Objective To investigate alterations in the microtubule-associated protein 2 (MAP-2) of neurons in Wistar rats and the effect of nimodipine (Nim), D-2-amino-5-phosphonovaleric acid (D-AP-5) and mild hypothermia on neuronal MAP-2 following fluid percussion injury (FPI). Methods Alterations of MAP-2 in Wistar rat neurons following FPI were measured by a confocal laser scanning microscope using MAP-2 immunofluorescence staining as a MAP-2 indicator. Results MAP-2 immunofluorescence staining was limited to the cell bodies and dendritic compartments of neurons and more intense in dendrites than in cell bodies. The loss of MAP-2 was marked at 3 h post trauma ( P ＜ 0.01 ), and reached a maximum at 48 h post-trauma. Afterwards, fluorescence recovered partly at 72 h post-trauma. The application of Nim markedly reduced the loss of MAP-2 immunoreectivity within 1 h post-trauma ( P ＜ 0.01 ), and the application of D-AP-5 markedly reduced the loss of MAP-2 immunoreactivity within 10 h post-injury ( P ＜ 0.01 ). The application of mild hypothermia decreased the loss of MAP-2 immunoreactivity within 1 h post-injury (P＜ 0.05). Conclusions The partial recovery of fluorescence at 72 h post-trauma indicate that the partial structure of the neuronal microtubules can be repaired by itself. Nim, D-AP-5 and mild hypothermia reduce the degradation of MAP-2 by different mechanisms. The treatment of neuronal cytoskeleton degradation following FPI must employ multiple therapeutic approaches.

OBJECTIVE: To investigate the cause of massive hemoptysis in critical patients, and to evaluate the effect of bronchial artery embolization (BAE) on critical patients with massive hemoptysis. METHODS: A retrospective controlled analysis was conducted. The clinical data of 35 patients with life-threatening massive hemoptysis admitted to intensive care unit (ICU) of the First Hospital Affiliated to Guangzhou Medical University from January 2009 to December 2017 were analyzed. The patients were divided into BAE and non-BAE group according to whether receiving BAE or not. BAE patients were subdivided into subgroups: hemoptysis after ventilation and hemoptysis before ventilation subgroups, as well as survival and non-survival subgroups. The etiology of all massive hemoptysis was analyzed. The gender, age, acute physiology and chronic health evaluation II (APACHE II) score, amount of hemoptysis, whether presence of pleural thickening in chest CT, the length of ICU stay, total length of hospital stay, the duration of mechanical ventilation (MV), clinical effective and prognostic indicators of patients were recorded. The correlation between variables was analyzed by Spearman correlation analysis. RESULTS: All 35 patients were enrolled in the finally analysis. The main cause of critical patients with massive hemoptysis was fungal infection [37.1% (13/35)], followed by pneumonia and abnormal coagulation [17.1% (6/35)], bronchiectasis [11.4% (4/35)], tumor [8.6% (3/35)], etc. In all 35 patients, 27 were treated with BAE and 8 were treated without BAE. There was no difference in gender, age, the length of ICU stay, total length of hospital stay, the duration of MV, amount of hemoptysis, APACHE II score, whether use antiplatelet agents or anticoagulants, or whether presence of pleural thickening in chest CT between the two groups. The rate of hemoptysis remission in BAE group was significantly higher than that of non-BAE group [92.6% (25/27) vs. 25.0% (2/8), P < 0.01], but there was no statistically significant difference in hospital survival as compared with that of non-BAE group [48.1% (13/27) vs. 25.0% (2/8), P > 0.05]. Subgroup analysis showed that 64.3% (9/14) of patients with hemoptysis after ventilation was caused by pulmonary fungal infection, which was significantly higher than those with hemoptysis before ventilation [15.4% (2/13), P = 0.018]. Compared with hemoptysis after ventilation group, the length of ICU stay and the duration of MV in hemoptysis before ventilation group were significantly shortened [the length of ICU stay (days): 12.0 (14.0) vs. 30.0 (81.8), the duration of MV (days): 10.0 (16.0) vs. 25.0 (68.3)], the patients using antiplatelet drugs or anticoagulant drugs was decreased significantly (case: 1 vs. 9, all P < 0.05). However, there was no statistically significant difference in gender, age, total length of hospital stay, amount of hemoptysis, APACHE II score, whether presence of pleural thickening in chest CT, the rate of hemoptysis remission, the incidence of secondary BAE or hospital survival rate between the two groups. Compared with the survival subgroup (n = 13), more patients in the non-survival subgroup (n = 14) were treated with antiplatelet or anticoagulants (P < 0.05); and Spearman correlation analysis showed that the survival of the patients with BAE was negatively correlated with the use of antiplatelet or anticoagulants (r = -0.432, P = 0.024). There was no significant difference in the gender, age, the length of ICU day, total length of hospitalization, duration of MV, estimated hemoptysis, APACHE II score, or the proportion of pleural thickening between the two groups. CONCLUSIONS The study indicated that the etiology of massive hemoptysis in critical patients was complicated. Fungal infection was the main cause in patients with hemoptysis after ventilation. BAE was effective in the control of massive hemoptysis in ICU, but it was not ideal for patients with abnormal coagulation function or abnormal platelet count or platelet dysfunction from antiplatelet or anticoagulant drugs, the overall survival rate was still low.
APACHE ; Bronchial Arteries ; Hemoptysis ; Humans ; Intensive Care Units ; Prospective Studies ; Retrospective Studies