Abstract
Background: Serum concentrations of adhesion molecules and oxidative stress is thought to participate in the pathobiology of secondary brain injury after acute traumatic brain injury (TBI). We aimed to study the hypothesis that hyperbaric oxygen therapy (HBOT) both improves the adhesion molecules levels and antioxidant capacity. Methods: Thirty blood samples from ten patients after acute TBI were obtained after injury and before and after HBOT. Four patients received early HBOT started two weeks after injury, four patients received late HBOT started ten weeks after injury and two patients did not receive HBOT and served as control in this study. The HBOT patients received total 30 times HBOT in six weeks period. Results: Those serum biomarkers in patients with TBI had not significantly difference in glutathione (GSH), thiobarbituric acid reactive substances (TBARS), soluble intercellular cell adhesion-molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1 (sVCAM-1) concentrations on admission between early HBOT, late HBOT, and control group (p = 0.916, p = 0.98, p = 0.306, and p = 0.548, respectively). Serum GSH levels were higher at 10 weeks after injury in the early HBOT group than in the late HBOT group and control group (mean, 1.40 μmol/L, 1.16 μmol/L, and 1.05 μmol/L, respectively). Then the serum GSH level was increased at 18 weeks after injury in the late HBOT group (mean, 1.49 μmol/L). However, there was only statistically significant difference at Weeks 18 (p = 0.916, p = 0.463, and p = 0.006, at Week 2, Week 10, and Week 18, respectively). Serum TBARS levels were decreased at 10 weeks after injury in the early HBOT group than in the late HBOT group and control group (mean, 11.21 μmol/L, 17.23 μmol/L, and 17.14 μmol/L, respectively). Then the serum TBARS level was decreased at 18 weeks after injury in the late HBOT group (mean, 12.06 μmol/L). There was statistically significant difference after HBOT (p = 0.98, p = 0.007, and p = 0.018, at Week 2, Week 10, and Week 18, respectively). There was no statistically significant difference between the three groups on sICAM-1 and sVCAM-1 levels from Week 2 to Week 18. Conclusions: HBOT can improve serum oxidative stress in patients after TBI. These molecules may be added as evaluation markers in clinical practice. Perhaps in the future it may also become part of the treatment of patients after acute traumatic brain injury. Further large-scale study may be warrant.
Highlights
Acute traumatic brain injury (TBI) is a disease process with an initial injury, involves inflammatory pathways activation, and contributes to continuing biochemical and cellular changes over time [1,2]
An imbalance of reactive oxidative stress (ROS) generation and the oxidative metabolism which leads to mitochondrial dysfunctions and apoptosis [4], and that apoptotic factor in different brain regions of rats might contribute to neurotoxicity [5]
Previous reports showed that excess oxidative stress can affect energy metabolism [4], block the electron transport chain of mitochondria and damage to neurocytes and cerebrovascular endothelium [11] causing neurotoxicity such as apoptosis [12,13,14]
Summary
Acute traumatic brain injury (TBI) is a disease process with an initial injury, involves inflammatory pathways activation, and contributes to continuing biochemical and cellular changes over time [1,2]. The brain has the highest oxygen metabolism rate among the organs of the body [3] This high rate of oxygen metabolism leads to the possibility of excessive reactive oxidative stress (ROS) production. An imbalance of ROS generation and the oxidative metabolism which leads to mitochondrial dysfunctions and apoptosis [4], and that apoptotic factor in different brain regions of rats might contribute to neurotoxicity [5]. Previous reports showed that excess oxidative stress can affect energy metabolism [4], block the electron transport chain of mitochondria and damage to neurocytes and cerebrovascular endothelium [11] causing neurotoxicity such as apoptosis [12,13,14]. Serum concentrations of adhesion molecules and oxidative stress is thought to participate in the pathobiology of secondary brain injury after acute traumatic brain injury (TBI). Results: Those serum biomarkers in patients with TBI had not significantly difference in glutathione (GSH), thiobarbituric acid reactive substances (TBARS), soluble intercellular cell adhesion-molecule-1 (sICAM-1) and soluble vascular cell adhesion molecule-1
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