ABSTRACT
Objective To investigate the effect of combined application of mannitol and monosialoganglioside on neurological function and its efficacy in brain edema after intracerebral hemorrhage. Methods 92 cases of cerebral edema in patients with cerebral hemorrhage in our hospital, were randomly divided into groups, each group of 46 cases, the control group on the basis of the treatment of mannitol (125mL per times, once per 8h) treatment, the study group on the basic of control group received monosialogangliosides (20mg per times, once daily), 10d for a course of treatment, determination of serum indexes, neurological functions were recorded. Results The effective rate of control group was 71.74%, which was lower than 91.30% of the study group, there was significant difference (P < 0.05); compared with control group after treatment , in study group the intracranial pressure, intracranial hematoma, edema decreased, the urine volume increased, National Institutes of Health Stroke Scale (NIHSS) and quality of life score decreased, interleukin (IL-1β), high sensitive C reaction protein (Hs-CRP), IL-6 and IL-8 levels decreased, Na+-K+-ATP enzyme increased, the ratio of cerebrospinal fluid albumin and serum albumin, matrix metalloproteinase (MMP-2) and MMP-9 decreased, there were significant differences (P < 0.05). Conclusion The effect of the combined application of mannitol and monosialoganglioside on cerebral edema after cerebral hemorrhage is exact and could improve neurologic function.
ABSTRACT
Objective To investigate the functional and ultrastructural changes of cerebral microvascular endothelial cells at early stage following traumatic brain injury (TBI) in rats. Methods The rat models with closed brain injury were established with the improved Marmarous method. The expressions of thrombomodulin (TM) and von Willebrand factor (vWF) were determined by immunohistochemical techniques (5 rats per group) and real-time quantitative RT-PCR (5 rats per group) respectively at 1, 4, 8, 12, 24 hours and at days 3 and 7 after injury. Results TM and vWF started expression at 4 hours, reached peak at 24 hours and recovered to normal at day 7 after TBI. The expression levels of TM and vWF at different time points in sham control group showed statistical difference compared with damage group (P < 0.05). Conclusion The activation of the cerebral microvascular endothelial cells at early stage after TBI is the main mechanism of early secondary brain injury.