1. Role of the abdominal vagus and hindbrain in inhalational anesthesia-induced vomiting
- Author
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Michael Sciullo, Yolande Ramaroson, Ragini G. Gupta, Charles C. Horn, and Claire E. Schafer
- Subjects
0301 basic medicine ,Stilbamidines ,Vomiting ,Nausea ,medicine.medical_treatment ,Vagotomy ,Article ,Random Allocation ,03 medical and health sciences ,Cellular and Molecular Neuroscience ,0302 clinical medicine ,Neural Pathways ,medicine ,Animals ,Dose-Response Relationship, Drug ,Isoflurane ,Endocrine and Autonomic Systems ,business.industry ,Shrews ,Area postrema ,Vagus Nerve ,Immunohistochemistry ,Vagus nerve ,Rhombencephalon ,030104 developmental biology ,Dorsal motor nucleus ,Anesthesia ,Anesthetics, Inhalation ,Models, Animal ,Female ,Neurology (clinical) ,medicine.symptom ,Anesthesia, Inhalation ,Emetics ,business ,Proto-Oncogene Proteins c-fos ,030217 neurology & neurosurgery ,Postoperative nausea and vomiting ,medicine.drug - Abstract
The incidence of postoperative nausea and vomiting (PONV) can be as high as 80% in patients with risk factors (e.g., females, history of motion sickness). PONV delays postoperative recovery and costs several hundred million dollars annually. Cell-based assays show that halogenated ethers (e.g., isoflurane) activate 5-HT3 receptors, which are found on gastrointestinal vagal afferents and in the hindbrain - key pathways for producing nausea and vomiting. This project evaluated the role of the vagus and activation of the hindbrain in isoflurane-induced emesis in musk shrews – a small animal model with a vomiting reflex, which is lacking in rats and mice. Sham-operated and abdominal vagotomized shrews were exposed to 1 to 3% isoflurane to determine effects on emesis; vagotomy was confirmed by lack of vagal transport of the neuronal tracer Fluoro-Gold. In an additional study, shrews were exposed to isoflurane and hindbrain c-Fos was measured at 90 min after exposure using immunohistochemistry. There were no statistically significant effects of vagotomy on isoflurane-induced emesis compared to sham-operated controls. Isoflurane exposure produced a significant increase in c-Fos-positive cells in the nucleus of the solitary tract and vestibular nuclei but not in the area postrema or dorsal motor nucleus. These results indicate that the abdominal vagus plays no role in isoflurane-induced emesis and suggest that isoflurane activates emesis by action on the hindbrain, as shown by c-Fos labeling. Ultimately, knowledge of the mechanisms of inhalational anesthesia-induced PONV could lead to more targeted therapies to control PONV.
- Published
- 2017