Hydrogen Gas Protects Baby Mice Brains from Anesthesia Damage
- Authors
- Ryuji Yonamine, Yasushi Satoh, Mitsuyoshi Kodama, Yoshiyuki Araki, Tomiei Kazama
- Journal
- Anesthesiology
- Year
- 2013
- DOI
- 10.1097/ALN.0b013e318275146d
- Study Type
- Mouse
- Outcome
- Positive
- Peer Reviewed
- Yes
- Country
- Japan
- Health Condition
- Anesthesia-Induced Neurotoxicity
- Body System
- Nervous System
TL;DR
Breathing in hydrogen gas can significantly protect baby mice's brains from damage and memory problems caused by a common anesthetic.
Key Finding
Adding hydrogen gas (1.3%) to sevoflurane anesthesia reduced neuronal cell death by approximately 60% and prevented long-term cognitive and behavioral deficits in neonatal mice.
Summary
This mouse study tested whether hydrogen gas could protect developing brains from damage caused by sevoflurane, a common anesthetic. Six-day-old mice were exposed to sevoflurane with or without hydrogen gas mixed in. Researchers found that hydrogen gas significantly reduced brain cell death and prevented memory and social behavior problems that normally occur from sevoflurane exposure alone.
Practical Takeaway
This early-stage animal research suggests hydrogen gas inhalation may protect developing brains from anesthetic damage, but these findings are from mice only and would need human studies before any clinical application. The study does not tell us whether this approach would work in human infants or what dose would be appropriate.
Abstract
Background: In animal models, several anesthetics induce widespread increases in neuronal apoptosis in the developing brain with subsequent neurologic deficits. Although the mechanisms are largely unknown, the neurotoxicity may, at least in part, be due to elevated oxidative stress caused by mitochondrial dysfunction. In an investigation of potential therapies that could protect against this type of damage, we studied the effects of molecular hydrogen on anesthetic-induced neurotoxicity in the developing mouse brain. Methods: Six-day-old C57BL/6 mice were exposed to 3% sevoflurane for 6 h with or without hydrogen (< 1.3%) as part of the carrier gas mixture. Apoptosis was evaluated by immunohistochemical staining for cleaved caspase-3 (n = 8-10/group). Western blot analysis for cleaved poly-(adenosine diphosphate-ribose) polymerase was also performed to examine apoptosis (n = 3-6/group). Oxidative stress was assessed by immunohistochemical staining for 4-hydroxy-2-nonenal (n = 8/group). Long-term memory and social behavior were examined using the fear conditioning test and the sociability test, respectively (n = 18-20/group). Results: Western blot analysis showed that coadministration of 1.3% hydrogen gas significantly (P < 0.001) reduced the level of neuronal apoptosis to approximately 40% compared with sevoflurane exposure alone. Immunohistochemical analysis showed that hydrogen reduced oxidative stress induced by neonatal sevoflurane exposure. Although neonatal sevoflurane exposure caused impairment in long-term memory and abnormal social behaviors in adulthood, mice coadministered hydrogen gas with sevoflurane did not exhibit these deficits. Conclusions: Inhalation of hydrogen gas robustly decreased neuronal apoptosis and subsequent cognitive impairments caused by neonatal exposure to sevoflurane.