ascorbic-acid and Craniocerebral-Trauma

Free radical hyperproduction may play an important role in brain hemorrhage and ischemia/reperfusion injury. The aims of this study were to assess whether antioxidant depletion occurs after intracranial hemorrhage (ICH) and head trauma (HT) and to evaluate the relation between the diameter of the brain lesion, the degree of the neurological impairment, and any observed antioxidant changes.. We measured plasma levels of vitamin C (ascorbic acid, AA), uric acid (UA), vitamin E (alpha-tocopherol), and ubiquinol-10 in 13 patients with ICH and 15 patients with HT on the day of the brain injury and subsequently every other day up to 1 week. Patients were compared with 40 healthy control subjects.. ICH and HT patients had significantly lower plasma levels of AA compared with healthy subjects, in contrast to plasma levels of UA, alpha-tocopherol, and ubiquinol-10. AA levels were significantly inversely correlated with the severity of the neurological impairment as assessed by the Glasgow Coma Scale and the National Institutes of Health Stroke Scale. AA levels were also significantly inversely correlated with the major diameter of the lesion. In addition, mean plasma AA levels were lower in jugular compared with peripheral blood samples obtained from 5 patients.. These findings suggest that a condition of oxidative stress occurs in patients with head trauma and hemorrhagic stroke of recent onset. The consequences of early vitamin C depletion on brain injury as well as the effects of vitamin C supplementation in ICH and HT patients remain to be addressed in further studies.

Topics: Adult; Antioxidants; Ascorbic Acid; Biomarkers; Brain; Craniocerebral Trauma; Female; Glasgow Coma Scale; Humans; Intracranial Hemorrhages; Male; Middle Aged; Oxidative Stress; Predictive Value of Tests; Severity of Illness Index; Tomography, X-Ray Computed; Ubiquinone; Uric Acid; Vitamin E

The state of processes of lipid peroxidation and antioxidant defense was studied in patients with severe isolated craniocerebral closed injury. It was found that starting from the first days in the hospital the patients demonstrated marked alterations in the thiol-disulfide and ascorbate metabolism, activation of lipid peroxidation processes and lower antioxidant defense. The use of Solcoseryl as a component of the antioxidant therapy in treatment of the above mentioned category of patients resulted in considerably better indices of the thiol-disulfide metabolism. The isolated use of Solcoseryl failed to influence the ascorbate metabolism and lipid peroxidation. Solcoseryl used in combination with the ascorbic acid led to normalization of the thiol-disulfide and ascorbade metabolism without influencing the lipid peroxidation processes. Combined use of Solcoseryl and ascorbic acid promoted normalization of the neurological status and stabilization of the arterial pressure level.

Topics: Actihaemyl; Acute Disease; Antioxidants; Ascorbic Acid; Craniocerebral Trauma; Critical Care; Drug Therapy, Combination; Free Radicals; Humans; Lipid Peroxidation; Oxidation-Reduction; Sulfhydryl Compounds; Time Factors

Antioxidative effect of nimodipine was investigated in patient with severe head trauma.. The patients in group A were treated according to the standard procedures without nimodipine. Other patients in group B were treated with standard procedures plus intravenous nimodipine for a week. Three times per day, blood samples were taken from internal jugular venous saturation probe and central venous catheter for a week. The levels of malondialdehyde (MDA), reduced glutathione (GSH), nitrite, and nitrate, ascorbic acid, retinol and β-carotene in the serum were measured.. MDA levels in group B were significantly lower than those in the group A (P<0.05). As for GSH levels, it was observed that there was a significant increase in GSH levels in group B when compared to those in group A (P<0.01). Comparison of nitrate and nitrite levels in the serum of patient groups showed that these parameters were significantly higher in group B than those in group A (P<0.01). It was seen that there were a significant increase in ascorbic acid (P<0.01) and β-carotene (P<0.05) levels in group B when compared to those in group A. Values of retinol levels were slightly higher in group B than that of group A, and there was no significant difference between the groups.. Severe head trauma may increase oxidative stress. Administration of nimodipine may prevent the oxidative stress and may augment endogenous antioxidative defense systems in patients with severe head trauma.

Topics: Adolescent; Adult; Antioxidants; Ascorbic Acid; beta Carotene; Calcium Channel Blockers; Child; Craniocerebral Trauma; Female; Glutathione; Humans; Injections, Intravenous; Lipid Peroxidation; Male; Malondialdehyde; Middle Aged; Nimodipine; Nitrates; Nitrites; Oxidative Stress; Trauma Severity Indices; Vitamin A; Young Adult

Diabetes mellitus is a metabolic disorder associated with central nervous system impairments. Recent studies implicate oxidative stress mediated by reactive oxygen species (ROS) in the pathogenesis of diabetic complications. ROS have been shown to play role in the pathophysiology of brain injury. In the present study, closed head injury (CHI) was induced in diabetic rats to test the hypothesis that chronic oxidative stress exacerbates brain damage following CHI. Neurological recovery, edema, levels of low molecular weight antioxidants (LMWA), and markers of lipid peroxidation were determined at different intervals after injury. Diabetic rats (4 weeks after induction with streptozotocin) were subjected to CHI. Brain edema (percent water) and clinical status (neurological severity score) were assessed during 7 days. Brain LMWA were determined using cyclic voltammetry (CV) and HPLC-EC. In addition, conjugated dienes and thiobarbituric acid reactive substances (TBARS) were measured. Diabetic-CHI rats exhibited a lower rate of recovery and greater and more sustained edema (p < 0.01), as compared with the controls. At all times diabetic rats had higher levels of TBARS and conjugated dienes and lower concentrations of LMWA, and of vitamins C and E, suggesting chronic oxidative stress. At 5 min of CHI, the amounts of LMWA in control-CHI brains decreased (approximately 50%, p < 0.01) and returned to normal by 48 h and 7 days. In the diabetic-CHI brain only one class of LMWA slightly declined but remained low for 7 days. The present results support the hypothesis that diabetic rats are under chronic oxidative stress, and suffer greater neurological dysfunction, associated with further lipid peroxidation following CHI.

Topics: Animals; Ascorbic Acid; Brain; Brain Edema; Craniocerebral Trauma; Diabetes Mellitus, Experimental; Electric Conductivity; Electrophysiology; Male; Oxidative Stress; Rats; Rats, Wistar; Recovery of Function; Severity of Illness Index; Thiobarbituric Acid Reactive Substances; Vitamin E; Wounds, Nonpenetrating

Reactive oxygen species (ROS) are normally generated in the brain during metabolism, and their production is enhanced by various insults. Low molecular weight antioxidants (LMWA) are one of the defense mechanisms of the living cell against ROS. The reducing capacity of brain tissue (total LMWA) was measured by cyclic voltammetry (CV), which records biological oxidation potential specific to the type of scavenger(s) present and anodic current intensity (Ia), which depends on scavenger concentration. In the present study, the reducing capacity of rat brain following closed head injury (CHI) was measured. In addition, CV of heat-acclimated traumatized rats was used to correlate endogenous cerebroprotection after CHI with LMWA activity. Sham-injured rat brains displayed two anodic potentials: at 350 +/- 50 mV (Ia = 0.75 +/- 0.06 microA/mg protein) and at 750 +/- 50 mV (Ia = 1.00 +/- 0.05 microA/mg protein). Following CHI, the anodic waves appeared at the same potentials as in the sham animals. However, within 5 min of CHI, the total reducing capacity was transiently decreased by 40% (p < 0.01). A second dip was detected at 24 h (60%, p < 0.005). By 48 h and at 7 days, the Ia levels normalized. The acclimated rats displayed anodic potentials identical to those of normothermic rats. However, the Ia of both potentials was lower (60% of control, p < 0.001). The Ia profile after CHI was the direct opposite of the normothermic Ia profile: no immediate decrease of Ia and an increase from 4 h and up to 7 days (40-50%, p < 0.001). We suggest that the lowered levels of LMWA in the post-CHI period reflect their consumption due to overproduction of free radicals. The augmented concentration of LMWA found in the brain of the heat-acclimated rats suggests that these rats are better able to cope with these harmful radicals, resulting in a more favorable outcome following CHI.

Topics: Acclimatization; Animals; Antioxidants; Ascorbic Acid; Brain Chemistry; Brain Injuries; Craniocerebral Trauma; Disease Susceptibility; Electric Conductivity; Free Radical Scavengers; Heart; Hot Temperature; Male; Myocardium; Oxidation-Reduction; Oxidative Stress; Rats; Reactive Oxygen Species; Tryptophan

Before microdialysis (MD) can be introduced into the clinic as an improved method of cerebral monitoring, certain ethical, methodological and clinical factors must be considered. Access to the brain for probe insertion is offered by craniotomy or by routine intracranial pressure (ICP) monitoring and the additional lesion is minimal. Care must be taken that the two devices do not interfere with each other. In contrast to ICP monitoring, MD provides information about multiple aspects of brain metabolism. We can monitor either still intact tissue to prevent additional damage, or injured brain to decide on and control therapies. The parameters used must reflect pathological changes an early stage, and the analysis should be available on-line or immediately after sample collection. The effects off factors such as tube length and flow rate on the behaviour of the chosen parameters (in our case on-line pH, radical scavengers and uric acid) in the MD set-up must be investigated in vitro and in animal models before use in the clinic. The range of non-pathological values of parameters of interest in human brain should be known For this purpose we took measurements during an extracranial-intracranial bypass operation, and were able to compare values with those in a severely damaged brain. The mutual chronology of parameter changes and clinical events must be clear. Future aspects include the use of low-flow methods offering nearly 100% recovery, improved analytical methods, and combination of MD with other monitoring methods to obtain more exact information.

Topics: Animals; Ascorbic Acid; Bicarbonates; Brain; Carbon Dioxide; Craniocerebral Trauma; Critical Care; Cysteine; Feasibility Studies; Glutathione; Humans; Hydrogen-Ion Concentration; Microdialysis; Nervous System Diseases; Rats; Rats, Inbred SHR; Uric Acid