PubMed · 11780170
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R Hürlmann. 2001-11-09. [Premedication before endoscopy].. https://doi.org/10.1055/s-2001-18327-2
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BACKGROUND: This double-blind randomized study was undertaken to assess agitation, Bispectral Index (BIS) and EEG changes during induction of anaesthesia with sevoflurane in children premedicated with midazolam or clonidine. METHODS: Children were allocated randomly to receive rectal midazolam 0.4 mg kg(-1) (n=20) or oral clonidine 4 microg kg(-1) (n=20) as premedication. Rapid induction of anaesthesia was achieved with inhalation of sevoflurane 8% in nitrous oxide 50%-oxygen 50%. After tracheal intubation, the children's lungs were mechanically ventilated and the inspired sevoflurane concentration was adjusted to achieve an end-tidal fraction of 2.5%. The EEG and BIS were recorded during induction until 10 min after tracheal intubation. The EEG was analysed using spectral analysis at five points: baseline, loss of eyelash reflex, 15 s before the nadir of the BIS (BIS(nadir)), when both pupils returned to the central position (immediately before intubation), and 10 min after intubation. RESULTS: Agitation was observed in 12 midazolam-treated and five clonidine-treated patients (P=0.05). At baseline, EEG rhythms were slower in the clonidine group. Induction of anaesthesia was associated with similar EEG changes in the two groups, with an increase in total spectral power and a shift towards low frequencies; these changes were maximal around the end of the second minute of induction (BIS(nadir)). When the pupils had returned to the central position, fast EEG rhythms increased and BIS was higher than BIS(nadir) (P<0.05). In both groups, agitation was associated with an increase in slow EEG rhythms at BIS(nadir). CONCLUSIONS: Compared with midazolam, clonidine premedication reduced agitation during sevoflurane induction. During induction with sevoflurane 8% (oxygen 50%-nitrous oxide 50%), the nadir of the BIS occurred at the end of the second minute of inhalation. Agitation was associated with a more pronounced slowing of the EEG rhythms at BIS(nadir) compared with inductions in which no agitation was observed. The BIS may not follow the depth of anaesthesia during sevoflurane induction in children.
BACKGROUND: We compared the cardioprotective effects of 1 minimum alveolar concentration (MAC) desflurane administered before, during or after ischaemia, or throughout the experiment (before, during and after ischaemia) on myocardial infarct size following 30 min occlusion of the left anterior descending coronary artery and 3 h reperfusion in adult rats. METHODS: Fifty male Sprague-Dawley rats were anaesthetized with pentobarbital, intubated and mechanically ventilated. Blood gases, pH and body temperature (37.5-38 degrees C) were controlled. Heart rate and arterial pressure were measured continuously. Animals were randomly assigned to the following groups (n=10 in each group): pentobarbital only ("Pento"); 15 min desflurane administration followed by 10 min of washout before 30 min ischaemia and 3 h reperfusion ("Precond"); 30 min desflurane administration during ischaemia period ('Isch'); desflurane administration during the 15 first min of reperfusion ("Reperf") and desflurane administration throughout the experiment (before, during and after ischaemia; "Long"). Volumes at risk and infarct sizes were assessed by Indian ink and with 2,3,5-triphenyltetrazolium chloride staining, respectively. RESULTS: Physiological parameters and volumes at risk were not significantly different between groups. In the Pento group, mean myocardial infarct size was 65 (sd 15)% of the volume at risk; myocardial infarct size was reduced to a significant and comparable extent in the desflurane-treated groups (Precond 42 (14)%; Isch 34 (11)%; Reperf 41 (15)%; Long 33 (10)%; P<0.0002 vs Pento group). CONCLUSIONS: In rats, desflurane 1 MAC significantly decreased myocardial infarct size whatever the period and duration of administration.
Gamma-hydroxybutyrate (GHB) has been shown to have therapeutical properties in various psychiatric disorders, especially in alcohol abuse, and to mimic different actions of ethanol at the cellular and system level. Using whole-cell patch-clamp recordings on brain slices of 21- to 25-day-old rats, the present study investigated the effects of GHB and ethanol on spontaneous excitatory postsynaptic currents (sEPSCs) in dopaminergic neurons of the substantia nigra pars compacta (SNc). sEPSCs are an index of glutamate release from the excitatory input to dopamine cells, which play a key role in different reward-related behaviors. We found that GHB and ethanol depressed both the frequency and the amplitude of sEPSCs. These effects were GABA(B)-independent and the GHB-induced depression was blocked by the GHB receptor antagonist 6,7,8,9-tetrahydro-5[H]benzocyclohepte-5-ol-4-ylidene acetic acid (NCS-382), pointing to a specific effect of this drug. The effects of ethanol were not affected by NCS-382. This study indicates that GHB and ethanol share the effect of reducing the efficacy of excitatory glutamatergic neurotransmission in the SNc by acting through different mechanisms.