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acute ischemic brain
相关语句
  急性缺血性脑
    OBJECTIVE: To discuss the protective effects of nimodipine on acute ischemic brain injury caused by activation of phospholipase A2. DESIGN: A completely randomized controlled trial.
    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。
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  “acute ischemic brain”译为未确定词的双语例句
    These suggested that AVP was involved in the pa-thophysiologic process of acute ischemic brain edema, and its mechanism mightbe the effect of AVP on AVP receptor mediated by cAMP, cGMP, and that in turn inhibited the Na+-K+ ATPase activity of brain cell membrane,then exaggerated the formation of ischemic brain edema
    提示AVP可能是通过cAMP、cGMP介导的AVP受体的作用,产生抑制脑细胞膜Na~+-K~+ATP酶活力的效应,从而促进缺血性脑水肿的形成。
短句来源
    Methods The perinatal acute ischemic brain damage model was established by ligation of both uterine arteries of full-term pregnant Wistar rats(n=315). They were divided randomly into topiramate one and five times groups and hypoxic-ischemia(HI) group(n=105),and normal collate group consisted of 105 normal Wistar rats.
    方法:夹闭足月妊娠大鼠子宫血管,制成急性脑缺血损伤的新生鼠模型(n=315),随机分为topiramate 1次和5次给药组及缺血组(n=105),另取105只正常Wistar大鼠作为正常对照组。
短句来源
    The Effect of Arginine Vasopressin ( AVP ) on Acute Ischemic Brain Edema in Gerbil
    精氨酸加压素对沙土鼠急性缺血性脑水肿的作用
短句来源
    These suggest AW was involved in the pathophysiologic process of acute ischemic brain edema.
    提示AVP参与了急性缺血性脑水肿的病理生理过程,且起着促进或加重缺血性脑水肿形成的作用。
短句来源
    The purpose of this experiments is to study the role of arginine vasopressin (AVP)iu acute ischemic brain edema and its mechanism.
    本文探讨了精氨酸加压素(AVP)对急性缺血性脑水肿的作用及其作用机理。
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The purpose of this experiment was to study the role of arginine vasopressin (AW) in acute cerebral ischemic edema in mongolian gerbils. The results showed that intracerebroventricular injection (ICV) of AVP exacerbated the ischemic brain edema, while ICV of AW antiserum significantly decreased the ischemic brain edema. Nimodipine couldn't block this role of AW in ischemic brain edema. The cortical Na+ -K+ ATPase activity was significantly decreased, the contents of cAMP in the ischemic cortex and hypothalamus...

The purpose of this experiment was to study the role of arginine vasopressin (AW) in acute cerebral ischemic edema in mongolian gerbils. The results showed that intracerebroventricular injection (ICV) of AVP exacerbated the ischemic brain edema, while ICV of AW antiserum significantly decreased the ischemic brain edema. Nimodipine couldn't block this role of AW in ischemic brain edema. The cortical Na+ -K+ ATPase activity was significantly decreased, the contents of cAMP in the ischemic cortex and hypothalamus and the contents of cGMP in the hypothalamus were remarkably increased after ICV of AW. These suggest AW was involved in the pathophysiologic process of acute ischemic brain edema. And its mechanism might be the effect of AW on AW receptor mediated by cAMP, cGMP, and that in turn inhibited the Na+ -K+ ATPase activity of brain cell membrane, then exaggerated the formation of ischemic brain edema.

本实验探讨了精氨酸加压素(AVP)对蒙古种沙土鼠急性缺血性脑水肿的作用及其机理。结果表明,给沙土鼠侧脑室注射AVP后,缺血性皮质水肿显著加重,尼莫地平不能阻断AVP对缺血性脑水肿的影响;侧脑室注射AVP抗血清后,缺血性皮质水肿明显减轻,侧脑室注射AVP后,缺血性皮质Na~+-K~+ATP酶活力显著降低,皮质和下丘脑cAMP以及下丘脑cGMP含量均显著升高。提示AVP参与了急性缺血性脑水肿的病理生理过程,且起着促进或加重缺血性脑水肿形成的作用。其作用机理可能是通过cAMP、cGMP介导的AVP受体的作用,产生抑制脑细胞膜Na~+-K~+ATP酶活力的效应,从而促进缺血性脑水肿的形成。

The purpose of this experiments is to study the role of arginine vasopressin (AVP)iu acute ischemic brain edema and its mechanism. The results showde that intracerebroventricular injection ( ICV ) of AVP exacerbated the ischemic corticalc edema,and the calcium entry Mocker couldn' t block this role of AVP in ischemi brain edema. ICV of AVP antiserum,m V2 and V1/V2 receptor antagonist respectively decreased significantly the ischemic cortical edema. In addition, the Na + -K+ATPase activity...

The purpose of this experiments is to study the role of arginine vasopressin (AVP)iu acute ischemic brain edema and its mechanism. The results showde that intracerebroventricular injection ( ICV ) of AVP exacerbated the ischemic corticalc edema,and the calcium entry Mocker couldn' t block this role of AVP in ischemi brain edema. ICV of AVP antiserum,m V2 and V1/V2 receptor antagonist respectively decreased significantly the ischemic cortical edema. In addition, the Na + -K+ATPase activity of ischemic cortex was significantly decreased, and the contents of cAMP in cortex, hy pothalamus, staiatumand pons-medulla were markedly increased, and the contents of cGMP in hypothalamus and staiatum alsoincreased after ICV of AVP. These suggested that AVP was involved in the pa-thophysiologic process of acute ischemic brain edema, and its mechanism mightbe the effect of AVP on AVP receptor mediated by cAMP, cGMP, and that in turn inhibited the Na+-K+ ATPase activity of brain cell membrane,then exaggerated the formation of ischemic brain edema

本文探讨了精氨酸加压素(AVP)对急性缺血性脑水肿的作用及其作用机理。结果表明,侧脑室注射AVP后,缺血性皮层水肿显著加重,且这一作用不能被钙通道拮抗剂所阻断。侧脑室注射AVP抗血清、V_2及V_1/V_2型AVP受体拮抗剂均显著减轻缺血性皮层水肿。此外,侧脑室注射AVP后,缺血皮屋Na~+-K~+ATP酶活力显著降低;皮层等脑区cAMP含量显著升高,下丘脑和纹状体cGMP含量亦显著升高。提示AVP可能是通过cAMP、cGMP介导的AVP受体的作用,产生抑制脑细胞膜Na~+-K~+ATP酶活力的效应,从而促进缺血性脑水肿的形成。

BACKGROUND: Activated by Ca2+, phospholipase A2 will aggravate the influx of Ca2+ or the release of intracellular Ca2+, and then forms a vicious circle, which results in a continuous increase in free calcium level and leads to server injury in neural cells. OBJECTIVE: To discuss the protective effects of nimodipine on acute ischemic brain injury caused by activation of phospholipase A2. DESIGN: A completely randomized controlled trial. SETTING: Intensive Care Unit (ICU) of Children's Hospital, Chongqing...

BACKGROUND: Activated by Ca2+, phospholipase A2 will aggravate the influx of Ca2+ or the release of intracellular Ca2+, and then forms a vicious circle, which results in a continuous increase in free calcium level and leads to server injury in neural cells. OBJECTIVE: To discuss the protective effects of nimodipine on acute ischemic brain injury caused by activation of phospholipase A2. DESIGN: A completely randomized controlled trial. SETTING: Intensive Care Unit (ICU) of Children's Hospital, Chongqing Medical University. MATERIALS: From January 2001 to October 2003, it was completed at the ICU of Children's Hospital, Chongqing Medical University. Thirty male rats were selected and divided into sham operation group, ischemia group and nimodipine 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 ischemia group, at 30 minutes before cerebral ischemia, 2 mL saline was injected intraperitoneally. In nimodipine treated group, at 30 minutes before cerebral ischemia, 0.2 g/L nimodipine (2 mg/kg) was injected intraperitoneally. In all the three groups, the duration between ischemia and decollation was 120 minutes. Rats were decollated under anesthesia and their brains were taken out to assess the activity of phospholipase A2, the free calcium level in brain cells, the brain water content and the changes in mRNA levels of type Ⅱ phospholipase A2 (secretive phospholipase A2) and type Ⅳ phospholipase A2 (cytoplasmic phospholipase A2) in brain tissue. MAIN OUTCOME MEASURES: ① The activity of phospholipase A2 in brain tissue; ② the free calcium 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 the 30 rats entered the statistical analysis. ① The activity of phospholipase A2 in brain tissue: In ischemia group and nimodipine treated group, the activity of phospholipase A2 were higher than that in sham operation group (57.8±7.2), (42.5±6.1), (17.1±5.3)%, P < 0.05-0.01, and it was a litter lower in nimodipine treated group than that in ischemia group (P < 0.05). ②The free calcium levels in brain cells: It was higher in nimodipine treated group and ischemia group than that in sham operation group (775.8±105.5), (497.2±45.9), (103.8±10.3) μmol/L, P < 0.05-0.01, and it was lower in nimodipine group than in ischemia group (P < 0.01). ③ The brain water content: It was higher in nimodipine group and ischemia group than that in sham operation group (82.9±0.5), (80.0±1.1), (72.1±0.01)%, P < 0.05-0.01, and it was lower in nimodipine treated group than that in ischemia group (P < 0.05). ④ In sham operation group, no significant mRNA of type Ⅱ phospholipase A2 could be detected in brain tissue. And the mRNA level of type Ⅱ phospholipase A2 in brain tissue was very low. At 120 minutes after ischemia, mRNA of type Ⅱ phospholipase A2 was detectable and the expression of type Ⅱ phospholipase A2 was increased. Compared to ischemia group, the expression of type Ⅱ phospholipase A2 was not decreased in nimodipine treated group while the expression of type Ⅱ phospholipase A2 was decreased. CONCLUSION: Nimodipine is capable of decreasing the free calcium level in brain cells, the activity of phospholipase A2 in brain tissue and the brain water content after ischemia. However, it cannot significantly inhibit the expressions of type Ⅱ phospholipase A2 and type Ⅱ phospholipase A2 after cerebral ischemia.

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...

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表达水平很低。缺血后120min后脑组织中出现Ⅱ类A型分泌型磷脂酶A2mRNA表达,胞浆型磷脂酶A2mRNA表达水平明显增强。尼莫地平干预组与缺血组比较,Ⅱ类A型分泌型磷脂酶A2mRNA表达水平无明显降低,胞浆型磷脂酶A2mRNA表达水平有所降低。结论:尼莫地平可降低缺血后脑细胞游离Ca2+浓度,脑组织中磷脂酶A2的活性和脑含水量,但不能明显抑制脑缺血后Ⅱ类A型分泌型磷脂酶A2mRNA及胞浆型磷脂酶A2mRNA的表达。

 
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