# Neonatal sevoflurane anesthesia can also affect rat medulla spinalis

**Authors:** Elvan Ocmen, Hale Aksu Erdost, Osman Yilmaz, Alper Bagriyanik, Muge Kiray, Necati Gokmen

PMC · DOI: 10.2478/abm-2025-0017 · 2025-06-30

## TL;DR

This study shows that neonatal sevoflurane anesthesia increases spinal cord cell death in rats, though motor function remains unaffected.

## Contribution

The study reveals a novel effect of sevoflurane on spinal cord apoptosis in neonatal rats.

## Key findings

- Chronic sevoflurane exposure significantly increased apoptotic cell count in the spinal cord.
- No significant difference in motor function was observed between sevoflurane and control groups.
- Tail flick test results showed significant differences on specific postnatal days.

## Abstract

Anesthesia has been linked to neuroapoptosis and prolonged neurocognitive disorders in the neonatal rat brain, but the full extent of damage induced by anesthesia on the central nervous system is still unknown.

We aim to investigate whether sevoflurane anesthesia affects the spinal cord.

After the approval of the ethics committee, 24 Wistar albino rat pups, weighing between 9 g and 11 g, on the postnatal 7th day were included in the study. In the sevoflurane groups, rats breathed 2.5% sevoflurane in oxygen. The tail flick tests were performed on postnatal 8th, 15th, and 30th days to evaluate motor functions. At the end of the experiments, rats were sacrificed by decapitation, and their spinal cords were taken for histopathological evaluation.

There was a significant difference between the tail pulling times on the 8th and 30th days in both groups (P = 0.036). No significant difference was found between the control and sevoflurane groups (P = 0.053). In histopathological assessments, the chronic sevoflurane group showed a significant increase in apoptotic cell count (P < 0.001).

This study showed that although there was a significant increase in apoptotic cells in the chronic sevoflurane group, motor function of the spinal cord was not affected. Further studies can be conducted to investigate the possible mechanisms.

## Linked entities

- **Chemicals:** sevoflurane (PubChem CID 5206)

## Full-text entities

- **Genes:** Dntt (DNA nucleotidylexotransferase) [NCBI Gene 294051], Mtor (mechanistic target of rapamycin kinase) [NCBI Gene 56718] {aka Frap1, RAFT1}
- **Diseases:** postsurgical (MESH:D010149), neuroinflammation (MESH:D000090862), neurodegeneration (MESH:D019636), neurocognitive disorders (MESH:D019965), neuronal injury (MESH:D009410), medulla spinalis injury (MESH:D013606), motor function deficits (MESH:D001289), chronic pain (MESH:D059350), hippocampal injury (MESH:D001930), depression (MESH:D003866), neurotoxic (MESH:D020258), pain (MESH:D010146), Learning and memory deficits (MESH:D007859)
- **Chemicals:** Crystal violet (MESH:D005840), formalin (MESH:D005557), Sevoflurane (MESH:D000077149), O2 (MESH:D010100), paraffin (MESH:D010232), xylene (MESH:D014992), ethanol (MESH:D000431), Isoflurane (MESH:D007530), N2O (MESH:D009609), Cresyl-violet (MESH:C028911), dUTP (MESH:C027078)
- **Species:** Homo sapiens (human, species) [taxon 9606], Rattus norvegicus (brown rat, species) [taxon 10116]
- **Mutations:** C-22 C

## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12303590/full.md

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Source: https://tomesphere.com/paper/PMC12303590