Introduction
Traumatic brain injury is a leading cause of death and disability among young adults (18–45 years old) and a leading combat casualty. This project examines the effects of hypercarbia on brain injury following fluid percussion injury in the rat.
Methods
Anaesthetized rats underwent tracheostomy, arterial cannulation, and moderate cerebral fluid percussion injury (2.75–3.00 atm). For one hour following fluid percussion injury the animal's PaCO2 was altered by adjusting minute ventilation, and maintained at a predetermined level for one hour. Each group was controlled for temperature and pO2. The rats were euthanized and perfused at 72 hours and their brains harvested for histopathology (H&E). Brain injury areas were demarcated and total volumes interpolated.
Results
Mean injury volumes (± SD) were 42. 39+12.17 mm3, 25.27 +12.62 mm3, 24.45+8.32 mm3, 16.46±21.73 mm3, in animals with mean pCO2 values of <40 (normal controls), 45, 55, and 60 mmHg, respectively. Statistical analysis revealed significant differences (P<0.05) in comparing brain injury volume of hypercarbic animals to normocarbic controls.
Discussion
In conclusion, rats sustaining a moderate fluid percussion injury have a significant decrease in injury volume when treated with one-hour of post-traumatic hypercarbia in the setting of normal oxygenation compared to rats with normal pCO2 values. These findings warrant further investigation into the mechanisms behind the neuroprotective effects of post-traumatic hypercarbia and the pathophysiological sequelae of its use in the setting of traumatic brain injury. Ongoing experiments are examining the effects of hypercarbia following penetrating brain injury measuring brain tissue O2, brain temperature, intracranial pressures (ICP), laser Doppler cerebral blood flow, DC/EGG, and 72 h histopathology.