British journal of anaesthesia
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We have studied rats with chronically implanted subarachnoid catheters. Xylazine, an alpha 2 adrenoceptor agonist, was injected intrathecally and nociceptive thresholds measured at two skin sites: the tail and the neck. Intrathecal xylazine (dose range 24.3-389 nmol) produced increases in electrical thresholds for nociception in the tail without any change in the neck; this observation suggested that the antinociceptive action of this drug was confined to the caudal part of the spinal cord responsible for tail innervation. ⋯ In contrast, the antinociceptive effects of intrathecal xylazine were not affected by concurrent administration of opioid or GABAA antagonists. We conclude that intrathecal xylazine produced spinally mediated antinociceptive effects by combination with spinal cord alpha 2 adrenoceptors and that neither opioid nor GABA-containing propriospinal neurones were involved in the mediation of this effect. However, alpha 2 adrenoceptors in the spinal cord appear to be involved with antinociception produced by intrathecal fentanyl.
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We have examined the effects of sedation with midazolam 0.1 mg kg-1 and reversal with flumazenil 0.5 mg on beat-to-beat heart rate (HR) variability (HRV), systolic arterial pressure (SAP), finger photoplethysmograph amplitude (PLA) and impedence pneumography in eight volunteers. With the onset of sedation there was a small decrease in SAP and increase in HR (ns). ⋯ These were thought to be secondary to activity of coupled cardiorespiratory neurones within the brain stem and the ventilatory periodicity appeared similar to that observed during the early stages of sleep. The diminished high frequency and increased low frequency oscillations induced by midazolam sedation were reversed by administration of flumazenil.
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Propofol is used widely during general anaesthesia but there has been concern that it may be implicated in provoking seizure activity. We have investigated the effects of low-dose propofol on the electrocorticogram of anaesthetized patients undergoing surgery for medically intractable epilepsy. During continuous peroperative recording of the electrocorticogram, propofol was administered in 25 mg increments until burst suppression occurred. ⋯ There was an increase in mean spike frequency in 16, extension of spike distribution in 15 and polyphasia in 13 patients. The mean dose of propofol required to cause burst suppression was 88.2 (range 25-175) mg. We conclude that at low doses, propofol caused activation of the electrocorticogram in epileptic patients but at higher doses burst suppression was induced.