People who climb too fast or too high are at risk of acute altitude sickness, which can lead to life-threatening hypoxic brain injury. When using live electrochemistry, the researchers demonstrated that characteristic changes occur in the oxygen content of several brain regions before injury. As the team reports in the magazine. Chemie AngewandteThe risk of brain damage could be predicted days in advance, perhaps a new approach to detecting hypoxic injuries at high altitude.
Due to the low air pressure and low partial pressure of oxygen at high altitude, the brain does not have an adequate supply of oxygen (hypoxia). This not only happens when skiing or climbing mountains, if you reach 2,500 m too quickly, but people living in regions above 3,000 m in South America or Asia, for example, can also be affected despite their acclimatization (chronic altitude sickness). The mild form of acute altitude sickness begins four to six hours after climbing, with a headache. If the climb is not interrupted, additional problems may develop, such as dizziness, nausea, and palpitations. At this point, descent to a lower altitude or treatment in a (portable) pressure chamber and administration of oxygen are essential to prevent hypoxia and life-threatening high-altitude hypoxic brain injury (HHBI).
Most current methods for early detection of HHBI leave much to be desired in terms of speed and accuracy. A team led by Lin Zhou and Bin Su from Zhejiang University (China) has proposed a novel strategy based on changes in the oxygen content of brain regions over time.
Using thin biocompatible electrodes, the team examined the relationship between the oxygen content in different brain areas of the mice and the degree of HHBI under simulated exposure to high altitude (3000 to 7500 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 oxygen: Brain regions with greater tolerance to hypoxia received less oxygen to support delivery to more important areas.
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) decreased more rapidly than that of the hippocampus (responsible for memory). In both areas, it sank faster than the reduction in blood oxygen saturation. These measurements correlate with sensory and memory tests. Under normal pressure, the animals recovered completely. In contrast, after three days at a simulated 7,500 m, the oxygen content of both zones fell to approximately similar values. The mice suffered severe HHBI, including cell death. At intermediate heights, individual animals reacted differently. Based on the currents measured during the first one to two hours of low-pressure simulation, it was possible to predict whether a mouse would suffer from HHBI and in which area three days later.
Based on the characteristics of changes in brain oxygen level, it was possible to predict the risk of HHBI several days in advance. The team hopes to use this knowledge as a basis for possible early detection of impending HHBI.