Hydrogen is neuroprotective against surgically induced brain injury

Abstract

Background: Neurosurgical operations cause unavoidable damage to healthy brain tissues. Direct surgical injury as well as surgically induced oxidative stress contributes to the subsequent formation of brain edema. Therefore, we tested the neuroprotective effects of hydrogen (H2) in an established surgical brain injury (SBI) model in rats. Materials and methods: Adult male Sprague - Dawley rats (weight 300-350g) were divided into three groups to serve as sham operated, SBI without treatment, and SBI treated with H2 (2.9%). Brain water content, myeloperoxidase (MPO) assay, lipid peroxidation (LPO), and neurological function were measured at 24 hrs after SBI. Results: SBI resulted in localized brain edema (p = < 0.001). Hydrogen (2.9%) administered concurrently with surgery significantly decreased the formation of cerebral edema (p = 0.028) and improved neurobehavioral score (p = 0.022). However, hydrogen treatment failed to reduce oxidative stress (LPO assay) or inflammation (MPO assay) in brain tissues. Conclusions: Hydrogen appears to be promising as an effective, yet inexpensive way to reduce cerebral edema caused by surgical procedures. Hydrogen has the potential to improve clinical outcome, decrease hospital stay, and reduce overall cost to patients and the health care system.

Study details

Article type

Original Research

Disease / injury model

Surgically induced brain injury (SBI) in rats (partial right frontal lobectomy)

Duration

24 hours

Dose-dependent effect

No

Outcome

Positive

Findings

Inhaled hydrogen (2.9%) administered during surgery significantly reduced cerebral edema and improved neurological function in rats with surgically induced brain injury, but did not reduce oxidative stress or inflammation markers.