesis, apomorphine antagonism, arousal inhibition, effect on striatal dopamine metabolism, and in vivo and in vitro anticholinergic potency. Thioridazine and the classical neuroleptics haloperidol and chlorpromazine were included in the study for comparison. The classical tests used to detect neuroleptic activity in laboratory animals were found to be poor predictors of possible clinical effectiveness of the dibenzo-epines.

Animals↗
PubMed1976

Anticholinergic properties of antipsychotic drugs and their relation to extrapyramidal side-effects.

The effects of haloperidol, alone and in combination with atropine, were compared with the effects of clozapine, alone and in combination with physostigmine, in a variety of tests commonly used to characterize neuroleptic compounds. It was found that clozapine in combination with physostigmine did not present the profile of activity of a classical neuroleptic agent; neither did haloperidol in combination with atropine present that of clozapine. In fact, some effects of haloperidol (catalepsy) were antagonized by atropine, while others (induction of striatal DA-receptor hypersensitivity) were enhanced. It is concluded that the interaction between dopaminergic and cholinergic systems in the striatum is highly complex, and that a neuroleptic possessing both potent DA-receptor blocking and muscarinic anticholinergic activity, while being less likely to cause parkinsonism in patients, would be more likely to induce tardive dyskinesias.

Animals↗
PubMed1976

Effect of clozapine on the metabolism of serotonin in rat brain.

Clozapine, but not chlorpromazine, haloperidol, thioridazine, or loxapine, increases the concentrations of tryptophan, serotonin, and 5-hydroxyindoleacetic acid in the brain of the rat. This effect of clozapine is due to an increased serotonin synthesis as demonstrated by an enhanced accumulation of 3H-serotonin in the brain after i.v. infusion of 3H-tryptophan. Clozapine also elevates the plasma concentration of free tryptophan, and reduces the plasma concentration of total tryptophan. Therefore, clozapine may increase the brain serotonin concentration by enhancing the availability of tryptophan in the brain, thereby promoting serotonin synthesis. Measurement of the rate of disappearance from the brain of 3H-serotonin or of endogenous serotonin after synthesis inhibition with 6-fluorotryptophan shows that clozapine has no direct effect on the release and degradation of serotonin. The effect of clozapine on brain serotonergic systems may possibly be related to the pronounced sedative and sleep-inducing properties of this drug.

Animals↗