DDFPe increased cerebral oxygen tension after traumatic brain injury in rats.

Hypoxia is a critical secondary injury mechanism in traumatic brain injury (TBI), and early intervention to alleviate post-TBI hypoxia may be beneficial. DDFPe was screened for its ability to increase brain tissue oxygen tension (PbtO2) when administered soon after TBI. DDFPe caused an increase in PbtO2 following TBI in rats and should be evaluated further as a possible immediate treatment for TBI.


Link to publication