Impaired cerebral mitochondrial function after traumatic brain injury in humans

Object. Oxygen supply to the brain is often insufficient after traumatic br ain injury (TBI), and this results in decreased energy production (adenosin e triphosphate [ATP]) with consequent neuronal cell death. It is obviously important to restore oxygen delivery after TBI; however, increasing oxygen delivery alone may not improve ATP production if the patient's mitochondria (the source of ATP) are impaired. Traumatic brain injury has been shown to impair mitochondrial function in animals; however, no human studies have b een previously reported. Methods. Using tissue fractionation procedures, living mitochondria derived from therapeutically removed brain tissue were analyzed in 16 patients wit h head injury (Glasgow Coma Scale Scores 3-14) and two patients without hea d injury. Results revealed that in head-injured patients mitochondrial func tion was impaired, with subsequent decreased ATP production. Conclusions. Decreased oxygen metabolism due to mitochondrial dysfunction m ust be taken into account when clinically defining ischemia and interpretin g oxygen measurements such as jugular venous oxygen saturation, arterioveno us difference in oxygen content, direct tissue oxygen tension, and cerebral blood oxygen content determined using near-infrared spectroscopy. Restorin g mitochondrial function might be as important as maintaining oxygen delive ry.