Articles: dexmedetomidine.
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Randomized Controlled Trial Clinical Trial
Effects of dexmedetomidine on isoflurane requirements in healthy volunteers. 2: Auditory and somatosensory evoked responses.
The anaesthetic-sparing activity of dexmedetomidine during isoflurane anaesthesia was examined, using the end-point of lack of response to tetanic nerve stimulation. Nine subjects were given two doses of dexmedetomidine (target plasma concentrations of 0.3 ng ml-1 and 0.6 ng ml-1, respectively) and saline on separate occasions. We measured auditory (AER) and somatosensory (SER) evoked responses at end-tidal isoflurane concentrations of 0.2-1.4%. ⋯ The dose of dexmedetomidine had a significant interaction with this trend (P < 0.002). Decreasing the concentration of isoflurane at the high dose of dexmedetomidine had less impact on P15-N20 amplitude than decreasing isoflurane at the low dose or with saline. The mechanism by which dexmedetomidine spares isoflurane is discussed in the light of these evoked response changes.
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Randomized Controlled Trial Clinical Trial
Effect of dexmedetomidine on the minimum alveolar concentration (MAC) of sevoflurane in adults age 55 to 70 years.
To determine the effect of two target dexmedetomidine infusions (0.3 ng/ml and 0.6 ng/ml) on the minimal alveolar concentration (MAC) of sevoflurane in adults age 55 to 70 years. ⋯ Dexmedetomidine 0.7 ng/ml decreased the MAC of sevoflurane by 17%, whereas there was no difference between the placebo and the dexmedetomidine 0.39 ng/ml group.
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Dexmedetomidine is an alpha 2 agonist and has been reported to have proconvulsant actions. To investigate the interaction of dexmedetomidine with convulsant anaesthetics, we studied effects on seizure threshold in cats during enflurane anaesthesia. Cats were prepared with chronic implantation of electrodes for recording of the cortical electroencephalogram (EEG) and midbrain reticular formation multi-unit activity (R-MUA). ⋯ The effects of dexmedetomidine 1, 10 and 100 micrograms kg-1 i.v. and yohimbine 500 micrograms kg-1, an alpha 2 antagonist, on SII during 3.5% enflurane anaesthesia were investigated. Dexmedetomidine significantly increased SII at 10 and 100 micrograms kg-1, and this effect was reversed by yohimbine. We found that high-dose dexmedetomidine reduced seizure threshold during enflurane anaesthesia.
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Journal of anesthesia · Sep 1996
Effects of spinal naloxone and naltrindole on the antinociceptive action of intrathecally administered dexmedetomidine.
Intrathecally administered alpha-2 adrenoceptor and opioid agonists are well known to exert antinociceptive effects in humans and various animals. To examine the interaction of these two groups of agents in the spinal cord, we tested the effect of the opioid antagonists naloxone or naltrindole on the antinociceptive action of an intrathecally administered alpha-2 agonist, dexmedetomidine, using a formalin test in rats. 19 groups of Sprague-Dawley rats (250-300 g) were prepared with chronic intrathecal catheters and examined for the effects of agents on the formalin test. Each group contained 6 animals. 50 μl of 5% formalin was injected subcutaneously in the plantar surface of one hind paw. ⋯ Intrathecal dexmedetomidine (1 μg) maximally depressed the behavioral changes in both phase 1 and phase 2 of the formalin test, which was antagonized by the alpha-2 adrenoceptor selective antagonist atipamezole (0.3 μg). Naloxone (0.1-10 μg) or naltrindole (1-10 μg), when coadministered with dexmedetomidine, showed a dose-dependent antagonism to the effect of dexmedetomidine, whereas naloxone, naltrindole, or atipamezole alone showed no effect on the nocieptive behavior due to formalin injection. These results indicate that the antinociceptive effect of intrathecally administered alpha-2 adrenoceptor agonists may involve opioid receptors in the spinal cord.
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alpha(2)-Adrenoceptor agonists like clonidine, dexmedetomidine, and ST-91, inhibit nociceptive reflex activity predominantly by a spinal mode of action. They mimic the action of the inhibitory transmitter noradrenaline, which is released from the terminals of bulbospinal monoaminergic pathways. The inhibition by noradrenaline is due partly to hyperpolarization of the postsynaptic neuronal membrane; however, the selective antinociceptive effect of the alpha(2)-adrenoceptor agonists results from reduction of the release of the excitatory transmitters such as glutamate and substance P, blockade of the binding of substance P to spinal neurones, and enhancement of the action of the inhibitory transmitter, 5-hydroxytryptamine. ⋯ Moreover, impulse conduction in C fibres of peripheral nerves is far more reduced by these compounds than that in A fibres. Antinociceptive effects are reported to occur in various models of clinical pain, e.g. the formalin test, adjuvans-induced arthritis, autotomy following deafferentation, and "hyperalgesia" after nerve ligation. Therefore, the mechanisms involved in antinociception may also be responsible for the analgesia produced by alpha(2)-adrenoceptor agonists.