Anesthesia and analgesia
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Anesthesia and analgesia · May 2013
Editorial CommentComparing apples to oranges: just say no to N2O?
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Anesthesia and analgesia · May 2013
The impact of hypothermia on emergence from isoflurane anesthesia in orexin neuron-ablated mice.
Orexin neurons regulate the sleep/wake cycle and are proposed to influence general anesthesia. In animal experiments, orexin neurons have been shown to drive emergence from general anesthesia. In human studies, however, the role of orexin neurons remains controversial, owing at least, in part, to the fact that orexin neurons are multifunctional. Orexin neurons regulate not only the sleep/wake cycle, but also body temperature. We hypothesized that orexin neurons do not directly regulate emergence from anesthesia, but instead affect emergence indirectly through thermoregulation because anesthesia-induced hypothermia can greatly influence emergence time. To test our hypothesis, we used simultaneous measurement of body temperature and locomotor activity. ⋯ The effect of orexin deficiency to impair thermoregulation during general anesthesia is of sufficient magnitude that body temperature must be appropriately controlled when studying the role of orexin neurons in emergence from anesthesia.
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Anesthesia and analgesia · May 2013
Train-of-four and tetanic fade are not always a prejunctional phenomenon as evaluated by toxins having highly specific pre- and postjunctional actions.
Nerve-stimulated fade in muscle is generally accepted as a prejunctional phenomenon mediated by block of prejunctional acetylcholine receptors (AChRs) at the nerve terminal, whereas decrease of twitch tension is considered a postjunctional effect due to block of muscle AChRs. Using ligands with specific pre- or postjunctional effects only, we tested the hypothesis that fade is not necessarily a prejunctional phenomenon. ⋯ Botx-induced decreased ACh release in and of itself does not cause fade but does cause decrease of absolute tensions. Decrease of available (functional) postjunctional AChRs by α-BTX did induce fade. The prejunctional fade effects of DHβE on α3β2 AChRs become manifest only when the margin of safety was decreased by concomitant administration of α-BTX. Thus, fade during repetitive stimulation is not always a prejunctional phenomenon and may also reflect the decreased margin of safety of neurotransmission, which can be due to a pure postjunctional AChRs block or to a combination of both pre- and postjunctional AChRs block. Block of prejunctional α3β2 AChRs alone is not necessary and sufficient to cause fade.
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Anesthesia and analgesia · May 2013
The antinociceptive effect of SNAP5114, a gamma-aminobutyric acid transporter-3 inhibitor, in rat experimental pain models.
Gamma-aminobutyric acid (GABA) is the primary inhibitory neurotransmitter in the mammalian central nervous system. GABAergic transmission has an important role in regulating nociception at the spinal dorsal horn. It is terminated by rapid uptake of the neurotransmitter from the synaptic cleft into neurons and glial cells, via specific GABA transporters (GATs). Among the 4 GATs, GAT-3 has the greatest expression in central nervous system regions closely associated with nociceptive transmission, including the spinal cord. In this study, we examined the antinociceptive effect of intrathecal administration of a selective GAT-3 inhibitor, SNAP5114, on acute, inflammatory, and neuropathic pain in experimental models. ⋯ These results suggest that SNAP5114 exerts antinociceptive effects by activating GABAA and GABAB receptors in the spinal cord. The GAT-3 inhibitor may prove useful in treatment of various painful conditions.