[Central anticholinergic syndrome during postoperative period].

The central anticholinergic syndrome (CAS) includes central signs (somnolence, confusion, amnesia, agitation, hallucinations, dysarthria, ataxia, delirium, stupor, coma) and peripheral signs (dry mouth, dry skin, tachycardia, visual disturbances and difficulty in micturition). It occurs when central cholinergic sites are occupied by specific drugs and also as a result of an insufficient release of acetylcholine. The CAS can be caused by atropine sulphate, hyoscine (scopolamine), promethazine, benzodiazepines, opioids, halothane, influrane, ketamine.

No effect of doxapram during enflurane-nitrous oxide anesthesia.

Doxapram was administered to 50 spontaneously breathing patients receiving enflurane and nitrous oxide for surgical anesthesia. A similar group acted as control. Significant depression of ventilation did not occur in the control group of patients, nor did doxapram produce a reduction of end tidal CO2 concentrations.

[Physostigmine--recent pharmacologic data and their significance for practical use].

Physostigmine is widely used for treatment of the central anticholinergic syndrome during recovery from anaesthesia. The drug is also very useful in treatment of intoxicated patients, in differential-diagnostic procedures of coma of unknown origin, and in restoration of vigilance after prolonged sedation for mechanical ventilation. Besides the specific central cholinergic action of physostigmine, several new pharmacological actions have now been established.

Atropine methylbromide and glycopyrrolate. A comparative study during reversal of neuromuscular block.

Two quaternary anticholinergics, atropine methylbromide (methylatropine bromide, MAB) and glycopyrrolate (ROBINUL) were compared as adjuncts to neostigmine for the reversal of residual nondepolarising neuromuscular block. MAB 0.75 mg in combination with neostigmine 2 mg produced a marked initial rise in heart rate.

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.

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.

Absence of electroencephalographic excitation pattern under isoflurane anesthesia.

In twelve patients the EEG was recorded under isoflurane--nitrous oxide inhalation anesthesia. A quiet EEG pattern was registered, without suppressions and seizures of spike activity which are often observed under enflurane. This was the case even when end expiratory CO2 shifted to low values (3-3.

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.

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.

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).

Physostigmine versus naloxone in heroin-overdose.

Two groups of 10 chronically heroin addicted patients who were admitted to the Emergency Ward because of hypoventilation and coma, were treated random- aselectively with naloxone, 3 micrograms kg-1 BW iv, or with physostigmine salicylate 0,04 mg kg-1 BW iv. Patients in both groups completely regained consciousness and breathed spontaneously, regularly and adequately within 10 minutes. One essential difference in the treatment was that physostigmine caused no signs of acute opiate withdrawal, the patients felt fine and stayed for further control, in contrast with naloxone where the patients felt bad and occasionally escaped prematurely from the ward.

Practical experiences with flunitrazepam in anesthesia.

Flunitrazepam was used in general and local anesthesia. Little effect was noted on the respiratory and cardiovascular systems. In our patients there was an impressive period of amnesia and often we observed a central anticholinergic syndrome, which could be reversed by the use of physostigmine salicylate (0.

Central anticholinergic syndrome in anesthetic practice.

Anticholinergic agents may lead to a syndrome described by Longo as the Central Anticholinergic Syndrome (CAS). Patients with this syndrome exhibit one or more of the following: though impairement, disturbance of recent memory, hallucinations, ataxia, excitement, drowsiness of coma. We have reviewed our use of anticholinergics and tried to correlate it with the occurrence of the above symptomatology and have treated 200 cases in which the CAS was diagnosed with physostigmine salicylate (0.