体温对沙鼠前脑缺血/再灌注Ca^(2+)/钙调素依赖性蛋白激酶Ⅱ活性变化的影响

EFFECTS OF BODY-TEMPERATURE ON THE CHANGE OF CALCIUM/CALMODULIN DEPENDENT PROTEIN KINASE Ⅱ ACTIVITY FOLLOWING CEREBRAL ISCHEMIA/REPERFUSION IN GERBILS

目的和方法 :本文以蒙古沙土鼠双侧颈动脉夹闭 (BCAO)形成前脑缺血模型 ,观察不同体温 (3 6.5℃、3 0 .0℃、3 9.0℃ )对脑缺血 /再灌注海马、皮质、纹状体、小脑Ca2 +/CaMPKⅡ活性变化的影响。结果 :①除小脑外 ,海马、皮质、纹状体Ca2 +/CaMPKⅡ活性在缺血后均有不同程度下降 ,该下降对缺血过程中体温变化十分敏感 :如分别于 3 6.5℃、3 0 .0℃、3 9.0℃时同样缺血 10min ,海马酶活性分别为对照组的 3 2 .2 %、10 1.3 %、9.1% ;②持续一定时间的低体温再灌注可显著促进海马、皮质、纹状体该酶活性的恢复 :如 3 6.5℃和 3 0 .0℃再灌注相同时间后 ,海马酶活性分别为对照组的 5 1.3 %和 5 3 .2 % (4h ,P >0 .0 5 )、5 8.0 %和 68.9% (8h ,P <0 .0 5 )、67.4 %和 84 .1% (16h ,P <0 .0 5 )。结论 :低体温可显著保护脑缺血 /再灌注缺血敏感组织Ca2 +/CaMPKⅡ活性 ,这可能与其保护缺血性脑损伤关系密切。

Aim:To investigate the effects of body temperature on the Ca 2+ /CaM PK Ⅱ activity in different cerebral tissues following ischemia/ reperfusion Methods:We used bilateral carotid artery occlusion in gerbils as ischemic models, examined the Ca 2+ /CaM PK Ⅱ activity in hippocampus, cerebral cortex, striatum and cerebellum at ① different intraischemic body temperature (30.0 ℃, 36.5 ℃, 39.0 ℃) and ischemic time (0 min, 10 min, 20 min, 30 min), ② different body temperature (30.0℃, 36.5 ℃) and time (4 h, 8 h> 16 h) of reperfusion following 10 min normathermic ischemia.Results:① ischemia decreased Ca 2+ /CaM PK Ⅱ activity at different degree in all the tissues except for cerebellum. These decreases were very sensitive to intraischemic body temperature. Hypothermia(30.0℃) protected Ca 2+ /CaM PK Ⅱ activity against ischemia, the protective efficiency depended on the time of ischemia: 30.0℃ could almost preserve the activity in all the tissues at 10 min ischemia, but at 20 min and 30 min the activity decreased gradually but was much higher than 36.5℃ ischemic control group ( P <0.05). Hyperthermia(39.0℃) exacerbated ischemia induced inhibition of Ca 2+ /CaM PK Ⅱ activity. ②Hypothermia accelerated the restoration of inhibited Ca 2+ /CaM PK Ⅱ activity in the three tissues during reperfusion, the accelerative efiiciency depended on the time of hypothermic reperfusion: 8 h and 16 h hypothermic reperfusuion accelerated the restoration of the activity, but 4 h couldn't. Conclusion:Hypothermia preserves Ca 2+ /CaM PK Ⅱ acti vity nearby to the normal level following ischemia/reperfusion, perhaps it is one of the molecular mechanisms of hypothermic protection against cerebral ischemia. To investigate the effects of body temperature on the Ca 2+ /CaM PK Ⅱ activity in different cerebral tissues following ischemia/ reperfusion Methods:We used bilateral carotid artery occlusion in gerbils as ischemic models, examined the Ca 2+ /CaM PK Ⅱ activity in hippocampus, cerebral cortex, striatum and cerebellum at ① different intraischemic body temperature (30.0 ℃, 36.5 ℃, 39.0 ℃) and ischemic time (0 min, 10 min, 20 min, 30 min), ② different body temperature (30.0℃, 36.5 ℃) and time (4 h, 8 h> 16 h) of reperfusion following 10 min normathermic ischemia.Results:① ischemia decreased Ca 2+ /CaM PK Ⅱ activity at different degree in all the tissues except for cerebellum. These decreases were very sensitive to intraischemic body temperature. Hypothermia(30.0℃) protected Ca 2+ /CaM PK Ⅱ activity against ischemia, the protective efficiency depended on the time of ischemia: 30.0℃ could almost preserve the activity in all the tissues at 10 min ischemia, but at 20 min and 30 min the activity decreased gradually but was much higher than 36.5℃ ischemic control group ( P <0.05). Hyperthermia(39.0℃) exacerbated ischemia induced inhibition of Ca 2+ /CaM PK Ⅱ activity. ②Hypothermia accelerated the restoration of inhibited Ca 2+ /CaM PK Ⅱ activity in the three tissues during reperfusion, the accelerative efiiciency depended on the time of hypothermic reperfusion: 8 h and 16 h hypothermic reperfusuion accelerated the restoration of the activity, but 4 h couldn't. Conclusion:Hypothermia preserves Ca 2+ /CaM PK Ⅱ acti vity nearby to the normal level following ischemia/reperfusion, perhaps it is one of the molecular mechanisms of hypothermic protection against cerebral ischemia. Methods:We used bilateral carotid artery occlusion in gerbils as ischemic models, examined the Ca 2+ /CaM PK Ⅱ activity in hippocampus, cerebral cortex, striatum and cerebellum at ① different intraischemic body temperature (30.0 ℃, 36.5 ℃, 39.0 ℃) and ischemic time (0 min, 10 min, 20 min, 30 min), ② different body temperature (30.0℃, 36.5 ℃) and time (4 h, 8 h> 16 h) of reperfusion following 10 min normathermic ischemia.Results:① ischemia decreased Ca 2+ /CaM PK Ⅱ activity at different degree in all the tissues except for cerebellum. These decreases were very