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Biomedical subjects

J Rupreht

Publications and source records attributed to J Rupreht.

At least 55 records · Page 3Linked to original sources
PubMed1986

Stimulus processing during apparent unconsciousness in anesthetized volunteers.

Return of motor-responses upon request as an indicator of stimulus processing during apparent unconsciousness in general anesthesia was studied in 8 healthy, male volunteers during prolonged inhalation of nitrous oxide. First the minimal effective concentration of nitrous oxide was established for each volunteer, based upon continued absence of motor-responses to repeated verbal commands. One week later this concentration of nitrous oxide was administered for a 3-hr. period; return of motor-responses after at least 30 min. of absence was considered a sign of so-called unconscious perception. Four volunteers showed return of motor-response within the 3 hr. of exposure, but two of these had been rather restless throughout the session. Results indicate that unexpected processing of information by patients may occur during presumed unconsciousness after a prolonged inhalation of nitrous oxide in general anesthesia.

Adult↗
PubMed1986

[Postanesthetic recall ability, anxiety and dreams in surgical patients. A clinical study].

The recall of stimuli registered during general anaesthesia is described. Patients were interviewed 2 days after surgery, concerning their experiences during anaesthesia. In a second series of observations, the interview was preceded by a short inquiry, which took place in the recovery room as soon as the patient awoke. Anxiety was also assessed by pre- and postoperative tests. Of 140 patients, 2 described recall of awareness during anaesthesia. There was no evidence that external stimuli had been incorporated into dream content.

Adolescent↗
PubMed1985

Tolerance to nitrous oxide in volunteers.

Nociception and loss of awareness during exposure to anaesthetic concentration of nitrous oxide (N2O) were studied in eight male medical students. The cold water nociception test, where a hand is immersed in 0 degree C stirred water, was used for measurement of nociception. At irregular intervals an auditory command was given to oppose two fingers, and this served to monitor consciousness. The selected inspiratory concentration of N2O used per individual was sufficient to induce a loss of consciousness for more than 2.5 min, within 10 min of exposure to N2O. This concentration of N2O varied from 60% to 80%. The experimental exposure to N2O lasted 3 h. In all volunteers significant antinociception was observed within 2 min of exposure to N2O. The maximal analgesic effect was observed between 20 and 30 min of exposure to N2O. The analgesic effect of N2O gradually decreased and was absent in all eight volunteers within 150 min. Two volunteers regained consciousness at 77 and 91 min of exposure, whilst still breathing 60 and 80% N2O. These results show that tolerance to antinociceptive effects of N2O in man rapidly develops and that awareness may occur in some volunteers during prolonged exposure to N2O.

Adult↗
PubMed1984

REM sleep deprivation decreases the antinociceptive property of enkephalinase-inhibition, morphine and cold-water-swim.

Rats treated with phosphoramidon (an enkephalinase-inhibitor 250 micrograms, i.c.v.), morphine (20 micrograms i.c.v.) or subjected to cold-water-swim (CWS, animals forced to swim in water at 5 degrees C for 5 min) showed consistent analgesia. The antinociceptive effect of phosphoramidon, morphine and CWS was antagonised by REM sleep deprivation (REMSD). It is suggested that normal duration of REM sleep is of importance for the anti-nociceptive activity of endogenous and exogenous opiates.

Analgesia↗
PubMed1984

Enkephalinase inhibition prevented tolerance to nitrous oxide analgesia in rats.

Tolerance to nitrous oxide (N2O) antinociception was studied in rats in accordance with the Randall-Selitto pressure nociception test. Both N2O (70% in 30% O2) and the relatively selective enkephalinase inhibitor phosphoramidon (350 micrograms i.c.v.), which blocks the biotransformation of enkephalins, were administered. They both induced a significant analgesic effect which vanished within 45 min. The rapidly developed tolerance to N2O analgesia does not affect the anaesthetic state since the animals remained motionless for the duration of exposure lasting 3 h. In the animals treated with the enkephalinase inhibitor phosphoramidon, no development of tolerance to N2O-antinociception occurred during the exposure lasting 3 h. The results indicate that tolerance to N2O analgesia can be abolished by activation of the enkephalinergic system, which might suggest a possible insufficiency of this system during tolerance to N2O.

Animals↗
PubMed1983

Effect of phosphoramidon - a selective enkephalinase inhibitor - on nociception and behaviour.

Phosphoramidon (100-350 micrograms i.c.v.), a selective enkephalinase inhibitor, induced in the rat a decrease of nociception to pressure stimulation without evident respiratory depression. In addition, intensive behavioural changes such as grooming (licking the fur, face washing and scratching), mounting behaviour and wet dog shakes were observed. Naltrexone pretreatment (1 mg/kg i.p.) caused a significant decrease in the phosphoramidon-induced nociception and behavioural changes. Puromycin (30 micrograms i.c.v. or 7.5 mg/kg i.p.) caused no changes in nociception or behaviour.

Animals↗
PubMed1983

The involvement of the central cholinergic and endorphinergic systems in the nitrous oxide withdrawal syndrome in mice.

The nitrous oxide withdrawal syndrome in mice was used as an experimental model to examine some of the factors which may play a role in postanesthetic excitation. Predisposition to nitrous oxide withdrawal convulsions as judged by duration of susceptibility was decreased significantly after pretreatment with the cholinesterase inhibitors, physostigmine and galanthamine, or with the opiate receptor blocking agent naloxone. Results are discussed in relation to the central anticholinergic syndrome, endorphin release, and disturbances which follow nitrous oxide anesthesia in humans and animals.

Animals↗
PubMed1983

Methyl atropine bromide versus atropine sulphate. A clinical comparison.

In a double blind clinical investigation we compared methyl atropine bromide to atropine sulphate in equivalent doses for their effects on changes in the heart rate and dryness of the mouth. Drugs were administered five minutes before the induction of anesthesia. Methyl atropine bromide appeared to have a stronger positive chronotropic effect on the heart rate and a more pronounced mouth drying action. Less dysrhythmias were observed after the methyl congener. Both drugs failed to alter blood pressure significantly. We concluded that methyl atropine bromide is superior to atropine sulphate because it does not produce side effects which may cause the central anticholinergic syndrome. For clinical use, however, methyl atropine bromide should be administered only in half-equivalent dose of atropine sulphate to prevent excessive tachycardia and dryness of the mouth.

Adult↗
PubMed1983

Electrocorticographic changes in cats after intoxication with anticholinergic drugs.

Atropine sulphate or atropine-methyl-bromide were administered to cats intravenously in a dose of 0.0115 mmol/kg (i.e 4 mg/kg). Electrocorticogram changes were studied. Atropine sulphate caused the classical shift of the electrocorticogram from high-frequency-low-voltage pattern to a low-frequency-high-voltage pattern. We observed no changes of the electrocorticogram after the administration of atropine-methyl-bromide.

Animals↗
PubMed1983

The role of a noradrenergic system in the antinociceptive effects of 4-aminopyridine in the rat.

Antinociceptive effects of physostigmine and 4-aminopyridine after i.p. administration were studied in rats according to the Randall-Selitto nociception method. The antinociceptive action of physostigmine was not significantly influenced by atropine, naloxone or alpha-methyl-p-tyrosine. The antinociceptive action of 4-aminopyridine was also unaffected by simultaneous administration of atropine, naloxone or pretreatment by DL-p-chlorophenylalanine. However, 4-aminopyridine was without antinociceptive effect in rats pretreated with alpha-methyl-p-tyrosine. It is suggested that the antinociceptive action of 4-aminopyridine is mediated by a noradrenergic system.

4-Aminopyridine↗
PubMed1982

Elimination of irritating compounds during chronic exposure to gases.

Ammonia (NH3, a degradation product of urine) and intestinal gases which accumulate in the experimental circuit during the long-term experimental exposure of rats to gases might cause disturbing irritation in the behavior of the animals. A relatively simple and cheap experimental arrangement has been suggested for the elimination of these irritating compounds. This system also guarantees the maintenance of a constant concentration of the investigated gases. In order to facilitate the comparison of the results of various studies, the standardization of the basic experimental procedure for the long-term exposure to gases has been suggested.

Ammonia↗