In vivo electrochemistry could provide early detection of high-altitude hypoxic brain injury

People who climb too fast or too high risk acute altitude sickness, which can lead to life-threatening hypoxic brain injury. By using in vivo electrochemistry, researchers have demonstrated that characteristic changes occur in the oxygen content of various brain regions before injury.

As a team reports in the journal Angewandte Chemie International Edition, the risk of brain damage could be predicted days in advance—perhaps a new approach for detecting high-altitude hypoxic injury.

Because of the low air pressure and low partial pressure of oxygen at high altitude, the brain does not receive an adequate oxygen supply, causing hypoxia. This not only happens when skiing or mountain climbing if one reaches 2,500 m too quickly, but it also affects people who live in regions above 3,000 m in South America or Asia, for example, despite their acclimation, causing chronic altitude sickness.

The mild form of acute altitude sickness begins about four to six hours after climbing, with a headache. If the climb is not interrupted, additional problems may develop, such as dizziness, nausea, and a racing heart. At this point, descent to lower altitude or treatment in a portable pressure chamber and administration of oxygen are critical to prevent hypoxia and life-threatening high-altitude hypoxic brain injury (HHBI).

Most current methods for the early detection of HHBI leave a lot to be desired with regard to speed and precision. A team led by Lin Zhou and Bin Su at Zhejiang University (China) has proposed an approach for a novel strategy based on changes in the oxygen content of regions of the brain over time.

By using fine biocompatible electrodes, the team examined the relationship between the oxygen content in different areas of mouse brains and the degree of HHBI under simulated exposure to high altitude (3,000 to 7,500 m) in a low-pressure chamber.

Hypoxia in the brain immediately triggered the transport of oxygen from other organs to the brain. Within about two hours, the brain additionally redistributed the oxygen: brain regions with higher tolerance for hypoxia received less oxygen to support supply to more important areas.

The electrochemical measurements showed that at a simulated altitude of 3,000 m, the oxygen content of the primary somatosensory cortex (responsible for the sense of touch) sank more rapidly than that of the hippocampus (responsible for memory). In both areas, it sank more rapidly than the reduction of blood oxygen saturation. These measurements correlate with memory and sensory tests.

Under normal pressure, the animals recovered completely. In contrast, after three days at simulated 7,500 m, the oxygen content of both areas sank to roughly similarly low values. The mice suffered from severe HHBI, including cell death.

At intermediate heights, individual animals reacted differently. Based on the currents measured within the first one or two hours of low-pressure simulation, it was possible to predict whether and in which area a mouse would suffer HHBI three days later.

Based on the characteristics of the changes in brain oxygen level, it was possible to predict the risk of HHBI several days in advance. The team hopes to use these insights as the basis for possible early detection of impending HHBI.