急性缺血性脑损伤后脑组织磷脂酶A2活性和脑细胞游离钙离子浓度变化及尼莫地平的保护作用(英文)  

Activation of phospholipase A_2, changes of free ca^(2+) concertration and protection of nimodipine in rats with acute cerebral ischemia injury

作　　者：王兴勇[1] 李晓文[1] 卢仲毅[1] 匡凤梧[1] 许峰[1] 

机构地区：[1]重庆医科大学儿童医院ICU,重庆市400014

出　　处：《中国临床康复》2005年第33期169-171,F0003,共4页Chinese Journal of Clinical Rehabilitation

基　　金：重庆市科学技术委员会科研基金资助(2001-54-85)~~

摘　　要：背景:磷脂酶A2能被Ca2+激活,而被激活的磷脂酶A2又能使Ca2+内流或细胞内Ca2+释放,形成恶性循环,使神经细胞游离Ca2+浓度持续增加,导致神经细胞严重损伤。目的:探讨尼莫地平对磷脂酶A2激活致急性缺血性脑损伤中的保护作用。设计:完全随机对照实验。单位:重庆医科大学儿童医院ICU。材料:实验于2001-01/2003-10在重庆医科大学儿科研究所完成,选择30只雄性Wistar大鼠,随机分为假手术组、缺血组、尼莫地平干预组,每组10只。方法:假手术组:大鼠仅在麻醉状态下分离右侧颈总动脉,不予阻断血流。缺血组:脑缺血前30min,每只大鼠腹腔注射2mL生理盐水。尼莫地平干预组:脑缺血前30min,每只大鼠腹腔注射0.2g/L的尼莫地平2mg/kg。3组大鼠自缺血开始至处死的时间均为120min。大鼠在麻醉状态下断头处死,取脑组织检测磷脂酶A2活性、脑细胞游离Ca2+浓度、脑组织水含量及检测脑组织中Ⅱ类A型分泌型磷脂酶A2和Ⅳ类胞浆型磷脂酶A2mRNA表达的改变。主要观察指标:①各组大鼠脑组织磷脂酶A2活性。②各组大鼠脑细胞游离Ca2+浓度。③各组大鼠脑含水量。④各组大鼠脑组织中Ⅱ类A型分泌型磷脂酶A2和胞浆型磷脂酶A2表达情况。结果:30只大鼠均进入结果分析。①各组大鼠脑组织磷脂酶A2活性:缺血组、尼莫地平干预组均高于假手术组([57.8±7.2),(42.5±6.1),(17.1±5.3)%,P<0.05～0.01],尼莫地平干预组低于缺血组(P<0.05)。②各组大鼠脑细胞游离Ca2+浓度:缺血组、尼莫地平干预组均高于假手术组([775.8±105.5),(497.2±45.9),(103.8±10.3)μmol/L,P<0.05～0.01],尼莫地平干预组低于缺血组(P<0.01)。③各组大鼠脑含水量:缺血组、尼莫地平干预组均高于假手术组([82.9±0.5),(80.0±1.1),(72.1±0.01)%,P<0.05～0.01],尼莫地平干预组低于缺血组(P<0.05)。④假手术组脑组织中无明显Ⅱ类A型分泌型磷脂酶A2mRNA表达,胞浆型磷脂酶A2mRNA�BACKGROUND： Aetivated by Ca^2±, phospholipase A2 will aggravate the influx of Ca^2± or the release of intraeeltular Ca^2±, anti then forms a vicious circle, which results in a continuous increase in free calcium level and leads to server injury in neural eells. OBJECTIVE： To discuss the protective effects of niraodipine on acute ischemic brain injury caused by activation of phospholipase A2. DESIGN： A completely randoraized controlled trial. SETTING： Intensive Care Unit （ICL） of Chihtren＇s Hospital, Chongqing Medical University. MATERIALS： From January 2001 to Oetober 2003, it was completed at the ICU of Children＇s Hospital, Chnngqing Medibal University. Thirty male rats were selected and divided into sham operation group, ischeraia group and niraodipine treated group randomly, with 10 rats in each group. METHODS： In sham operation group, the right common carotid artery was identified by blunt dissection without ligation under anesthesia in rats. In ischeraia group, at 30 minutes before cerebral iseheraia, 2 raL saline was injected intraperitoneally. In niraodipine treated group, at 30 minutes before cerebral ischeraia, 0.2 g/L niraodipine （2mg/kg） was injected intraperitoneally. In all the three groups, the duration between istrheraia and deeollation was 120 minutes. Rats were deeollated under anesthesia and their brains were taken out tn assess the activity of phosphnlipase A2, the free calcium level in brain cells, the brain water content and the changes in raRNA levels of type Ⅱ phospholipase A2 （secretive phospholipase A2） and type Ⅳ phospholipase A： （cytoplasraie phospholipase A2） in brain tissue. MAIN OUTCOME MEASURES： ① The activity of phospholipase A2 in brain tissue： ② the free ealciura levels in brain cells; ③ the brain water content; ④ the mRNA levels of type Ⅱ phospholipase A2 （secretive phospholipase A2） and type Ⅱ phospholipase A2 （cytoplasmic phospholipase A2） in brain tissue were measured in rats in all the groups. RESULTS： All of

关 键 词：脑缺血 尼莫地平 磷脂酶A类 

分 类 号：R742[医药卫生—神经病学与精神病学]