OBJECTIVE: To investigate the capacity of serum samples draining from the neuronal lesions to induce apoptosis of the lymphoid Jurkat cells in vitro and to analyze whether this effect is related to patient outcome. DESIGN AND SETTING: Prospective clinical investigation in a 21-bed intensive care unit (ICU) in a university hospital. PATIENTS: Forty-two patients who had suffered from acute brain injury (traumatic brain injury or spontaneous intracranial hemorrhage) requiring intensive care. INTERVENTIONS: Blood samples were obtained simultaneously from jugular bulb vein (regional) and from central venous catheter (systemic) on admission to the ICU and after 24, 48, and 72 h. Jurkat cells were incubated in the presence of 10% of heat-inactivated patients sera. The percentages of apoptotic cultured cells was measured by staining with annexin V and propidium iodide. MEASUREMENTS AND RESULTS: Regional serum draining from the lesions induced higher percentages of early and late apoptotic cells than systemic serum. The apoptotic effect was clearer with the sera from the patients who developed brain death. The apoptotic effect maintained a relationship with the mortality and the functional outcome at 6 months after the injury. CONCLUSIONS: Despite being performed on lymphoid cells because of the easier technical handling, our data help to elucidate the role of apoptosis for brain damage in acute brain injury. This and other undergoing studies on neuronal cells will enhance the understanding and management of apoptotic cell death in patients with acute brain injury admitted to the ICU.
OBJECTIVE: To investigate the capacity of serum samples draining from the neuronal lesions to induce apoptosis of the lymphoid Jurkat cells in vitro and to analyze whether this effect is related to patient outcome. DESIGN AND SETTING: Prospective clinical investigation in a 21-bed intensive care unit (ICU) in a university hospital. PATIENTS: Forty-two patients who had suffered from acute brain injury (traumatic brain injury or spontaneous intracranial hemorrhage) requiring intensive care. INTERVENTIONS: Blood samples were obtained simultaneously from jugular bulb vein (regional) and from central venous catheter (systemic) on admission to the ICU and after 24, 48, and 72 h. Jurkat cells were incubated in the presence of 10% of heat-inactivated patients sera. The percentages of apoptotic cultured cells was measured by staining with annexin V and propidium iodide. MEASUREMENTS AND RESULTS: Regional serum draining from the lesions induced higher percentages of early and late apoptotic cells than systemic serum. The apoptotic effect was clearer with the sera from the patients who developed brain death. The apoptotic effect maintained a relationship with the mortality and the functional outcome at 6 months after the injury. CONCLUSIONS: Despite being performed on lymphoid cells because of the easier technical handling, our data help to elucidate the role of apoptosis for brain damage in acute brain injury. This and other undergoing studies on neuronal cells will enhance the understanding and management of apoptotic cell death in patients with acute brain injury admitted to the ICU.
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