The cerebrospinal fluid thromboxane A(2) and prostaglandin I-2 levels in patients with severe head injury

The aim of this study was to evaluate the levels of thromboxane A, (TXA(2)) and prostacyclin (also called prostaglandin I-2 or PGI(2)) production in the ventricular cerebrospinal fluid (CSF) in patients with severe head injury (SHI). CSF samples in the trauma group, which included 15 patients, were obtained via insertion of an intraventricular catheter, and in the control group, which included 5 patients, they were obtained while the patients' shunt procedures were being performed. Levels were measured using the corresponding kits for TXB2 and 6-keto PGF(1a) metabolites of TXA(2) and PGI(2) respectively, during the following four periods after trauma: 6 to 10 hours, 20 to 28 hours, 40 to 56 hours, and 64 to 74 hours. CSF concentrations of TXB2 significantly increased in patients with SHI at all times after trauma (P < 0.0001). There was a variation in the levels of 6-keto-PGF(1a), however. Between 6 and 10 hours after trauma, a significant decline was noted (P < 0.05). By the first day, levels were markedly increased, on average, three times those found in the controls, but there was a tendency for levels to decline again later. The TXA(2)/PGI(2) ratio was studied, and it remained high, particularly at 6 to 10 hours and 64 to 74 hours after trauma. The ratio revealed the close relation between the severity of injury and a poor Glasgow Outcome Scale score, with the latter being higher in more severe injury. These results suggest that an increased TXA(2)/PGI(2) ratio was closely related to the severity of the brain injury and therefore appears to be an important indicator of secondary brain damage

Nitric oxide levels in rat cortex, hippocampus, cerebellum, and brainstem after impact acceleration head injury

Nitric oxide (NO) is a potential mediator of secondary brain injury in the settings of cerebral ischemia and inflammation. Traumatic brain injury (TBI) alters the levels of stable end products of NO metabolism. We investigated these changes and attempted to identify brain regions that were unique with regard to NO production in the period immediately after TBI. The experiment involved assaying nitrite-nitrate concentrations in the rat cortex, cerebellum, hippocampus, and brainstem after impact-acceleration head injury, Five rats comprised the sham-operated (control) group, five sustained mild head injury (MHI), and five sustained severe head injury (SHI). There was a uniform decline in the tissue concentrations of NO metabolites in all four brain regions in both injured groups. There were no significant differences in the concentrations of NO metabolites among the various sites tested in the MHI group; however, there appeared to be a relationship between degree of decline in NO levels and amount of trauma sustained by a given region in the SHI group. In these rats, NO dropped to the lowest levels in the brain region where the direct trauma was most severe. The results suggest that nitrite-nitrate levels in these four brain regions fall below normal in the first 5min after impact trauma. This decrease may, in part, be related to reduced activity of all nitric oxide synthase isoforms, which would cause a drop in the levels of NO metabolites. We believe that this decline may be linked to, and may even cause, the global decrease in cerebral blood flow that occurs in the initial stages of TBI. [Neurol Res 2003; 25: 31-34]