Articles: anesthesia.
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Anesthesia and analgesia · Feb 2025
Substantia Innominata Glutamatergic Neurons Modulate Sevoflurane Anesthesia in Male Mice.
Accumulated evidence suggests that brain regions that promote wakefulness also facilitate emergence from general anesthesia (GA). Glutamatergic neurons in the substantia innominata (SI) regulate motivation-related aversive, depressive, and aggressive behaviors relying on heightened arousal. Here, we hypothesize that glutamatergic neurons in the SI are also involved in the regulation of the effects of sevoflurane anesthesia. ⋯ Our study shows that SI glutamatergic neuronal activity facilitates emergence from sevoflurane anesthesia and provides evidence for the involvement of the SI-LH glutamatergic pathway in the regulation of consciousness during GA.
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Journal of anesthesia · Feb 2025
Post-esophagectomy patients presenting for general anesthesia induction: a survey of practice among US anesthesiologists (PESO-GAIN-S).
Following esophagectomy, annually several thousand patients in the United States (US) reach a stable post-esophagectomy status. Such patients may require general anesthesia (GA) for elective procedures, but no generally accepted guidelines exist for the induction of GA in post-esophagectomy patients. ⋯ US attending anesthesiologists' approach to induction of GA in a patient with a history of successful esophagectomy was not uniform. The majority of responses reflected a concern for aspiration in such a patient. Considering surgical and non-surgical upper gastrointestinal changes, establishment of practice guidance to optimize perioperative care is an unmet need.
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Spinal cord stimulation (SCS) is an effective modality for pain treatment, yet its underlying mechanisms remain elusive. Neurokinin 1 receptor-positive (NK1R + ) neurons in spinal lamina I play a pivotal role in pain transmission. To enhance our mechanistic understanding of SCS-induced analgesia, we investigated how different SCS paradigms modulate the activation of NK1R + neurons, by developing NK1R-Cre;GCaMP6s transgenic mice and using in vivo calcium imaging of superficial NK1R + neurons under anesthesia (1.5% isoflurane). ⋯ However, at low intensity (20% MoT), the 30-minute 900-Hz SCS only induced persistent neuronal inhibition in naïve mice, but not in SNI-t mice. In conclusion, both 10-minute high-intensity SCS and 30-minute SCS at moderate intensity inhibit the activation of superficial NK1R + neurons, potentially attenuating spinal nociceptive transmission. Furthermore, in vivo calcium imaging of NK1R + neurons provides a new approach for exploring the spinal neuronal mechanisms of pain inhibition by neuromodulation pain therapies.