[Practical aspects of use of nitrous oxide in children].
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Anesthetics, Inhalation↗
Biomedical subjects
J Rupreht
Publications and source records attributed to J Rupreht.
[Fatal arrhythmia following administration of suxamethonium in a postpartum woman subsequently found to have dystrophia myotonica].
A 28-year-old woman died of irreversible ventricular fibrillation after administration of succinylcholine because of post partum curettage. Afterwards it became known she had undiagnosed myotonic dystrophy. She also had metabolic acidosis because of haemorrhagic hypovolaemia resulting in a probably elevated serum K+ concentration preoperatively. Succinylcholine given to patients with myotonic dystrophy may lead to life threatening hyperkalaemia and cardiac arrest. Therapy should be aimed at immediate lowering of serum K+ concentration with calcium, sodium bicarbonate and hyperventilation.
Adult↗
Behavioral and electrophysiological aspects of nitrous oxide dependence.
We examined the effect of 70% nitrous oxide (N2O) on locomotion and visual-evoked potentials (VEP) in rats. The animals exposed to N2O showed an initial decrease of locomotion, followed by development of tolerance and unaltered motor activity during N2O withdrawal. Similarly, an initial decrease of VEP amplitudes was followed by tolerance to N2O. In addition, some amplitudes (N2-P3, P3-N3, and N3-P4) exceeded the control values, indicating an increase of neuronal excitability of the visual system during a long lasting exposure to N2O. The increase of VEP amplitudes was further potentiated by cessation of this gas. The VEP latencies after initial increase, returned to normal and remained unaltered during N2O withdrawal suggesting that the speed of neurotransmission is not essentially changed during chronic exposure to N2O. However, a significant increase of neuronal excitability during chronic N2O exposure, which further increased by cessation of N2O, could be of clinical importance. Therefore, monitoring of VEP, particularly the amplitude values, may significantly improve a detection of altered neuronal excitability during anaesthesia and drug withdrawal.
Animals↗
Effects of morphine and physostigmine on the ventilatory response to carbon dioxide.
BACKGROUND: It has been reported that physostigmine antagonizes morphine-induced respiratory depression, but it is not known whether this is due to a central chemoreceptor effect, an effect on the peripheral chemoreflex loop, or both. We therefore assessed the effect of morphine and physostigmine on the normoxic hypercapnic ventilatory response mediated by the central and peripheral chemoreceptors in ten alpha-chloralose-urethan-anesthetized cats. METHODS: The breath-by-breath ventilatory responses to stepwise changes in end-tidal CO2 tension were determined before (control), after administration of morphine hydrochloride (0.15 mg.kg-1) and during intravenous infusion of physostigmine salicylate (bolus of 0.05 mg.kg-1 followed by 0.025 mg.kg-1.h-1). Each response was separated into a central and a peripheral chemoreflex characterized by CO2 sensitivity (Sc and Sp), time constant, time delay, and apneic threshold (a single off-set B). RESULTS: Morphine increased B and decreased Sc and Sp (P < 0.01), but not the ratio Sp/Sc. Subsequent infusion of physostigmine decreased B (P < 0.01), without further change of Sp and Sc. Premedication with physostigmine decreased B, Sp and Sc (P < 0.01) vs. control, but not Sp/Sc. Subsequent administration of morphine decreased Sp and Sc further but increased B (P < 0.01), while Sp/Sc remained constant. CONCLUSIONS: Because morphine diminishes the Sc and Sp of the chemoreflex loop to the same extent this depressant effect is presumably due to an action on the respiratory integrating centers rather than on the peripheral and central chemoreceptors as such and is not antagonized by physostigmine. We argue that the increase in B may be due to changes in the amount of acetylcholine available in the brain and can be antagonized by physostigmine.
Anesthesia↗
Effects of eseroline on the ventilatory response to CO2.
The effect of eseroline on the normoxic hypercapnic ventilatory response was assessed in nine alpha-chloralose-urethane-anaesthetized cats. The ventilatory responses to step changes in end-tidal PCO2 were determined before (control), during i.v. infusion of eseroline (bolus of 1.2 mg.kg-1 followed by 0.65 mg.kg-1 x h-1) and 1 h after the end of the infusion. Each response was separated into central and peripheral chemoreflexes, characterized by CO2 sensitivity, time constant, time delay and apnoeic threshold. We found that eseroline depressed ventilation by affecting both tidal volume and breathing frequency. The ventilatory response to CO2 was depressed due to a decrease in the CO2 sensitivity of peripheral chemoreceptors from 0.20 to 0.12 l.min-1 x kPa-1 and in the CO2 sensitivity of central chemoreceptors from 1.04 to 0.50 l.min-1 x kPa-1 (P < 0.01). However, the ratio of these sensitivities was not changed, like the apnoeic threshold. The depressant effect was reversed by naloxone. We conclude that the depressant effect of eseroline on ventilatory response to CO2 is mainly due to an action on the respiratory integrating centres in the brainstem rather than on the CO2 sensitivity of peripheral and central chemoreceptors.
Analgesics↗
Patient-controlled analgesia (PCA) leads to more postoperative pain relief, but also to more fatigue and less vigour.
This investigation evaluated patient-controlled analgesia (PCA) for subjective well-being and mood in the postoperative period in comparison with the intramuscular (im) administration of morphine given on demand. Patients scheduled for elective upper abdominal surgery were assigned at random to either PCA (n = 17) or im morphine (n = 14). The PCA group experienced significantly more pain relief and consumed more morphine than those who received im morphine. The PCA patients suffered from more fatigue and showed less vigour than the im group. Neither preoperative trait anxiety nor locus of control was associated with postoperative pain in either of the groups.
Adult↗
The effects of orally active enkephalinase inhibitors on morphine withdrawal syndrome.
Considerable evidence has accumulated to suggest that intracerebroventricular administration of enkephalinase inhibitors, which do not penetrate the blood-brain barrier, significantly attenuates opioid withdrawal syndrome. Therefore, the aim of this study was to examine the effect of intraperitoneal (i.p.) administration of orally active enkephalinase inhibitors, acetorphan (2.5-20 mg kg-1) and SCH 34826 (15-120 mg kg-1). These drugs significantly decreased the severity of the naloxone precipitated withdrawal syndrome in morphine dependent rats and mice. It therefore appears that these orally active enkephalinase inhibitors are promising tools in studying modulation of opioid dependence phenomena.
Administration, Oral↗
Monitoring cobalamin inactivation during nitrous oxide anesthesia by determination of homocysteine and folate in plasma and urine.
The effects of nitrous oxide-induced cobalamin inactivation on homocysteine and folate metabolism have been investigated. Plasma levels of cobalamin, folate, homocysteine, and methionine were determined in 40 patients before and after operation under nitrous oxide anesthesia (range of exposure time, 70 to 720 minutes). Twelve patients anesthetized with total intravenous anesthesia served as control subjects (range of exposure time, 115 to 600 minutes). Postoperative plasma levels of folate and homocysteine increased (p less than 0.001) up to 220% and 310%, respectively, in nitrous oxide-exposed patients, whereas plasma levels of methionine decreased (p less than 0.025). Response occurred after 75 minutes of nitrous oxide exposure. The percentage increase of plasma folate and homocysteine correlated significantly with exposure time (p less than 0.025 and p less than 0.0001, respectively). In eight patients receiving nitrous oxide anesthesia plasma homocysteine levels had not returned to preoperative levels within 1 week (p less than 0.01). Urinary excretion of folate and homocysteine increased during and after nitrous oxide exposure (p less than 0.01 and p less than 0.002, respectively) and correlated with exposure time (p less than 0.01 and p less than 0.005, respectively). It can be concluded that disturbance of homocysteine and folate metabolism by nitrous oxide develops with little delay and return to normal levels requires several days. Elevation of plasma homocysteine levels may therefore be used for monitoring nitrous oxide-induced cobalamin inactivation.
Adult↗
Hyoscine derivative in children--but was it hyoscine?
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Anesthesia Recovery Period↗
Effect of aminophylline or physostigmine on recovery from nitrous oxide-enflurane anaesthesia.
If facilities for recovery are limited, shortening the recovery time from general anaesthesia is important. A comparative study on the effect of 3 mg.kg-1 aminophylline or 0.04 mg.kg-1 physostigmine on duration and quality of the recovery time from nitrous oxide-enflurane anaesthesia is presented. Three groups of 35 patients were observed, placebo being included for comparison in this double-blind study. Without treatment, recovery from nitrous oxide-enflurane inhalation anaesthesia lasted 18.8 +/- 5.80 min. Aminophylline considerably shortened the recovery time (12.06 +/- 3.52 min), whereas physostigmine did not (18.97 +/- 9.18 min). In the physostigmine group, however, a remarkably calm recovery and early return of protective reflexes was observed. Although aminophylline shortens the recovery time, due to earlier incidence of pain and other disturbances, it cannot be recommended for general improvement of recovery, whereas physostigmine clearly improves the quality of recovery from nitrous oxide-enflurane anaesthesia.
Adult↗
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↗
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↗
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↗
Suppressive effects of enkephalins and REM sleep deprivation on seizures.
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Animals↗
[Patient-controlled analgesia in postoperative pain--PCA].
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Analgesia, Patient-Controlled↗
[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↗
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↗
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↗