Xenon Gas May Mitigate Blast-Induced Brain Injury

A new study demonstrates that xenon treatment after blast traumatic brain injury (bTBI) reduces initial injury and prevents subsequent injury development.

Researchers at Imperial College London (ICL; United Kingdom), the Royal Centre for Defence Medicine (RCDM; Birmingham, United Kingdom), and other institutions conducted a murine study that examined slices of mouse brain tissue after exposing them to blast shockwaves that emulated those produced by improvised explosive devices (IEDs). Using a dye that highlights damaged brain cells, the researchers were able to monitor injury development up to three days after exposure.

They then compared brain slices of mice given xenon treatment starting one hour after exposure to slices of mice exposed to blast, but without xenon treatment, assessing injury development at 24, 48, and 72 hours using propidium iodide fluorescence. They found that slices treated with xenon suffered significantly less injury than the untreated control slices. The blast-injured slices treated with xenon were not significantly different to uninjured slices at 24 hours and 72 hours after injury, indicating that xenon gas prevented injury from developing. The study was published on February 8, 2018, in the Journal of Neurotrauma.

“One of the most insidious aspects of TBI in general, and it is believed bTBI also, is that the damage can continue to grow long after the initial injury. The secondary injury can be many times worse than the primary injury, so our goal is to stop the damage from spreading as early as possible,” said lead author Rita Campos-Pires, PhD, of ICL. “Xenon could be delivered easily by inhalation shortly after brain injury with relatively simple equipment. In addition to its potential for arresting injury development, xenon has an additional advantage of simultaneously providing analgesia.”

Xenon is a nonflammable inert gas that has been used as a general anesthetic since the 1950s. It is a pleiotropic drug known to act via a number of targets implicated in secondary injury development, including inhibition of N-methyl-D-aspartate receptors, activation of potassium channels, and anti-apoptotic action. Xenon has a number of unique advantages, including not being metabolized and rapidly crossing the blood–brain barrier, facilitating a rapid onset and offset of action, within minutes.