[Balanced general anesthesia by the combination of sodium 4-hydroxybutyrate dehydrobenzperidol and dextromoramide].
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The effects of verapamil were studied in anaesthetised dogs administered dextromoramide intrathecally to provide background vagal tone. Measurements were made of spontaneous heart rate, and, in paced hearts, of conduction times in atrial muscle, the atrioventricular node (A-V node) and His-Purkinje system by means of His bundle potential recording. The effective refractory period (ERP) of A-V node was measured by the extrastimulus method. In atropinised and vagotomised animals, verapamil reduced sinus rate and increased A-V nodal conduction time. In dogs high vagal tone after dextromoramide, however, verapamil increased sinus rate and reduced A-V nodal ERP. After dextromoramide alone, A-V block was observed at an atrial pacing rate of 150 beats X min-1, but after verapamil 1:1 A-V conduction was restored. The decrease in conduction velocity in the A-V node due to ACh was neither attenuated nor enhanced by verapamil.
This study reports the in vitro influence of morphine, dextromoramide, levomoramide, and methionine-enkephalin upon normal human T blood lymphocytes by using the active and total rosette tests. Morphine and dextromoramide inhibited the percentage of active T rosettes. This effect was completely reversed in the presence of naloxone, their specific antagonist. The specificity was further demonstrated by the absence of the effect of levomoramide, the inactive enantiomere, upon the rosette system. Methionine-enkephalin increased the percentage of active T rosettes. This effect was specifically inhibited by naloxone. These observations suggest that normal human blood T lymphocytes bear surface receptor-like structures for morphine, dextromoramide, and methionine-enkephalin. Such findings may provide a link between the central nervous system and the immune system.
We are reporting on a case of polyintoxication by cocaine, lidocaine, methadone, and dextromoramide. This conclusion is supported by the analysis of a strand of hair. We note for the first time the detection of dextromoramide as well as lidocaine and desethyl-lidocaine in hair. Concentrations in hair were: cocaine = 2.4 ng/mg, benzoylecgonine = 0.3 ng/mg, methadone = 10.2 ng/mg, EDDP = 1.5 ng/mg, dextromoramide = 1.6 ng/mg, lidocaine = 115.9 ng/mg and desethyl-lidocaine = 1.6 ng/mg. The victim who was seeking an anesthesia effect without the loss of consciousness ingested cocktails during episodes of self mutilation. The wounds were of two different types and with different morphological locations: long and deep without ablation of tissue, clean lacerations found on the neck, the pectoral region, and the left upper extremity; either round or discoid with deep excavation found on the head (ears, forehead, chin, and lips) and also, on the neck and on the left upper extremity. Near the most recent wounds, needle marks were noticed indicating probable local infiltration of lidocaine.
The neuroleptic drugs used in anesthetics belong to the group of phenothiazines or butyrophenones. The endocrine response to their intravenous administration is still ill-known and usually only concerns the association of anesthetics and neuroleptics. However, as far as the catecholamines are concerned, it is known that neuroleptic drugs do not prevent either their secretion nor their liberation but, depending on their dosage, they block the dopaminergic receptors and the alpha-receptors and induce disturbances in the metabolism of the mono-amines. The injection of neuroleptics associated with analgesics, raises the blood levels of catecholamines, does not induce a rise in ACTH and cortisol levels in the absence of stress, but does not totally prevent their rise in cases of aggression. As far as growth hormone is concerned, the effects are variable depending on the association studied. There is a rise with droperidol + pethidine or pentazocine, no change with chloroprotixene-dextromoramide. In both cases, the blood sugar rises. As far as STH, or growth hormone, free fatty acids and insulin are concerned, one may note a rise with associations containing droperidol even in the absence of any stress and stability with a mixture of chlorprotixene and dextromoramide. With none of these well known associations was there any variation either in levels of pituitary thyreo-stimulin, nor in thyroxine levels. Testosterone becomes reduced with the association of droperidol + analgesics but this effect does not seem to be specific to droperidol. These responses are frequently disturbed in case of additional stress.
Isoflurane and halothane, two anaesthetics agents have been compared. Forty young and healthy patients were divided into two randomly selected group. Each of them was anaesthetized either with isoflurane or with halothane. Anaesthesia was maintained with nitrous-oxide and dextromoramide. During induction, the ventilation was spontaneous. Blood-gas, ventilation rate and tidal-volume were studied before induction, during anaesthesia and at the end of the surgery. Statistical data show a higher PaCO2 and a lower pH with isoflurane. This was increased by dextromoramide. During induction, complications occurred more after than with halothane but the emergence was better.
Morphine, dextromoramide (4 mumol/kg i.p.) and vimonol R2 (17 mumol/kg i.p.) in analgesic doses (28 to 112 mumol/kg i.p.) decreased 3',5'-cyclic guanosine monophosphate (cGMP) in rat cerebellar cortex; morphine also decreased the cGMP content in deep cerebellar nuclei. Intrastriatal but not intracerebellar injections of morphine (20 mug) decreased cerebellar cGMP content. Naltrexone, an opiate receptor antagonist, but only apomorphine, a dopaminergic receptor agonist, blocked the effect of morphine on cerebellar cGMP. Pretreatment with 3-acetylpyridine (3-AP) which destroys the climbing fibers, failed to antagonize the effect of morphine on cerebellar cGMP. These results suggest that activation of opiate receptors in striatum decreases cerebellar cGMP content presumably by reducing activity in the mossy fiber excitatory input to cerebellum.
The changes in core temperature induced by low (5 mg/kg) and high (40 mg/kg) doses of morphine were compared in Wistar and Sprague-Dawley rats. In Sprague-Dawley rats the low dose caused a hyperthermia and the high dose a hypothermia but in Wistar rats both doses caused a hyperthermia. In either case the change in core temperature was antagonized by naloxone (2 mg/kg). Tolerance to the effects of the high dose of morphine developed in both strains of rat. Dextromoramide (3.75 and 15 mg/kg) also had an effect on core temperature, but in this case the responses of the strains were opposite to those seen with morphine. Laevomoramide was relatively ineffective. Naloxone (2 mg/kg) had no effect on the ability of rats of either strain to withstand heat or cold stress, providing no evidence that endogenous morphine-like substances have a physiological role in thermoregulation.
Transcutaneous cranial electrical stimulation (TCES) with high frequency (166 kHz) intermittent current (100 Hz: Limoge current) has been used for several years in cardiac, thoracic, abdominal, urological and micro-surgery. The main benefits are a reduced requirement for analgesic drugs, especially opiates, and a long-lasting postoperative analgesia. We have confirmed these clinical observations in rats using the tail-flick latency (TFL) test to measure pain threshold. TCES was not found to modify the pain threshold in drug-free rats, but it potentiated morphine-induced analgesia (systemic injection). To obtain a maximal effect, the stimulation must be initiated 3 h before the drug injection and be maintained throughout the duration of its pharmacological action. TCES potentitation was found to depend on the dose of the drug, the intensity of the current and the polarity of electrodes. These findings were confirmed by blind tests of the efficiency of TCES on several opiate analgesic drugs currently used in human surgery (morphine, fentanyl, alfentanil and dextromoramide). The analgesic effect of these 4 opiates (TFL as % of baseline without or with TCES) were respectively: 174%, 306%; 176%, 336%; 160%, 215%; and 267%, 392%. The results were obtained not only after systemic opiate treatment, but also after intracerebroventricular injection of morphine (10 micrograms; analgesic effect 152%, 207% with TCES) suggesting that TCES potentiation of opiate-induced analgesia is centrally mediated.
BACKGROUND: To compare the acceptability and effectiveness of three pre-medication regimens for manually activated cardioversion of recurrent persistent atrial fibrillation. METHODS: Eighteen patients implanted with the Jewel AF atrial defibrillator for drug-resistant persistent atrial fibrillation only were studied in an open-labelled randomised crossover study. Patients were assigned to sedation (S) with midazolam elixir, analgesia (A) with morphine sulphate or combination therapy (C) with dextromoramide and lorazepam. Pre-medication was taken up to 1 h before cardioversion. Patients rotated through each type of medication after undertaking at least one cardioversion. Visual analogue scales were completed immediately post-cardioversion and 24 h later for pain, anxiety and 'unpleasantness'. Higher scores represented a worse outcome. RESULTS: After 2 years' follow-up, 238 cardioversions were performed with S, 17 with A and 35 with C. The mean immediate combined score for S (10.9, 95% confidence interval (CI) 8.2-13.6) was significantly lower than for A (17.3, 95% CI 15.1-19.5, P = 0.01) and for C (15.9, 95% CI 12.3-19.6, P = 0.02). All patients who used S chose it as the most favourable pre-medicant. All patients who used A found it the least acceptable. CONCLUSION: Sedation rather than analgesia enhanced the acceptability of manually activated atrial defibrillation.
In the rat, the ratio of the analgesic to the respiratory depressant potency was the same for morphine, codeine, diamorphine, methadone, dipipanone, piperidylisomethadone, phenadoxone, dextromoramide, and propoxyphene. The relative respiratory depressant activity of pethidine tended to be less, but the difference was not significant. The ratio of the analgesic dose to the dose preventing transport of a charcoal meal in the rat was about the same for morphine, codeine, pethidine, methadone, phenadoxone, dimethylthiambutene, and propoxyphene; the relative activities of these compounds in inhibiting the peristaltic reflex of the isolated guinea-pig ileum were also similar. However, because of differences in the slopes of regression lines in the charcoal meal test, some compounds (for example, morphine) had a greater effect on gastrointestinal propulsion than others (for example, pethidine) when given at moderate analgesic dose levels.In studies of the effects of intracisternal morphine in the rat, effects on the spinal reflex of the tail were to some extent dissociated from effects on the threshold for a squeak response. Further, the delaying of transport of a charcoal meal paralleled depression of respiratory rate, and this is evidence for the participation of a central as well as a peripheral action in the effect of morphine on the gastrointestinal tract. The delay in propulsion was reduced by nalorphine and increased by atropine and two general anaesthetic substances, but was unaffected by a number of other pharmacological agents.