Simulated Aeromedical Evacuation Causes Hippocampal Neuronal Damage in Rats With Acute Lung Injury

Aeromedical rescue plays an important role in the extensive evacuation of war casualties, sudden natural disasters (e.g., earthquakes, tsunamis), major public health events, and special needs across borders and regions. The most prominent environmental consideration in aeromedical evacuation (AE) is the impact of changes in barometric pressure on oxygen delivery and gas expansion. However, the hypobaric and hypoxic environment sustained by critically ill patients in flight can cause lung injury, leading to hypoxemia, which remains one of the few limiting factors for AE. Previous studies have focused primarily on secondary damage to brain and lung tissues during AE, with limited investigations into potential injuries to other organ systems. The purpose of this study was to investigate the effects of hypobaric hypoxia on the brain tissue of rats with acute lung injury (ALI).

Sprague-Dawley (SD) rats with lipopolysaccharide (LPS)-induced ALI were allocated to either a normoxic environment or a simulated AE environment (hypobaric hypoxic conditions). Hematoxylin-eosin staining was used to evaluate brain tissue damage, and single-cell RNA sequencing technology was used to analyze the injured brain tissue.

Sprague-Dawley rats with lipopolysaccharide-induced ALI presented with hippocampal neuronal damage after undergoing simulated AE. The analysis of the interaction of neurons with other hippocampal tissue cells suggested that the expression level of NRG1-ErbB4 was significant.

This study demonstrated that ALI results in hippocampal neuronal damage after simulated aeromedical treatment in rats. In this study, single-cell RNA sequencing revealed that the NRG1/ErbB4 signaling pathway may play an important role in hippocampal neuronal injury. In contrast to previous studies on secondary injury to lung tissue, this study examined secondary injury to brain tissue caused by simulated AE.