Der Anaesthesist
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Randomized Controlled Trial Clinical Trial Controlled Clinical Trial
[Esmolol as a bolus for prevention of sympathetic adrenergic reactions following induction of anesthesia].
In addition to laryngoscopy, endotracheal intubation, and other stressful intraoperative phases, hypertension occurs during recovery from anaesthesia, provoking post-operative complications like bleeding and increased intracranial or intraocular pressure. Furthermore, these hypertensive reactions result in life-threatening complications, especially in patients with pre-existing cardiovascular diseases. In this study, the effect of the new, short-acting beta-blocker esmolol given as a single bolus for preventing the increases in blood pressure and heart rate during recovery from anaesthesia and extubation in patients with hypertension was investigated. ⋯ Thus, the potential risks of beta-blockers due to half-life are minimised. The results of this study show that a dangerous increase in BP and HR with increased myocardial oxygen consumption can be prevented by a single bolus, and better by a double bolus of 100 mg esmolol. Although bradycardia with HR below 50.min-1 in 8 patients might indicate a risk of cardiac instability, the systolic BP did not fall below 100 mm Hg, and the episode of bradycardia was so short that there was no risk to the patients.
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Clinical Trial
[Topographic electroencephalometry following anesthesia induction with ketamine-midazolam].
The neurophysiological action of ketamine has attracted increasing interest in recent years, with special interest in receptor action and in neurophysiological differences between and psychomimetic side effects of the two enantiomorphs. Most of the neurophysiological examinations published deal with ketamine as a single anaesthetic agent, although it has been suggested to that psychomimetic side-effects and haemodynamic deterioration could be avoided by combining ketamine with a sedative drug. The primary aim of our study was to examine the combined ketamine-midazolam action on cerebral activity; secondly, we planned to look at these interactions topographically at different points of the cortex to evaluate topographical differences in the combination's action; thirdly, the cerebral and haemodynamic reactions to anaesthesiological stimuli (intubation, gastric tube) were evaluated and compared. ⋯ Thus, the action of combined ketamine and midazolam on cerebral function is not an additive, but an interactive process. Despite a relatively high induction dosage, haemodynamic changes during intubation occurred and were accompanied by changes in cerebral activity. This can be regarded as incomplete cerebral suppression even by these induction dosages.
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Slices of the rabbit caudate nucleus were incubated with [3H]choline for 30 min and then superfused continuously with Mg(2+)-free medium at 37 degrees C. Stimulation with N-methyl-D-aspartate (NMDA) caused a concentration-dependent release of [3H]acetylcholine (ACh), which was abolished in the presence of MG2+. This release of ACh was exocytotic and mediated by action potentials. ⋯ At the neuropathologic level, Parkinson's disease is characterized by an overshoot of striatal cholinergic transmission due to the decreased inhibitory dopaminergic input from the substantia nigra. The well-known antiparkinsonian effect of memantine and amantadine is most probably due to a blockade of NMDA-receptor-linked ion channels on striatal cholinergic interneurons, leading in turn to a diminished release of ACh. Since ketamine diminished cholinergic neurotransmission to a similar degree to that achieved with memantine and amantadine and even more potently than the adamantanes, and that at concentrations far below those needed for its anaesthetic and analgesic properties, it seems worthwhile to test this drug as an antiparkinsonian agent clinically.
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Review Randomized Controlled Trial Clinical Trial
[Medical therapy for coronary heart disease. Perioperative relevance].
The aim of our review is to summarize relevant data on the perioperative use of anti-ischaemic drugs in patients at risk for or with proven coronary heart disease. ⋯ Beta-blockers, calcium channel blockers, nitrates, and possibly alpha 2-agonists lead to reduced rates of PMI and other cardiac complications in risk patients. Current anti-anginal medications, with the exception of anti-platelet agents, should be maintained to the day of surgery and continued as soon as possible thereafter. All of these drugs except anti-platelet agents may also be used intra-operatively, however, possible interactions with anaesthetic agents should be carefully considered.
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Randomized Controlled Trial Comparative Study Clinical Trial
[Ketamine racemate versus S-(+)-ketamine with or without antagonism with physostigmine. A quantitative EEG study on volunteers].
The potency of S-(+)-ketamine is approximately double that of the racemic ketamine. This study was carried out to investigate the recovery of cerebral electrical function after a bolus of 1.3 mg/kg ketamine or 0.65 mg/kg S-(+)-ketamine and subsequent continuous application of 4 mg/kg h ketamine per h or 2 mg/kg S-(+)-ketamine, per h for 15 min. Furthermore, the centrally acting, cholinergic agonist physostigmine has been reported to antagonize ketamine and to shorten the recovery period. ⋯ The spectral edge frequency did not differ between measurement points, and is therefore not suitable for assessment of the depth of anaesthesia reached with ketamine/S-(+)-ketamine. The dose of physostigmine tested was probably too low to produce antagonism of S-(+)-ketamine. An increased dosage of physostigmine has yet to be studied, but is likely to cause a higher rate of side effects, such as nausea, vomiting and bradycardia, and possibly even tonic-clonic seizures.