Differential gene transcription following intravenous injection of air bubbles in rats with varying resistance to decompression sickness (DCS)

Decompression sickness (DCS) is a pathology caused by the appearance of gas emboli in the bloodstream and tissues. However, the weak correlation between the amount of venous gas emboli (VGE) and the development of DCS, as well as the considerable inter-individual variability in DCS-susceptibility, suggest that a higher DCS resistance could be associated with a better management of VGE-induced stress. To study the effects of VGE independently of the hyperbaric stress induced by diving, Wistar and DCS-resistant male and female rats received 5 ml/kg of a NaCl solution 0.9 % filled with air microbubbles through the tail vein. After 120 minutes, the liver and lungs were harvested. Wet to dry weight ratio was determined in the lungs. Gene expression was quantified by RT-PCR in the liver. Compared to Standard Wistar, DCS-resistant rats exhibited a lower lung wet to dry weight ratio after air microbubble injection, suggesting lower pulmonary fluid accumulation. In the liver, DCS-resistant rats showed higher tissue factor (TF) transcription at basal state and post-air microbubble injection. Tissue factor pathway inhibitor (TFPI) was lower in DCS-resistant rats at basal state but higher following air microbubble injection. Levels of HSP70, HSP27, and Egr-1, were higher in DCS-resistant rats after air microbubble injection. At the basal state, only HSP27 was higher in DCS-resistant rats, with HSP70 lower and Egr-1 not different. These results help clarifying the pathways involved in the response to VGE and highlight potential mechanisms underlying resistance to DCS, including enhanced anticoagulant pathways and improved cellular stress responses.