METHODS: This prospective observational study was conducted for a year in 2007 among 294 patients who had been treated for TBI in Hospital Kuala Lumpur. Patients fulfilling the set criteria were recruited into the study and data, including blood glucose level and Glasgow Outcome Score at 3-month follow-up, were collected.
RESULTS: 294 patients were included in the study: 50 females (17.0%) and 244 males (83.0%). The majority of cases were young adult patients (mean age of 34.2 years, SD 13.0). The mean blood glucose level during admission and post-surgery were 6.26 mmol/L (SD 1.30, n = 294) and 6.66 mmol/L (SD 1.44, n = 261), respectively. Specifically, the mean admission glucose level associated with mild TBI was 5.04 mmol/L (SD 0.71); moderate TBI, 5.78 mmol/L (SD 1.02); and severe TBI, 7.04 mmol/L (SD 1.18). The mean admission glucose level associated with a poor outcome in patients with isolated TBI was 6.98 mmol/L (SD 1.21). Patients with admission glucose of 5.56 mmol/L (SD 1.21) were more likely to have a favourable outcome.
CONCLUSION: Mild, moderate, and severe TBI were associated with an increase in blood glucose levels during admission, and the mean increase in glucose levels is based on the severity of the isolated TBI. Surgical intervention did not cause further significant changes in blood glucose levels. Patients with isolated TBI and minimal increases in blood glucose levels were more likely to have a favourable outcome.
Methods: For the optimisation and validation protocol, β-cells were plated onto 35 mm plastic petri dishes and maintained in RPMI-1640 media supplemented with 10 mM glucose, 10% FCS and 25 mM of N-2-hydroxyethylpiperazine-N-ethanesulfonic acid (HEPES). The treatment effects of 10 mM glucose and 30 μM fluoxetine on KATP channels NPo of β-cells were assessed via cell-attached patch-clamp recordings. For hippocampus cell experiments, hippocampi were harvested from day 17 of maternal Lister-hooded rat foetus, and then transferred to a Ca2+ and Mg2+-free HEPES-buffered Hank's salt solution (HHSS). The dissociated cells were cultured and plated onto a 25 mm round cover glasses coated with poly-d-lysine (0.1 mg/mL) in a petri dish. The KATP channels NPo of hippocampus cells when perfused with 1 mM and 10 mM of KA were determined.
Results: NPo of β-cells showed significant decreasing patterns (P < 0.001) when treated with 10 mM glucose 0.048 (0.027) as well as 30 μM fluoxetine 0.190 (0.141) as compared to basal counterpart. In hippocampus cell experiment, a significant increase (P < 0.001) in mean NPo 2.148 (0.175) of neurons when applied with 1 mM of KA as compared to basal was observed.
Conclusion: The two concentrations of KA used in the study exerted contrasting effects toward the mean of NPo. It is hypothesised that KA at lower concentration (1 mM) opens more KATP channels, leading to hyperpolarisation of the neurons, which may prevent neuronal hyper excitability. No effect was shown in 10 mM KA treatment, suggesting that only lower than 10 mM KA produced significant changes in KATP channels. This implies further validation of KA concentration to be used in the future.