Hypoxia/reoxygenation decreases endothelial glycocalyx via reactive oxygen species and calcium signaling in a cellular model for shock

CONCLUSION
In our cellular model for shock, we demonstrate that although hypoxia alone is sufficient to produce glycocalyx loss, H/R causes a greater decrease in glycocalyx thickness. Under both conditions damage is dependent on ROS and Ca2+ signaling. Notably, we found that ROS are generated upstream of Ca2+, but that ROS-mediated damage to the glycocalyx is dependent on Ca2+.

Source: The Journal of Trauma: Injury, Infection, and Critical Care - November 1, 2019 Category: Orthopaedics Tags: 2019 WTA PODIUM PAPERS Source Type: research