Location-dependent effects of trauma on oxidative stress in humans.

Though circulating antioxidant capacity in plasma is homeostatically regulated, it is not known whether acute stressors (i.e. trauma) affecting different anatomical locations could have quantitatively different impacts. For this reason, we evaluated the relationship between the anatomical location of trauma and plasma total antioxidant capacity (TAC) in a prospective study, where the anatomical locations of trauma in polytraumatic patients (n = 66) were categorized as primary affecting the brain -traumatic brain injury (TBI)-, thorax, abdomen and pelvis or extremities. We measured the following: plasma TAC by 2 independent methods, the contribution of selected antioxidant molecules (uric acid, bilirubin and albumin) to these values and changes after 1 week of progression. Surprisingly, TBI lowered TAC (919 ± 335 μM Trolox equivalents (TE)) in comparison with other groups (thoracic trauma 1187 ± 270 μM TE; extremities 1025 ± 276 μM TE; p = 0.004). The latter 2 presented higher hypoxia (PaO2/FiO2 272 ± 87 mmHg) and hemodynamic instability (inotrope use required in 54.5%) as well. Temporal changes in TAC are also dependent on anatomical location, as thoracic and extremity trauma patients' TAC values decreased (1187 ± 270 to 1045 ± 263 μM TE; 1025 ± 276 to 918 ± 331 μM TE) after 1 week (p < 0.01), while in TBI these values increased (919 ± 335 to 961 ± 465 μM TE). Our results show that the response of plasma antioxidant capacity in trauma patients is strongly dependent on time after trauma and location, with TBI failing to induce such a response.