目标性体温管理（targeted temperature management，TFM）以前称为治疗性低温、保护性低温（在中国通常称为亚低温治疗），2002年以来已经成为心脏骤停复苏后治疗的重要内容。加拿大急诊医师协会在2006年发布了相应的指南，2015年联合...目标性体温管理（targeted temperature management，TFM）以前称为治疗性低温、保护性低温（在中国通常称为亚低温治疗），2002年以来已经成为心脏骤停复苏后治疗的重要内容。加拿大急诊医师协会在2006年发布了相应的指南，2015年联合加拿大危重病医学会、神经重症学会、危重病研究协作组联合更新了指南。展开更多
Objective To evaluate the influence of hypothermia to Ca 2+/calmodulin-dependent kinase Ⅱ during global brain ischemia in rats. Methods Fifteen male SD rats were randomly divided into 3 groups: control group (group ...Objective To evaluate the influence of hypothermia to Ca 2+/calmodulin-dependent kinase Ⅱ during global brain ischemia in rats. Methods Fifteen male SD rats were randomly divided into 3 groups: control group (group Ⅰ, n=5), hepothermia group (group Ⅱ, n=5) and reperfusion group (group Ⅲ, n=5). Only sugery was performed without hypothermia and clipping bilateral carotids in group Ⅰ. Ice was used covering head of rats in group Ⅱ to get hypothermia around 32℃, and bilateral carotids were clipped 20 min of ischemia followed by 60 min reperfusion keeping tympanum temperature 32℃. Bilateral carotids were clipped 20 min of ischemia followed by 60 min reperfusion without hypothermia in Group Ⅲ. Brain tissues were saved in three groups after experiments for evaluating Ca 2+/calmodulin-dependent kinase Ⅱ. Results Left tympanum temperature in the group Ⅱ is significantly lower than group Ⅰ during global ischemia and reperfusion(p<0.05). Those are no difference between group Ⅰ and group Ⅲ. The activity of Ca 2+/calmodulin-dependent kinase Ⅱ after 60 min reperfusion in both Group Ⅱ and group Ⅲ was significantly lower than those in the group Ⅰ(P<0.05), which is significantly higher in the group Ⅱ than in the group Ⅲ(P<0.05). Conclusion Hypothermia can increase the activity of Ca 2+/calmodulin-dependent kinase Ⅱ after global ischemia reperfusion. Hypothermia has significant protection during ischemia reperfusion injury.展开更多
目的探讨心跳骤停心肺复苏后脑损伤(BIC)模型中,治疗性低温(TH)对神经元氧化应激损伤的作用及相关机制。方法雄性SD大鼠60只,7~10周,体重280~320 g。采用随机数字表法分为五组:假手术组(S组)、BIC组、低温治疗组(TH组)、沉默冷诱导RNA...目的探讨心跳骤停心肺复苏后脑损伤(BIC)模型中,治疗性低温(TH)对神经元氧化应激损伤的作用及相关机制。方法雄性SD大鼠60只,7~10周,体重280~320 g。采用随机数字表法分为五组:假手术组(S组)、BIC组、低温治疗组(TH组)、沉默冷诱导RNA结合蛋白(CIRP)后低温治疗组(THC组)和空载后低温治疗组(THN组),每组12只。采用经食管连续快速起搏诱发室颤,心跳骤停4 min后,行心肺复苏术(CPR),建立BIC模型。于BIC模型制备后1 d,采用免疫荧光法检测海马活性氧簇(ROS)荧光强度,Western blot法检测海马CIRP、硫氧还蛋白1(Trx1)、磷酸化凋亡信号调节激酶1(ASK1)蛋白含量及其下游p38和c-Jun N-末端激酶(JNK)磷酸化含量。于BIC模型制备后3 d,采用原位末端标记(TUNEL)法检测海马神经元凋亡细胞百分比。结果与S组比较,BIC模型制备后1 d BIC组ROS荧光强度明显升高,CIRP含量明显降低,p-ASK1、p-p38含量明显升高;TH组和THN组ROS荧光强度均明显升高,CIRP含量明显升高,p-JNK含量明显降低;THC组ROS荧光强度明显升高,CIRP、Trx1含量明显降低,p-ASK1、p-p38含量明显升高(P<0.05)。与BIC组比较,BIC模型制备后1 d TH组和THN组ROS荧光强度明显降低,CIRP、Trx1含量明显升高,p-ASK1和p-JNK含量明显降低;TH组p-p38含量明显降低;THC组ROS荧光强度明显降低,p-ASK1和p-p38含量明显升高(P<0.05)。与THC组比较,BIC模型制备后1 d TH组和THN组ROS荧光强度明显降低,CIRP、Trx1含量明显升高,p-ASK1、p-p38和p-JNK含量明显降低(P<0.05)。与S组比较,BIC模型制备后3 d BIC组、TH组、THC组和THN组神经元凋亡细胞百分比明显升高(P<0.05)。与BIC组比较,BIC模型制备后3 d TH组、THC组和THN组凋亡细胞百分比明显降低(P<0.05)。与THC组比较,BIC模型制备后3 d TH组和THN组凋亡细胞百分比明显降低(P<0.05)。结论TH可以减轻BIC模型制备后神经元氧化应激反应以及减少神经元凋亡,沉默CIRP后该作用�展开更多
文摘目标性体温管理（targeted temperature management，TFM）以前称为治疗性低温、保护性低温（在中国通常称为亚低温治疗），2002年以来已经成为心脏骤停复苏后治疗的重要内容。加拿大急诊医师协会在2006年发布了相应的指南，2015年联合加拿大危重病医学会、神经重症学会、危重病研究协作组联合更新了指南。
文摘Objective To evaluate the influence of hypothermia to Ca 2+/calmodulin-dependent kinase Ⅱ during global brain ischemia in rats. Methods Fifteen male SD rats were randomly divided into 3 groups: control group (group Ⅰ, n=5), hepothermia group (group Ⅱ, n=5) and reperfusion group (group Ⅲ, n=5). Only sugery was performed without hypothermia and clipping bilateral carotids in group Ⅰ. Ice was used covering head of rats in group Ⅱ to get hypothermia around 32℃, and bilateral carotids were clipped 20 min of ischemia followed by 60 min reperfusion keeping tympanum temperature 32℃. Bilateral carotids were clipped 20 min of ischemia followed by 60 min reperfusion without hypothermia in Group Ⅲ. Brain tissues were saved in three groups after experiments for evaluating Ca 2+/calmodulin-dependent kinase Ⅱ. Results Left tympanum temperature in the group Ⅱ is significantly lower than group Ⅰ during global ischemia and reperfusion(p<0.05). Those are no difference between group Ⅰ and group Ⅲ. The activity of Ca 2+/calmodulin-dependent kinase Ⅱ after 60 min reperfusion in both Group Ⅱ and group Ⅲ was significantly lower than those in the group Ⅰ(P<0.05), which is significantly higher in the group Ⅱ than in the group Ⅲ(P<0.05). Conclusion Hypothermia can increase the activity of Ca 2+/calmodulin-dependent kinase Ⅱ after global ischemia reperfusion. Hypothermia has significant protection during ischemia reperfusion injury.
文摘目的探讨心跳骤停心肺复苏后脑损伤(BIC)模型中,治疗性低温(TH)对神经元氧化应激损伤的作用及相关机制。方法雄性SD大鼠60只,7~10周,体重280~320 g。采用随机数字表法分为五组:假手术组(S组)、BIC组、低温治疗组(TH组)、沉默冷诱导RNA结合蛋白(CIRP)后低温治疗组(THC组)和空载后低温治疗组(THN组),每组12只。采用经食管连续快速起搏诱发室颤,心跳骤停4 min后,行心肺复苏术(CPR),建立BIC模型。于BIC模型制备后1 d,采用免疫荧光法检测海马活性氧簇(ROS)荧光强度,Western blot法检测海马CIRP、硫氧还蛋白1(Trx1)、磷酸化凋亡信号调节激酶1(ASK1)蛋白含量及其下游p38和c-Jun N-末端激酶(JNK)磷酸化含量。于BIC模型制备后3 d,采用原位末端标记(TUNEL)法检测海马神经元凋亡细胞百分比。结果与S组比较,BIC模型制备后1 d BIC组ROS荧光强度明显升高,CIRP含量明显降低,p-ASK1、p-p38含量明显升高;TH组和THN组ROS荧光强度均明显升高,CIRP含量明显升高,p-JNK含量明显降低;THC组ROS荧光强度明显升高,CIRP、Trx1含量明显降低,p-ASK1、p-p38含量明显升高(P<0.05)。与BIC组比较,BIC模型制备后1 d TH组和THN组ROS荧光强度明显降低,CIRP、Trx1含量明显升高,p-ASK1和p-JNK含量明显降低;TH组p-p38含量明显降低;THC组ROS荧光强度明显降低,p-ASK1和p-p38含量明显升高(P<0.05)。与THC组比较,BIC模型制备后1 d TH组和THN组ROS荧光强度明显降低,CIRP、Trx1含量明显升高,p-ASK1、p-p38和p-JNK含量明显降低(P<0.05)。与S组比较,BIC模型制备后3 d BIC组、TH组、THC组和THN组神经元凋亡细胞百分比明显升高(P<0.05)。与BIC组比较,BIC模型制备后3 d TH组、THC组和THN组凋亡细胞百分比明显降低(P<0.05)。与THC组比较,BIC模型制备后3 d TH组和THN组凋亡细胞百分比明显降低(P<0.05)。结论TH可以减轻BIC模型制备后神经元氧化应激反应以及减少神经元凋亡,沉默CIRP后该作用�
