Increased leakage of brain antigens after traumatic brain injury and effect of immune tolerance induced by cells on traumatic brain injury.

BACKGROUND: Although traumatic brain injury can lead to opening the blood-brain barrier and leaking of blood substances (including water) into brain tissue, few studies of brain antigens leaking into the blood and the pathways have been reported. Brain antigens result in damage to brain tissues by stimulating the immune system to produce anti-brain antibodies, but no treatment has been reported to reduce the production of anti-brain antibodies and protect the brain tissue. The aim of the study is to confirm the relationship between immune injury and arachnoid granulations following traumatic brain injury, and provide some new methods to inhibit the immune injury. METHODS: In part one, methylene blue was injected into the rabbits' cisterna magna after traumatic brain injury, and concentrations of methylene blue and tumor necrosis factor (TNF)-α in blood were detected to determine the permeability of arachnoid granulations. In part two, umbilical cord mesenchymal stem cells and immature dendritic cells were injected into veins, and concentrations of interleukin 1 (IL-1), IL-10, interferon (IFN)-γ, transforming growth factor (TGF)-ß, anti-brain antibodies (ABAb), and IL-12 were measured by ELISA on days 1, 3, 7, 14 and 21 after injury, and the numbers of leukocytes in the blood were counted. Twenty-one days after injury, expression of glutamate in brain tissue was determined by immunohistochemical staining, and neuronal degeneration was detected by H&E staining. RESULTS: In part one, blood concentrations of methylene blue and TNF-α in the traumatic brain injury group were higher than in the control group (P < 0.05). Concentrations of methylene blue and TNF-α in the trauma cerebrospinal fluid (CSF) injected group were higher than in the control cerebrospinal fluid injected group (P < 0.05). In part two, concentrations of IL-1, IFN-γ, ABAb, IL-12, expression of glutamate (Glu), neuronal degeneration and number of peripheral blood leukocytes were lower in the group with cell treatment compared to the control group. IL-10 and TGF-ß were elevated compared to the control group. CONCLUSIONS: Traumatic brain injury can lead to stronger arachnoid granulations (AGs) permeability; umbilical cord mesenchymal stem cells and immature dendritic cells can induce immune tolerance and reduce inflammation and anti-brain antibodies to protect the brain tissue.

Extracellular glycerol in patients with severe traumatic brain injury.

OBJECTIVE: To study the factors affecting extracellular glycerol (Gly) in patients with severe traumatic brain injury (STBI). METHODS: Perilesional extracellular Gly and cerebral blood flow (CBF) in 53 patients with STBI were consecutively monitored. Simultaneously, the intracranial pressure (ICP) and cerebral perfusion pressure (CCP) were monitored. The hourly minimum of CCP and CBF and the hourly maximum of ICP levels were matched with the hourly Gly. Gly values were divided into several groups according to regional ICP (less than 15 mm Hg or larger than 15 mm Hg), CCP (less than 70 mm Hg or larger than 70 mm Hg), CBF (less than 50 AU or 50-150 AU) and the outcomes (death or persistent vegetative state group, severe or moderate disability group, and good recovery group). RESULTS: In comparison with the severe or moderate disability group, the Gly concentration of the death or persistent vegetative state group increased significantly, but CBF and CCP decreased significantly. In comparison with the good recovery group, the Gly concentration of the severe or moderate disability group increased significantly, but CBF and CCP decreased significantly. The Gly concentrations in patients with ICP larger than 15 mm Hg, CCP less than 70 mm Hg and CBF less than 50 AU were respectively higher than those of patients with ICP less than 15 mm Hg, CCP larger than 70 mm Hg and 50 AU less than CBF less than 150 AU. In patients with diffuse axial injury, the mean Gly concentration was (201.17+/-55.00) micromol/L, which was significantly higher than that of the patients with epidural hematoma (n equal to 7, 73.26+/-8.37, P less than 0.05) or subdural hematoma (n equal to 9, 114.67+/-62.88, P less than 0.05), but it did not increase significantly when compared with those in patients with contusion(n equal to 24, 167.48+/-52.63). CONCLUSION: Gly can be taken as a marker for degradation of membrane phospholipids and ischemia, which reflects the severity of primary or secondary insult.

Effect of mild hypothermia on glucose metabolism and glycerol of brain tissue in patients with severe traumatic brain injury.

OBJECTIVE: To study the effect of mild hypothermia on glucose metabolism and glycerol of brain tissue in patients with severe traumatic brain injury (STBI) using clinical microdialysis. METHODS: Thirty-one patients with STBI(GCS less than or equal to 8) were randomly divided into hypothermic group(Group A) and control group(Group B). Microdialysis catheters were inserted into the cerebral cortex of perilesional and normal brain tissue. All samples were analyzed using CMA microdialysis analyzer. RESULTS: In comparison with the control group, lactate/glucose ratio(L/G), lactate/pyruvate ratio(L/P) and glycerol(Gly) in perilensional tissue were significantly decreased; L/P in normal brain tissue was significantly decreased. In control group, L/G, L/P and Gly in perilensional tissue were higher than that in normal brain tissue. In the hypothermic group, L/P in perilensional tissue was higher than that in relative normal brain. CONCLUSIONS: Mild hypothermia protects brain tissues by decreasing L/G, L/P and Gly in perilensional tissue and L/P in "normal brain" tissues. The energy crisis and membrane phospholipid degradation in perilensional tissue are easier to happen after traumatic brain injury, and mild hypothermia protects brain better in perilensional tissue than in normal brain tissue.

[Influence of temperature on extracellular glucose and lactate after traumatic brain injury].

OBJECTIVE: To study the changes of extracellular glucose (Glu), lactate (Lac), and the ratio of lactate/pyruvate (L/P) in patients with traumatic brain injury under different body temperatures. METHODS: Catheters for microdialysis were punctured into the penumbra zone of injured brain tissue (INJ), relatively normal brain tissue (NOR), and abdominal subcutaneous tissue (ABD) respectively in 51 patients to collect the fluid. The perfusion rate was 0.3 microl/min and one tube of fluid was collected for each hour. The average collection time was (67.10 +/- 18.27) hours. Concentrations of Glu, Lac, and pyruvate (Pyru) in the fluid were analyzed using CMA microdialysis analyzer. Patients were divided into 7 groups according to their rectal temperature (RT) values, which were RT < 33.0 degrees C, 33.0-33.9 degrees C, 34.0-34.9 degrees C, 35.0-35.9 degrees C, 36.0-36.9 degrees C, 37.0-37.9 degrees C, and > or = 38.0 degrees C. RESULTS: The concentration of Glu in ABD was significantly higher than that in the brain tissue (P < 0.05). The Glu in NOR were significantly higher and the highest in 33.0 degrees C compared with that in the INJ when RT < 36.0 degrees C (P < 0.05). The concentration of Lac in ABD was significantly lower than that in brain (P < 0.05). The Lac in NOR were much higher than that in INJ when RT < 35.0 degrees C or > or = 37.0 degrees C (P < 0.05). The ratio of L/P decreased along with the increase of body temperature (P < 0.001). The ratio of L/P significantly decreased in an order of INJ > ABD > NOR when RT was lower than 33.0 degrees C, which was changed to the order of NOR > INJ > ABD when RT was higher than 34.0 degrees C. CONCLUSION: Treatment of hypothermia may play more protective role when RT were between 33-34 degrees C or 36-37 degrees C.