目的探讨心脏上的阿片受体是否介导了瑞芬太尼预适应对缺血后心脏保护作用。方法麻醉开胸大鼠心脏缺血再灌注模型。分为对照组(CON),缺血预适应组(IPC)和瑞芬太尼预适应组(RPC);瑞芬太尼预适应的方法:在缺血再灌注前分别静注瑞芬太尼5 m...目的探讨心脏上的阿片受体是否介导了瑞芬太尼预适应对缺血后心脏保护作用。方法麻醉开胸大鼠心脏缺血再灌注模型。分为对照组(CON),缺血预适应组(IPC)和瑞芬太尼预适应组(RPC);瑞芬太尼预适应的方法:在缺血再灌注前分别静注瑞芬太尼5 m in,停止5 m in共3个循环。三种阿片受体阻断剂Naltrindole(NTD,δ受体阻断剂,5 mg.kg-1)、nor-B inaltorph im ine(nor-BNI,к受体阻断剂,5 mg.kg-1)、CTOP(μ受体阻断剂,1 mg.kg-1),分别在RPC(NTD+RPC,BNI+RPC和CTOP+RPC组)和IPC(NTD+IPC,BNI+IPC和CTOP+IPC组)前静脉注射。观察指标包括:平均动脉压(MBP),心率(HR),记算收缩压心率乘积(RPP);缺血危险区(AAR),梗死区(IS)的体积,心肌梗死面积以IS/AAR来表示。结果在IS/AAR方面:NTD+RPC与CTOP+RPC与CON组之间无差别,与RPC有差别;nor-BNI+RPC与RPC及CON组之间都有差别;NTD+IPC和no-BNI+IPC与IPC组之间有差别,并且nor-BNI与CON组之间也有差别。结论μ,δ和κ-阿片受体介导了RPC对大鼠缺血后心脏的保护作用,μ-阿片受体的作用可能来至心脏之外的组织或器官。展开更多
Background The optimal time window for the administration of hypothermia following cerebral ischemia has been studied for decades, with disparity outcomes. In this study, the efficacy of mild brain hypothermia beginni...Background The optimal time window for the administration of hypothermia following cerebral ischemia has been studied for decades, with disparity outcomes. In this study, the efficacy of mild brain hypothermia beginning at different time intervals on brain endogenous antioxidant enzyme and energy metabolites was investigated in a model of global cerebral ischemia. Methods Forty-eight male Sprague-Dawley rats were divided into a sham-operated group, a normothermia （37℃-38℃） ischemic group and a mild hypothermic （31℃-32℃） ischemia groups. Rats in the last group were subdivided into four groups： 240 minutes of hypothermia, 30 minutes of normothermia plus 210 minutes of hypothermia, 60 minutes of normothermia plus 180 minutes of hypothermia and 90 minutes of normothermia plus 150 minutes of hypothermia （n=8）. Global cerebral ischemia was established using the Pulsinelli four-vessel occlusion model for 20 minutes and mild hypothermia was applied after 20 minutes of ischemia. Brain.tissue was collected following 20 minutes of cerebral ischemia and 240 minutes of reperfusion, and used to measure the levels of superoxide dismutase （SOD）, glutathione peroxidase （GSH-Px）, reduced glutathione （GSH） and adenosine triphosphate （ATP）. Results Mild hypothermia that was started within 0 to 60 minutes delayed the consumption of SOD, GSH-Px, GSH, and ATP （P 〈0.05 or P 〈0.01） in ischemic tissue, as compared to a normothermic ischemia group. In contrast, mild hypothermia beginning at 90 minutes had little effect on the levels of SOD, GSH-Px, GSH, and ATP （P〉0.05）. Conclusions Postischemic mild brain hypothermia can significantly delay the consumption of endogenous antioxidant enzymes and energy metabolites, which are critical to the process of cerebral protection by mild hypothermia. These results show that mild hypothermia limits ischemic injury if started within 60 minutes, but loses its protective effects when delayed until 90 minutes following cerebral ischemia.展开更多
文摘目的探讨心脏上的阿片受体是否介导了瑞芬太尼预适应对缺血后心脏保护作用。方法麻醉开胸大鼠心脏缺血再灌注模型。分为对照组(CON),缺血预适应组(IPC)和瑞芬太尼预适应组(RPC);瑞芬太尼预适应的方法:在缺血再灌注前分别静注瑞芬太尼5 m in,停止5 m in共3个循环。三种阿片受体阻断剂Naltrindole(NTD,δ受体阻断剂,5 mg.kg-1)、nor-B inaltorph im ine(nor-BNI,к受体阻断剂,5 mg.kg-1)、CTOP(μ受体阻断剂,1 mg.kg-1),分别在RPC(NTD+RPC,BNI+RPC和CTOP+RPC组)和IPC(NTD+IPC,BNI+IPC和CTOP+IPC组)前静脉注射。观察指标包括:平均动脉压(MBP),心率(HR),记算收缩压心率乘积(RPP);缺血危险区(AAR),梗死区(IS)的体积,心肌梗死面积以IS/AAR来表示。结果在IS/AAR方面:NTD+RPC与CTOP+RPC与CON组之间无差别,与RPC有差别;nor-BNI+RPC与RPC及CON组之间都有差别;NTD+IPC和no-BNI+IPC与IPC组之间有差别,并且nor-BNI与CON组之间也有差别。结论μ,δ和κ-阿片受体介导了RPC对大鼠缺血后心脏的保护作用,μ-阿片受体的作用可能来至心脏之外的组织或器官。
文摘Background The optimal time window for the administration of hypothermia following cerebral ischemia has been studied for decades, with disparity outcomes. In this study, the efficacy of mild brain hypothermia beginning at different time intervals on brain endogenous antioxidant enzyme and energy metabolites was investigated in a model of global cerebral ischemia. Methods Forty-eight male Sprague-Dawley rats were divided into a sham-operated group, a normothermia （37℃-38℃） ischemic group and a mild hypothermic （31℃-32℃） ischemia groups. Rats in the last group were subdivided into four groups： 240 minutes of hypothermia, 30 minutes of normothermia plus 210 minutes of hypothermia, 60 minutes of normothermia plus 180 minutes of hypothermia and 90 minutes of normothermia plus 150 minutes of hypothermia （n=8）. Global cerebral ischemia was established using the Pulsinelli four-vessel occlusion model for 20 minutes and mild hypothermia was applied after 20 minutes of ischemia. Brain.tissue was collected following 20 minutes of cerebral ischemia and 240 minutes of reperfusion, and used to measure the levels of superoxide dismutase （SOD）, glutathione peroxidase （GSH-Px）, reduced glutathione （GSH） and adenosine triphosphate （ATP）. Results Mild hypothermia that was started within 0 to 60 minutes delayed the consumption of SOD, GSH-Px, GSH, and ATP （P 〈0.05 or P 〈0.01） in ischemic tissue, as compared to a normothermic ischemia group. In contrast, mild hypothermia beginning at 90 minutes had little effect on the levels of SOD, GSH-Px, GSH, and ATP （P〉0.05）. Conclusions Postischemic mild brain hypothermia can significantly delay the consumption of endogenous antioxidant enzymes and energy metabolites, which are critical to the process of cerebral protection by mild hypothermia. These results show that mild hypothermia limits ischemic injury if started within 60 minutes, but loses its protective effects when delayed until 90 minutes following cerebral ischemia.
