ABSTRACT
Objective:To investigate the correlation between endothelial dysfunction and cardiomyocyte apoptosis during myocardial ischemia-reperfusion.Methods:A total of 63 male rats were selected to establish the rat model of myocardial ischemia-reperfusion by the ligation of the left anterior descending(LAD)coronary artery to simulate myocardial ischemia.Rats were divided into the control group and group Ⅰb, group Ⅰa, group Ⅱb, group Ⅱa, group Ⅲb and group Ⅲa.Control rats were treated only with LAD threading without ligation.In observation group, at 30, 90, 120 min after LAD ligation(marked as Ⅰ, Ⅱ, Ⅲ group respectively), loosen the ligation to simulate ischemia-reperfusion.In the observation group, captopril sublingual injection of 0.25 mg/kg before ligation were marked as group b, and as group a with no captopril injection.The circulating endothelial cells(CEC), endothelin(ET), nitric oxide(NO)and the apoptosis rate of cardiomyocytes in each group were measured.Results:The CEC and ET levels showed a continuous upward trend, and a NO level showed a continuous downward trend from group Ⅰa to Ⅱa to Ⅲa as compared with the control group( P<0.05). After using preventive intervention of captopril, the CEC and ET levels were lower and NO levels were higher in group Ⅱb and Ⅲb than in group Ⅱa and Ⅲa, respectively( P<0.05). The apoptotic rate of cardiomyocytes was higher in group Ⅰa than in the control group, and the apoptotic rate from high to low were from group Ⅲa[(235.71±40.25)%]to group Ⅱa[(197.28±43.56)%]to group Ⅰa[(138.55±32.87)%]and to the control group[(5.81±2.02)%]( P<0.05). The apoptotic rate of cardiomyocytes was lower in group Ⅱb[(125.67±26.51)%]and Ⅲb[(124.91±33.28)%]than in group Ⅱa and Ⅲa, respectively( P<0.05). Conclusions:The ischemia-reperfusion can cause endothelial dysfunction and the apoptosis of cardiomyocytes, and there is a close relationship between the degree of this lesions and the duration of ischemia-reperfusion.While, the appropriate application of angiotensin converting enzyme inhibitor can inhibit the damage of cardiomyocytes to a some extent.
ABSTRACT
Objective To discuss the emergency management and treatment measures of critically severe craniocerebral trauma.Methods A retrospective study was conducted on the emergency management in 82 patients with critically severe craniocerebral trauma admitted to our hospital from September 2005 to May 2011.Results According to the Glasgow Outcome scale ( GOS),there were 10 patients with good recovery (12％),17 with moderate disability (21％),12 with severe disability (20％),four in vegetable status (2％) and 39 deaths (48％).Conclusion The success rate in the treatment of critically severe craniocerebral injury can be enhanced through rapid and effective pre-hospital care,prompt surgical intervention,standardized subsequent therapy,adherence to damage control surgery concept,and emphasis on prevention and cure of secondary brain injury.