摘要
目的研究头部贴敷式亚低温治疗对缺氧缺血脑损伤(hypoxic-ischemic brain damage,HIBD)新生大鼠的脑组织线粒体ATP酶活性的影响,以进一步探讨亚低温对缺氧缺血脑组织的保护机制。方法将84只Wistar新生鼠随机分为4组:假手术常温对照组、假手术亚低温对照组、HIBD模型常温恢复组、HIBD模型亚低温治疗组。各组动物在HI后不同时间点(2,6,12h)断头取脑,提取脑组织线粒体并测定其中Na+-K+-ATP酶和Ca2+-ATP酶活性。结果①HIBD常温恢复组及亚低温治疗组在2,6,12h时Ca2+-ATP酶活性均呈下降趋势,分别为3.17±0.81,2.26±0.53,1.31±0.78μmol/mgPr.h及5.25±0.61,4.59±0.81,4.61±0.62μmol/mgPr.h,但亚低温治疗各组该酶活性均明显高于相应的常温组(P<0.01)。②HIBD常温及亚低温2h组Na+-K+-ATP酶活性较之假手术组无明显改变,6h、12h组该酶活性明显低于假手术组,分别为3.76±0.78,3.12±0.53μmol/mgPr.h及5.25±0.66、4.74±0.80μmol/mg Pr.h,但亚低温治疗组明显高于相应常温组(P<0.01)。结论贴敷式局部亚低温可增加HIBD后脑线粒体ATP酶活性,保护脑组织。
Objective To study the effect of cerebral mild hypothermia on cerebral mitochondrial ATPase activities in neonatal rats with hypoxlc-ischemic brain damage（HIBD）. Methods Eighty-four seven-day-old Wistar rats were randomly assigned into four groups：sham-operated normothermic, sham-operated mild hypothermic, HIBD normothermic and HIBD mild hypothemic. HIBD was induced by left common carotid artery ligation, followed by 8% hypoxia exposure. At each time interval of 2,6 ,and 12 hrs post-hypoxia-ischemia （HI）, 7 rats were sacrificed and the brain tissues were sampled for Ca -ATPase. Results The activities of mitochondrial Ca2^＋ detecting the activities of mitochondrial Na^＋ -K^＋ -ATPase and C2^＋ ATPase decreased significantly in the two HIBD groups compared with those of the two sham-operated groups at 2,6, and 12 hrs post-HI. The HIBD mild hypothemic group had higher mitochondrial Ca2^＋ -ATPase activities compared with the HIBD normothermic group at 2,6,and 12 hrs post-HI （5.25 ±0.61 μmol/mgPr, h vs 3.17 ±0.81 μmol/mgPr, h, 4.59 ±0.81 μmol/mgPr, h vs 2.26 ±0. 53 μmol/mgPr, h,4.61 ±0. 62 μmol/mgPr, h vs 1.31 ±0. 78 μmol/mgPr. H, respectively） （P 〈 0.0l ）. The activities of mitochondrial Na^＋ -K ^＋ -ATPase decreased significantly in the two HIBD groups compared with those of the two sham-operated groups at 6 and 12 hrs post-HI. A significant difference was observed in the mitochondrial Na^＋ -K^＋ -ATPase activities between the HIBD mild hypothemic and HIBD normothermic groups at 6 and 12 hrs post-HI （5.25 ±0.66 μmol/mg Pr. h vs 3.76 ±0.78 μmol/mgPr, h, 4.74 ±0.80 μmol/mgPr, h vs 3.12 ±0.53 μmol/mgPr, h; P 〈0. O1 ）. Conclusions Mild hypothermia following HIBD inhibits the decline in cerebral mitochondrial Ca^2＋ - and Na^＋ - K^＋ ATPase activities in neonatal rats, thus providing protective effects against HIBD.
出处
《中国当代儿科杂志》
CAS
CSCD
2007年第4期305-307,共3页
Chinese Journal of Contemporary Pediatrics
关键词
亚低温
HIBD
线粒体
ATP酶
新生大鼠
Mild hypothermia
Hypoxie-isehemie brain damage
Mitoehondria
ATPase
Neonatal rats
