ABSTRACT
Objective:To observe the effect of early temperature control on the prognosis of brain injury patients after severe carbon monoxide poisoning (COP).Methods:A total of 277 patients hospitalized with severe COP were randomly divided into a fever group ( n=78), a normal temperature group ( n=113) and a mild hypothermia group ( n=86). All were given hyperbaric oxygen therapy and any necessary supportive treatment. The mild hypothermia group were kept in a room at 34 to 35℃. Evaluation was with the Glasgow Coma Scale (GCS), version II of the Acute Physiology and Chronic Health Evaluation (APACHE), the Hasegawa dementia scale (HDS) and the mini mental state examination (MMSE). The incidence of delayed encephalopathy (DEACMP) and mortality were compared among the three groups. The bispectral index (BIS) and neuron-specific enolase (NSE) levels were correlated with DEACMP. Results:After the treatments, improvement was observed in multiple indexes of all three groups compared with before the treatment. Compared with the fever group, the average GCS of the mild hypothermia group was significantly higher on the 2nd, 4th, 8th and 31st day after the intervention. It was significantly higher than the normal temperature group′s averages on the 4th, 8th and 31st day. The average APACHE scores of the normal temperature and the mild hypothermia groups were significantly lower than the fever group′s average, with that of the mild hypothermia group significantly lower than that of the normal group. The average HDS scores of the normal temperature and mild hypothermia groups were significantly higher than the fever group′s average, with that of the mild hypothermia group significantly higher than that of the normal group. The average MMSE score of the mild hypothermia group was significantly improved after 7 days, one month and three months of treatment. That of the normal group showed significant improvement after one and three months, but the mild hypothermia group′s averages were superior. Compared with the fever group, the average BIS score of the mild hypothermia group was significantly better after one, three and seven days, and one month. This was true for the normal group beyond three days after the intervention. The average NSE concentration of the normal group after 7 days and one month was significantly lower than that of the fever group. For the mild hypothermia group this was true after only 3 days. Compared with the other two groups, the average coma time, incidence of DEACMP and nervous system injury were significantly lower in the hypothermia group. The average GCS, BIS and NSE values were closely related to the occurrence of DEACMP.Conclusions:Early temperature control can significantly reduce the severity of brain injury after COP and reduce the incidence of neurological sequelae. Early dynamic detection of GCS, NSE concentration and BIS is of great significance for predicting the incidence of DEACMP.
ABSTRACT
Objective To investigate the effect of Xing-Zhi-Yi-Nao (XZYN) particles on the expressions of Nogo and OMgp proteins in brain of rats after acute carbon monoxide (CO) poisoning.Methods A total of 120 Sprague-Dawley rats were randomly divided into normal group,CO poisoning group and XZYN particles treatment group (40 rats in each group).The rats in CO poisoning group and treatment group of acute CO poisoning were established by using an animal chamber,and then received hyperbaric oxygen therapy.Meanwhile,rats in treatment group were further given additional XZYN particles twice a day by gavage.At 1 day,1 week,1 month and 2 months after CO poisoning,the neurobehavioral score of rats was evaluated by a Morris water maze test and a shuttle box test,and the expressions of neurite outgrowth inhibitor (Nogo) and oligodendrocyte-myelin glycoprotein (OMgp) were investigated in rat brain tissue by immunohistochemistry staining and western blotting assay,respectively.Results Compared with those in normal control group((11.6±8.4)s,(41.8±4.4)%,(16.1±2.3)s,and (1.2±0.2)s),the escape latency in CO group was significantly prolonged ((14.1±6.1)s),and the T1/ T total was obviously decreased (23.6±2.4) %,the escape time ((26.3±3.8)s),the active escape latency ((2.3±0.3)s) were notably extended at 1 d (P1 week) in Xing-Zhi-Yi-Nao treatment group (P0.05).Conclusion The expression of Nogo and Omgp proteins may be associated with brain injury and demyelination in rats induced by CO poisoning.XZYN particles can down-regulate the expression of Nogo,and pave a way for the treatment of acute brain damage and delayed encephalopathy after CO poisoning.
ABSTRACT
Objective To investigate the effects of N-butylphthalide (NBP) on cognitive function in acute severe carbon monoxide (CO) poisoning rats and its mechanism. Methods 120 health Sprague-Dawley (SD) rats were randomly divided into three groups (n = 40): normal control group (NC group), CO poisoning group (CO group) and NBP treatment group (NBP group). The acute severe CO poisoning model was established in a hyperbaric oxygen chamber by intoxicated with 1 000 ×10-6CO for 40 minutes, followed with 3 000 ×10-6CO for another 20 minutes, and then received hyperbaric oxygen therapy 1.5 hours once a day until sacrificed. Rats in NBP group were administered orally NBP 60 mg/kg for 2 times daily until death. NC group and CO group were treated with equal amount of pure olive oil. Four rats in each group were taken from 1, 3, 7, 14, 30 days after model setup, respectively. The cognitive function score was assessed by Morris water maze test. The changes in ultrastructure of hippocampus were observed under transmission electron microscope. The expressions of calpain 1 and Ca2+/calmodulin dependent protein kinase Ⅱ(CaMK Ⅱ) in hippocampus of brain tissue were detected by immunofluorescence staining, and the localization of the two target proteins in neurons was observed by immunofluorescence double staining. Results Compared with NC group, the escape latency at 1 day after poisoning in CO group was significantly prolonged (s: 55.6±3.2 vs. 44.5±3.5, P < 0.05), and the times of the platform crossing was significantly decreased (times: 1.3±0.8 vs. 6.6±1.2, P < 0.05);the ultrastructure of hippocampus was obviously injured; the protein expressions of calpain 1 and CaMK Ⅱ in brain tissue were significantly increased at 1 day after CO poisoning [calpain 1 (A value): 41.24±5.21 vs. 6.44±1.13, CaMK Ⅱ (A value): 56.19±5.04 vs. 9.84±1.53, both P < 0.05], and the protein expression of calpain 1 reached the peak at 3 days (A value: 59.34±6.11), the protein expression of CaMK Ⅱ reached the peak at 1 day (A value:56.19±5.04). Compared with CO group, the cognitive function was significantly improved in NBP group in the late stage of poisoning [7-30 days, escape latency (s): 40.3±1.9 vs. 49.1±3.1 at 7 days, 30.1±2.9 vs. 39.4±3.1 at 30 days;times of the platform crossing (times): 2.8±1.0 vs. 1.0±0.9 at 14 days, 3.2±0.8 vs. 1.0±0.9 at 30 days, all P < 0.05];the degree of injury of hippocampal neuron was relatively slight; the protein expression of calpain 1 in brain tissue was significantly decreased from 3 days after CO poisoning (A value: 39.63±3.03 vs. 59.34±6.11, P < 0.05), and the protein expression of CaMK Ⅱ was significantly decreased from 1 day after CO poisoning (A value: 42.22±3.84 vs. 56.19±5.04, P < 0.05). Immunofluorescence double staining suggested that calpain 1 and CaMK Ⅱ protein could not only coexist in the same cell, but also could be expressed separately in different cells. Linear regression analysis showed that the expression of calpain 1 and CaMK Ⅱ was positively correlated (R 2= 0.852, P = 0.002). Conclusions NBP treatment could maintain ultrastructure integrity of hippocampus, balance the expression levels of calpain 1 and CaMK Ⅱproteins, and significantly improve cognitive impairment induced by CO poisoning, thus play a protective role against hippocampus damage in rats with acute severe CO poisoning.