TY - JOUR
T1 - Oxidative damage after severe head injury and its relationship to neurological outcome
AU - Paolin, Adolfo
AU - Nardin, Lorella
AU - Gaetani, Paolo
AU - Rodriguez y Baena, Riccardo
AU - Pansarasa, Orietta
AU - Marzatico, Fulvio
AU - Kelly, Daniel F.
AU - Robertson, Claudia
AU - Marshall, Lawrence F.
PY - 2002/10/1
Y1 - 2002/10/1
N2 - OBJECTIVE: We sought to establish the time course of reactive oxygen species after severe head injuries in humans and to investigate their relationship with clinical outcomes. METHODS: Both the markers of oxidative damage - malonylaldehyde (MDA) and the enzymatic and nonenzymatic antioxidant defenses (i.e., superoxide dismutase [SOD] and vitamin E [VE], respectively) - were studied. To assess the time course of MDA, SOD, and VE, jugular bulb (JB) and peripheral venous blood samples were obtained from 30 patients within 8 hours of severe head trauma onset (T0) and 6 (T1), 12 (T2), 24 (T3), and 48 hours (T4) after trauma onset. Patients were divided into good and poor outcome groups according to their 6-month neurological outcome as determined on the basis of their Glasgow Outcome Scale scores and biochemical profiles. RESULTS: In JB samples, MDA levels increased significantly at T1, T2, T3, and T4 as compared with T0; SOD activity increased significantly at T2 and T3 as compared with T0; and VE levels decreased significantly at T1, T2, and T3 as compared with T0. The same variables did not change significantly over time in peripheral venous blood samples. Moreover, the MDA levels and SOD activity detected in JB samples were significantly higher in the poor outcome group at T1 and T2. No significant difference in VE levels was observed between the two outcome groups. CONCLUSION: Reactive oxygen species-mediated oxidative damage can play an important role in determining the prognosis of severe brain injury in humans.
AB - OBJECTIVE: We sought to establish the time course of reactive oxygen species after severe head injuries in humans and to investigate their relationship with clinical outcomes. METHODS: Both the markers of oxidative damage - malonylaldehyde (MDA) and the enzymatic and nonenzymatic antioxidant defenses (i.e., superoxide dismutase [SOD] and vitamin E [VE], respectively) - were studied. To assess the time course of MDA, SOD, and VE, jugular bulb (JB) and peripheral venous blood samples were obtained from 30 patients within 8 hours of severe head trauma onset (T0) and 6 (T1), 12 (T2), 24 (T3), and 48 hours (T4) after trauma onset. Patients were divided into good and poor outcome groups according to their 6-month neurological outcome as determined on the basis of their Glasgow Outcome Scale scores and biochemical profiles. RESULTS: In JB samples, MDA levels increased significantly at T1, T2, T3, and T4 as compared with T0; SOD activity increased significantly at T2 and T3 as compared with T0; and VE levels decreased significantly at T1, T2, and T3 as compared with T0. The same variables did not change significantly over time in peripheral venous blood samples. Moreover, the MDA levels and SOD activity detected in JB samples were significantly higher in the poor outcome group at T1 and T2. No significant difference in VE levels was observed between the two outcome groups. CONCLUSION: Reactive oxygen species-mediated oxidative damage can play an important role in determining the prognosis of severe brain injury in humans.
KW - Glasgow Outcome Scale
KW - Malonylaldehyde
KW - Oxidative damage
KW - Severe brain injury
KW - Superoxide dismutase
KW - Vitamin E
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U2 - 10.1097/00006123-200210000-00018
DO - 10.1097/00006123-200210000-00018
M3 - Article
C2 - 12234402
AN - SCOPUS:0036820493
VL - 51
SP - 949
EP - 955
JO - Neurosurgery
JF - Neurosurgery
SN - 0148-396X
IS - 4
ER -