Serum levels of S100B from jugular bulb as a biomarker of poor prognosis in patients with severe acute brain injury.

AIMS/BACKGROUND: To evaluate the correlation between protein S100B concentrations measured in the jugular bulb as well as at peripheral level and the prognostic usefulness of this marker. METHODS: A prospective study of all patients admitted to the intensive care unit with acute brain damage was carried out. Peripheral and jugular bulb blood samples were collected upon admission and every 24h for three days. The endpoints were brain death diagnosis and the Glasgow Outcome Scale score after 6months. RESULTS: A total of 83 patients were included. Jugular protein S100B levels were greater than systemic levels upon admission and also after 24 and 72h (mean difference>0). Jugular protein S100B levels showed acceptable precision in predicting brain death both upon admission [AUC 0.67 (95% CI 0.53-0.80)] and after 48h [AUC 0.73 (95% CI 0.57-0.89)]. Similar results were obtained regarding the capacity of jugular protein S100B levels upon admission to predict an unfavourable outcome (AUC 0.69 (95% CI 0.56-0.79)). The gradient upon admission (jugular-peripheral levels) showed its capacity to predict the development of brain death [AUC 0.74 (95% CI 0.62-0.86)] and together with the Glasgow Coma Scale constituted the independent factors associated with the development of brain death. CONCLUSION: Regional protein S100B determinations are higher than systemic determinations, thus confirming the cerebral origin of protein S100B. The transcranial protein S100B gradient is correlated to the development of brain death.

Effect of neuroprotective therapies (hypothermia and cyclosporine a) on dopamine-induced apoptosis in human neuronal SH-SY5Y cells.

INTRODUCTION: This study aimed to evaluate the effect of hypothermia and CyA on neuronal survival after induced injury in a neuronal model. METHODS: Human neuroblastoma SH-SY5Y cells were seeded and allowed to grow. To determine whether lower temperatures protect from dopamine-induced apoptosis, cells were treated with dopamine at 100 µM, at 300 µM or without dopamine and incubated at 32 °C or 37 °C for 24 hours. To assess the effect of CyA, cells were pre-incubated with CyA at 37 °C and after dopamine was added. RESULTS: After 24 hours of incubation at 37 °C, 100 µM and 300 µM dopamine induced 42% (SD = 21) and 58% (SD = 7.9) apoptotic SH-SY5 cells, respectively. In cultures at 32 °C dopamine-induced apoptosis could be reversed by hypothermia [7% (SD = 1.4) and 3.45% (SD = 1.1) for 100 µM and 300 µM, respectively], similar to levels obtained in non-treated cells [2.4% (SD = 1.5)]. Cyclosporine A treatment did not render the expected result, since CyA-pre-treated cells and SH-SY5Y cells showed higher levels of apoptosis than those observed with dopamine alone CONCLUSIONS: Hypothermia has a marked protective effect against apoptotic cell death induced by dopamine in a human neuroblastic cell line. The neuroprotective effect of CyA described with other apoptotic cell death stimuli was not demonstrated with our experimental conditions.