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Bumetanide alleviates epileptogenic and neurotoxic effects of sevoflurane in neonatal rat brain.
Anesthesiology. 2010 Mar; 112(3):567-75.A

Abstract

BACKGROUND

We tested the hypothesis that in newborn rats, sevoflurane may cause seizures, neurotoxicity, and impairment in synaptic plasticity-effects that may be diminished by the Na-K-2Cl cotransporter 1 inhibitor, bumetanide.

METHODS

Electroencephalography, activated caspase-3, and hippocampal long-term potentiation were measured in rats exposed to 2.1% sevoflurane for 0.5-6 h at postnatal days 4-17 (P4-P17).

RESULTS

Arterial blood gas samples drawn at a sevoflurane concentration of 2.1% showed no evidence of either hypoxia or hypoventilation in spontaneously breathing rats. Higher doses of sevoflurane (e.g., 2.9%) caused respiratory depression. During anesthesia maintenance, the electroencephalography exhibited distinctive episodes of epileptic seizures in 40% of P4-P8 rats. Such seizure-like activity was not detected during anesthesia maintenance in P10-P17 rats. Emergence from 3 h of anesthesia with sevoflurane resulted in tonic/clonic seizures in some P10-P17 rats but not in P4-P8 rats. Bumetanide (5 micromol/kg, intraperitoneally) significantly decreased seizures in P4-P9 rats but did not affect the emergence seizures in P10-P17 rats. Anesthesia of P4 rats with sevoflurane for 6 h caused a significant increase in activated caspase-3 and impairment of long-term potentiation induction measured at 1 and 14-17 days after exposure to sevoflurane, respectively. Pretreatment of P4 rats with bumetanide nearly abolished the increase in activated caspase-3 but did not alleviate impairment of long-term potentiation.

CONCLUSION

These results support the possibility that excitatory output of sevoflurane-potentiated gamma-aminobutyric acid type A/glycine systems may contribute to epileptogenic and neurotoxic effects in early postnatal rats.

Authors+Show Affiliations

Department of Anesthesiology, University of Florida, Gainesville, Florida 32610-0254, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

20124973

Citation

Edwards, David A., et al. "Bumetanide Alleviates Epileptogenic and Neurotoxic Effects of Sevoflurane in Neonatal Rat Brain." Anesthesiology, vol. 112, no. 3, 2010, pp. 567-75.
Edwards DA, Shah HP, Cao W, et al. Bumetanide alleviates epileptogenic and neurotoxic effects of sevoflurane in neonatal rat brain. Anesthesiology. 2010;112(3):567-75.
Edwards, D. A., Shah, H. P., Cao, W., Gravenstein, N., Seubert, C. N., & Martynyuk, A. E. (2010). Bumetanide alleviates epileptogenic and neurotoxic effects of sevoflurane in neonatal rat brain. Anesthesiology, 112(3), 567-75. https://doi.org/10.1097/ALN.0b013e3181cf9138
Edwards DA, et al. Bumetanide Alleviates Epileptogenic and Neurotoxic Effects of Sevoflurane in Neonatal Rat Brain. Anesthesiology. 2010;112(3):567-75. PubMed PMID: 20124973.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Bumetanide alleviates epileptogenic and neurotoxic effects of sevoflurane in neonatal rat brain. AU - Edwards,David A, AU - Shah,Hina P, AU - Cao,Wengang, AU - Gravenstein,Nikolaus, AU - Seubert,Christoph N, AU - Martynyuk,Anatoly E, PY - 2010/2/4/entrez PY - 2010/2/4/pubmed PY - 2010/3/31/medline SP - 567 EP - 75 JF - Anesthesiology JO - Anesthesiology VL - 112 IS - 3 N2 - BACKGROUND: We tested the hypothesis that in newborn rats, sevoflurane may cause seizures, neurotoxicity, and impairment in synaptic plasticity-effects that may be diminished by the Na-K-2Cl cotransporter 1 inhibitor, bumetanide. METHODS: Electroencephalography, activated caspase-3, and hippocampal long-term potentiation were measured in rats exposed to 2.1% sevoflurane for 0.5-6 h at postnatal days 4-17 (P4-P17). RESULTS: Arterial blood gas samples drawn at a sevoflurane concentration of 2.1% showed no evidence of either hypoxia or hypoventilation in spontaneously breathing rats. Higher doses of sevoflurane (e.g., 2.9%) caused respiratory depression. During anesthesia maintenance, the electroencephalography exhibited distinctive episodes of epileptic seizures in 40% of P4-P8 rats. Such seizure-like activity was not detected during anesthesia maintenance in P10-P17 rats. Emergence from 3 h of anesthesia with sevoflurane resulted in tonic/clonic seizures in some P10-P17 rats but not in P4-P8 rats. Bumetanide (5 micromol/kg, intraperitoneally) significantly decreased seizures in P4-P9 rats but did not affect the emergence seizures in P10-P17 rats. Anesthesia of P4 rats with sevoflurane for 6 h caused a significant increase in activated caspase-3 and impairment of long-term potentiation induction measured at 1 and 14-17 days after exposure to sevoflurane, respectively. Pretreatment of P4 rats with bumetanide nearly abolished the increase in activated caspase-3 but did not alleviate impairment of long-term potentiation. CONCLUSION: These results support the possibility that excitatory output of sevoflurane-potentiated gamma-aminobutyric acid type A/glycine systems may contribute to epileptogenic and neurotoxic effects in early postnatal rats. SN - 1528-1175 UR - https://www.unboundmedicine.com/medline/citation/20124973/Bumetanide_alleviates_epileptogenic_and_neurotoxic_effects_of_sevoflurane_in_neonatal_rat_brain_ L2 - http://anesthesiology.pubs.asahq.org/article.aspx?doi=10.1097/ALN.0b013e3181cf9138 DB - PRIME DP - Unbound Medicine ER -