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Biomedical subjects

J Rupreht

Publications and source records attributed to J Rupreht.

At least 37 records · Page 2Linked to original sources
PubMed1991

Decrease of beta-endorphin in the brain of rats following nitrous oxide withdrawal.

beta-Endorphin levels in the whole rat brain were not changed during acute (25 min) or chronic (48 h) exposure of rats to N2O. However, a significant decrease of beta-endorphin was found in the whole brain, brain stem and subcortex during the withdrawal from chronic exposure to N2O. It has been suggested that decrease of beta-endorphin levels during N2O withdrawal could be ascribed to unspecific stress accompanying drug withdrawal. Decrease of central beta-endorphin during N2O withdrawal might have a significant modulatory effect on transmitter balance, neuronal excitability and corresponding withdrawal behaviour. Furthermore, the decrease of beta-endorphin levels in the whole brain during N2O withdrawal might contribute to the postanaesthesia N2O-excitatory syndrome in humans. This might explain the known therapeutic effect of the opioid drug, meperidine on the excitatory N2O withdrawal phenomena during recovery from N2O anaesthesia in man.

Animals↗
PubMed1991

The central muscarinic transmission during anaesthesia and recovery--the central anticholinergic syndrome.

Clinically relevant aspects of the muscarinic transmission in the CNS are mentioned. This transmission depends on the action of acetylcholine (ACh) on the muscarinic receptor and has been better elucidated than the CNS-cholinergic transmission subserved by the nicotinic receptor. Sub-types of the muscarinic receptor have been demonstrated. They are involved in many functions of the CNS. Therefore, disturbance of the CNS muscarinic transmission by ACh-antagonists or lack of ACh results in a colorful but unpredictable behavioural syndrome which is known as the central anticholinergic syndrome (CAS). To a certain degree, the CAS follows all forms of general anaesthesia. It can be prevented or treated by physostigmine which can elevate ACh-levels in the CNS. Postoperative restitution of the CNS-muscarinic transmission results in appropriate behavioural functioning early recovery. Normalization of ACh in the CNS also enhances analgesia and helps to sustain adequate breathing, heart rate and cardiovascular tone.

Anesthesia↗
PubMed1991

Propofol safely used in a neuroleptic malignant syndrome patient.

Anaesthetic regimens for patients with the poorly understood neuroleptic malignant syndrome (NMS) are not well outlined. In this case report, NMS and its questionable relation to malignant hyperpyrexia are outlined. Satisfactory use of total intravenous anaesthesia, based on propofol, in an NMS-susceptible patient is presented.

Anesthesia, Intravenous↗
PubMed1990

[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. The incidence of CAS during the postoperative period depends on choice and dose of anaesthetic agents, type of surgery, patient's condition and diagnostic criteria. It is close to 10% following general anaesthesia and 4% following regional anaesthesia with sedation. The differential diagnosis of CAS includes an overdose of anaesthetic drugs or an alteration in pharmacokinetics, altered hydratation, electrolyte or acid-base state, hypoglycaemia, hypoxia, hypercapnia, hypocapnia, hyperthermia, hypothermia, hormonal disorders, neurological damage resulting from surgery, embolism, haemorrhage or trauma. The diagnosis of CAS is often determined by a process of exclusion and not actually made until a positive therapeutic response to physostigmine, a centrally active anticholinesterase agent has taken place.

Anesthesia Recovery Period↗
PubMed1990

Haemodynamic and neurohumoral effects of xenon anaesthesia. A comparison with nitrous oxide.

Thirty-two patients were randomly allocated to be anaesthetised either with nitrous oxide or xenon. Those who received nitrous oxide required significantly more fentanyl peroperatively. Arterial blood pressure and heart rate were adequately controlled during surgery in both groups. Plasma noradrenaline and prolactin increased peroperatively in both groups, but plasma adrenaline and cortisol, which increased in the nitrous oxide group, did not change in the xenon group. Growth hormone was below control in those given xenon, but not in the nitrous oxide group, while dopamine remained unchanged in both groups. Postoperative plasma concentrations of noradrenaline, adrenaline, cortisol and prolactin (in both groups) and dopamine (in the nitrous oxide group) were elevated, and slowly returned to control. No differences were seen between the two gases in effects on plasma sodium and potassium. Xenon, because of its favourable haemodynamic, neurohumoral and antinociceptive properties, deserves a more prominent place in anaesthetic practice than it has so far occupied.

Adult↗
PubMed1990

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. It is suggested that surgical stimulation and concomitant nitrous oxide administration reduced the ventilatory depressant effect of enflurane and that the effect of doxapram was attenuated by the actions of enflurane on the peripheral chemoreceptors.

Adult↗
PubMed1989

Tolerance to N2O-induced alterations in somatosensory evoked potentials.

The effect of nitrous oxide (N2O) on somatosensory evoked potentials from the cortical (CEP) and spinal cord (SCP) regions in response to forepaw stimulation was studied in ketamine-anesthetized and mechanically ventilated rats. The CEP was recorded from the skull over the contralateral somatosensory area; the SCP was recorded from the supraspinous ligament at C57-6 and L1-2 levels of the spine. Rats were exposed to 70% N2O for 5 h, whereupon N2O was withdrawn for 2 h. Thereafter, the rats were re-exposed to N2O for 10 min. The N13-P21 component of the CEP, the slow positive wave (P2) of the segmental SCP, and the heterosegmental positive cord dorsum potential (HSP) were significantly suppressed by N2O, while the large negative (N1) component of the segmental SCP remained unchanged. A partial recovery of the CEP and HSP was observed during the 5 h of N2O anesthesia, while significant recovery of the P2 component of the SCP was not observed. The withdrawal from N2O following 5 h exposure caused an augmentation of the CEP (When compared to the control values). Re-exposure of rats to N2O again caused the suppression of these potentials as in the initial exposure. The results suggest that the phenomenon of tolerance to N2O in terms of evoked potentials develops within 5 h in the brain but not in the spinal cord.

Journal Article↗
PubMed1989

[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. Analgesic action is dependent on the interaction with the 5-HT (serotoninergic) system and is independent of narcotic or cholinergic agonists. The antianalgetic stress hormone, ACTH, also does not interfere with this action. Physostigmine does not interfere with the anaesthetic state when given during general anaesthesia. It attenuates several withdrawal states, especially alcohol delirium, opiate and nitrous oxide withdrawal syndromes. The drug may offer a protective mechanism against hypoxic damage of the brain and may also be beneficial in amnestic syndromes and sleep disorders. Physostigmine produces central and peripheral cardiovascular stimulation. It has been shown that physostigmine can be useful in prevention and treatment of postanaesthetic behavioural disturbances following anaesthesia with propofol. Number of indications for use of physostigmine has increased considerably.

Animals↗
PubMed1989

Central anticholinergic syndrome (CAS) in anesthesia and intensive care.

Many of the drugs used in anesthesia and intensive care may cause blockade of the central cholinergic neurotransmission. Acetylcholine is of significance in modulation of the interaction among most other central transmitters. The clinical picture of the central cholinergic blockade, known as the central anticholinergic syndrome (CAS), is identical with the central symptoms of atropine intoxication. This behaviour consists of agitation including seizures, restlessness, hallucinations, disorientation or signs of depression such as stupor, coma and respiratory depression. Such disturbances may be induced by opiates, benzodiazepines, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and halogenated inhalation anesthetics as well as by H2-blocking agents such as cimetidine. There is an individual predisposition for CAS--but unpredictable from laboratory findings or other signs. Reports of postanesthetic occurrence of the CAS requiring treatment are not unanimous, varying between 1 and 40%. Differential diagnosis of the CAS includes disorders of glucose and electrolyte metabolism, severe hormonal imbalance, respiratory disorders (hypoxia, hypercarbia), hypothermia, hyperthermia and neuropsychiatric diseases (cerebral hypoxia, stroke, catatony, acute psychosis). The CAS may considerably impair the postanesthetic period especially when agitation is prevalent, which may endanger the patient or the surgical results. The diagnosis is confirmed ex iuvantibus by the sudden increase in the acetylcholine level in the brain. This is achieved with physostigmine, a cholinesterase inhibitor able to easily cross the blood-brain barrier. Its peripheral muscarinic effects are minimal. Postanesthetic CAS can be prevented by administration of physostigmine during the anesthesia procedure. During intensive care (IC), agitated forms of CAS may occur in patients undergoing mechanical ventilation, particularly during prolonged high-dose sedation. Artificial ventilation of such patients becomes very difficult and muscle relaxation may be necessary. In these cases of IC-CAS, physostigmine is of value and has proven beneficial during weaning from mechanical ventilation. Dealing with the CAS for more than a decade has improved knowledge of the central cholinergic transmission. For example, it can be said that CAS occurs alongside general anesthesia, being no more than a frequent side-effect. Furthermore, acetylcholine is involved in nociception through the endorphinergic and the serotoninergic systems. There is a close relation between the central cholinergic transmission and actions of nitrous oxide. Moreover, cholinergic transmission is involved in withdrawal from (among others) alcohol, opiates, hallucinogens and nitrous oxide. In some intoxications with psychoactive agents, physostigmine is useful for reversal of the central nervous symptoms of the acute intoxication itself. In addition it can be used for prevention of some withdrawal states. In

Anesthetics↗
PubMed1989

[Nitrous oxide in anesthesia--present status of the use of nitrous oxide, risks for patients and personnel and treatment of side effects].

Mechanisms of some effects of nitrous oxide have recently been elucidated. Its antinociceptive action depends partly on the involvement of the endorphinergic system. Although vitamin B 12 becomes biologically inactive in the presence of nitrous oxide, this certainly is of no clinical consequence in exposures lasting less than eight hours. Should exposures last over 8 hours, effects of vitamin B 12 inactivation can be compensated for by administration of folinic acid. In contrast, professional exposure to trace levels of nitrous oxide seems not to interfere with human health. Furthermore, closed circle apparatus should be used and operating room air be well scavenged when nitrous oxide is used.

Anesthesia, Inhalation↗
PubMed1987

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. This was significantly greater than that produced by the administration of glycopyrrolate 0.4 mg with neostigmine. The antisialogogue effects of the two anticholinergics were identical and the central nervous system status of the patients was similar. It is concluded that, with the doses used in this study, glycopyrrolate is a superior alternative to MAB and is the drug of choice if a quaternary ammonium anticholinergic is required.

Adolescent↗
PubMed1986

An analgesic effect of enkephalinase inhibition is modulated by monoamine oxidase-B and REM sleep deprivations.

Both the MAO-B inhibitor deprenyl (2.5-10 mg/kg, ip, 60 min prior) and the MAO-B substrate beta-phenylethylamine (PEA, 40 micrograms, icv) potentiated the analgesic action of the enkephalinase inhibitor phosphoramidon (250 micrograms, icv) in animals allowed normal sleep. The enhancing effect of PEA on phosphoramidon analgesia was further potentiated by deprenyl (5 mg/kg, ip) pretreatment. Deprenyl (5 mg/kg, ip) or PEA (40 micrograms, iv) given alone did not induce analgesia in animals allowed undisturbed sleep. REM sleep deprivation (REMSD) decreased the basal pain threshold and abolished the analgesic effect of phosphoramidon. The administration of deprenyl and/or PEA failed to restore the analgesic effect of phosphoramidon in REM sleep deprived animals. The results indicate that excess PEA has a stimulatory effect on the analgesic activity of endogenously released enkephalins in rats allowed undisturbed sleep but not in REM sleep deprived animals. It is suggested that the failure of phosphoramidon to induce analgesia after REMSD, is probably due to a functional insufficiency of an enkephalinergic system.

Animals↗