Objective To investigate the standards for management of traumatic intrapulmonary hematoma and hematocele.Methods A retrospective study was conducted on the data of 21 patients with traumatic pulmonary hematoma or hematocele (AIS≥4 points) treated at Chongqing Emergency Medical Center from August 1999 to August 2010.Results The overall mortality was 14％ (3/21)and death causes were respiratory passage hemorrhea and asphyxia.About 67％ of patients ( 14/21 ) were associated with hemoptysis,which lasted for 1-240 days (mean,15.8 days).The duration of hemoptysis due to traumatic intrapulmonary hematoma hematocele was about 3.4 times longer than that due to simple traumatic pneumatocele.The hematoma or cyst disappeared at average 61.6 days,with 3.4 times longer than the disappearance time of intrapulmonary hematoma or hematocele in comparison with that of simple pneumatocele.The size and position of traumatic pulmonary hematoma or pneumatocele influenced the treatment methods,outcomes and prognosis.Conclusions Standardized treatment for traumatic pulmonary hematoma or hematocele is key to improving the cure rate.Early emergency definitive surgery is required for patients with traumatic intrapulmonary hematoma or hematocele greater than 6.0 cm in diameter and for those with pneumatocele greater than 6.0 cm in diameter combined with incapability of keeping breathing due to severe air leakage.

Objective To explore the neuroprotection of Shuxuetongmai capsule pretreatment, and the effect on the expression of p38 mitogen-activated protein kinase (p38MAPK) in rats with middle cerebral artery occlusion. Methods Ninety-six male SD rats were divided randomly into sham-operated group,ischemia/reperfusion group (I/R),ischemia preconditioning group (IP),and Shuxuetongmai group(n=24). Each group was further randomly divided into 4 subgroups by 3 h, 6 h, 24 h and 72 h after reperfusion, 6 rats in each subgroup. Sham-operated group was only performed artery separation . The middle cerebral artery occlusion (MCAO) model was set up in I/R rats by Longa method. The IP rats were performed for three minutes on the bilateral carotid artery ligation, and formed MCAO model 24 hours later. The rats in the Shuxuetongmai group were pretreated with Shuxuetongmai capsules for 14 days on gavage before the establishment of MCAO model. The neurological deficits were graded in rats by Zea Longa method. Western Blot was used to determine the protein expression of p38MAPK and P-p38MAPK. Tunel method was applied to detect the apoptosis of neurons and the relationship between expression of p38MAPK, P-p38MAPK and apoptosis of neuron. Results No neurological dysfunction appeared in the sham-operated group at each time points, but not for the other groups, which reached the peak at 24 h. Compared with the I/R group, IP group and Shuxuetongmai group presented the mild neurologic function deficiency at different time points in rats (P<0. 05), and no significant differences occurred between ischemia preconditioning group and Shuxuetongmai group (P>0.05). The obvious variation of the value of P-p38MAPK/p38MAPK wasn't detected in sham-operated group at different time points, while obviously presented in I/R group, and the ratios of P-p38MAPK/p38MAPK were increased gradually followed with reperfusion, approaching to the highest level at 24 h. Compared with the I/R group, the P-p38MAPK/p38MAPK declined from 3 h and to the lowest level at 24 h of reperfusion, in both IP and Shuxuetongmai groups(P<0. 05), and with similar phosphorylation. At different time points,very few neurons apoptosis were detected in sham-operated groups, but which increased gradually after reperfusion in other groups, and reached to the peak at 24 h. The neurons apoptosis in both IP group and Shuxuetongmai group were less than that in IR group ( P<0. 05 ) at different time points, and it showed no significant differences on neurons apoptosis between ischemia/preconditioning group and Shuxuetongmai group in rats (P>0. 05). Conclusion Shuxuetongmai capsule pretreatment can induce brain ischemic tolerance, attenuate the apoptosis of neurons in cerebral ischemia reperfusion, and improve neurologic function. The mechanism may be related to the inhibition of p38MAPK phosphorylation.