Articles: function.
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Anesthesia and analgesia · Mar 2016
Incomplete Spontaneous Recovery from Airway Obstruction During Inhaled Anesthesia Induction: A Computational Simulation.
Inhaled induction with spontaneous respiration is a technique used for difficult airways. One of the proposed advantages is if airway patency is lost, the anesthetic agent will spontaneously redistribute until anesthetic depth is reduced and airway patency can be recovered. There are little and conflicting clinical or experimental data regarding the kinetics of this anesthetic technique. We used computer simulation to investigate this situation. ⋯ Spontaneous recovery after complete airway obstruction during inhaled induction is plausible, but the recovery time is highly variable and depends on the clinical and physiologic situation. These results emphasize that induction is a non-steady-state situation, thus effect-site anesthetic levels should be modeled in future research, not alveolar concentration. Finally, this study provides an example of using computer simulation to explore situations that are difficult to investigate clinically.
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The spinal dorsal horn contains numerous inhibitory interneurons that control transmission of somatosensory information. Although these cells have important roles in modulating pain, we still have limited information about how they are incorporated into neuronal circuits, and this is partly due to difficulty in assigning them to functional populations. Around 15% of inhibitory interneurons in laminae I-III express neuropeptide Y (NPY), but little is known about this population. ⋯ Our results suggest that this input originates from a small subset of NPY-expressing interneurons, with the projection cells representing only a minority of their output. Taken together with results of previous studies, our findings indicate that somatodendritic morphology is of limited value in classifying functional populations among inhibitory interneurons in the dorsal horn. Because many NPY-expressing cells respond to noxious stimuli, these are likely to have a role in attenuating pain and limiting its spread.
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Although neonatal exposure to anesthetic drugs is associated with memory deficiency in rodent models and possibly in pediatric patients, the underlying mechanisms remain elusive. The authors tested their hypothesis that exposure of the developing brain to anesthesia triggers epigenetic modification, involving the enhanced interaction among transcription factors (histone deacetylase 2, methyl-cytosine-phosphate-guanine-binding protein 2, and DNA methyltransferase 1) in Bdnf promoter region(s) that inhibit brain-derived neurotrophic factor (BDNF) expression, resulting in insufficient drive for local translation of synaptic mRNAs. The authors further hypothesized that noninvasive environmental enrichment (EE) will attenuate anesthesia-induced epigenetic inhibition of BDNF signaling and memory loss in rodent models. ⋯ The findings of this study elucidated the epigenetic mechanism underlying memory deficiency induced by neonatal anesthesia and propose EE as a potential therapeutic approach.
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Understanding the mechanisms underlying neuronal death in spinal cord injury (SCI) and developing novel therapeutic approaches for SCI-induced damage are critical for functional recovery. Here we investigated the role of heme oxygenase-1 (HO-1) in neuroprotection after SCI. ⋯ HO-1 protects spinal cord neurons after SCI through inhibiting NLRP1 inflammasome formation.