查询词典 ischemic

Both brain ischemic pre-conditioning and PGE1 could induce cerebral ischemic tolerance through increasing Bcl-2 expression and reducing Bax expression. The effect of PGE1 in inducing cerebral ischemic tolerance was better than that of brain ischemic pre-conditioning.

预缺血及PGE1预处理后，使Bax蛋白表达减少，Bcl-2蛋白表达增高能够诱导脑缺血耐受，且PGE1的作用优于预缺血。

INTERVENTIONS: 4 vessel occlusion(4VO) brain ischemic models in rats stained with thionine staining and GFAP immunohistochemistry staining. were used. Sixty-four rats, of which bilateral vertebral arteries were occluded permanently by electrocautery, were divided into the following 8groups: sham operation group, cerebral ischemic preconditioninggroup, ischemic insult group; BIT group; MTPG + sham operation group;MTPG+BIT group; MTPG+ischemia group and -4C3HPG+BIT coup. All the rats were killed 7 days after the operation or the final ischemic treatment. Cerebral sections were selected and stained with thionine staining and GFAP immunohistochemistry staining.

干预：采用大鼠四血管闭塞全脑缺血模型，应用硫堇染色和胶质纤维酸性蛋白免疫组化法。64只大鼠椎动脉凝闭后分为假手术组、单纯预处理组、单纯缺血组、脑缺血耐受组，MTPG+假手术组、MTPG+脑缺血耐受组、MTPG+缺血组和-4C3HPG+脑缺血耐受组，所有动物均在手术后或末次缺血后7 d处死取材，行脑组织切片，硫堇染色和胶质纤维酸性蛋白免疫组化染色。

There was an obvious increase of insulin receptor gene and protein in the cerebral ischemia reperfusion tissues in rats. The positive cells such as neuron, neuroglia cells, vascular endothelium cells possibly participated in regulating the processes of energy metabolism of cells and neovascularization. It implied that the high expressions of insulin receptors in vascular endothelium cells in ischemic zones possibly participated in regulating the pathophysiological changes of the blood vessels in ischemic zones; The higher expressions of insulin receptors in different cells were possibly one of the self-protective machanisms in which the ischemic tissues confront the anoxemia injury.

脑缺血再灌注大鼠脑组织胰岛素受体基因和蛋白水平表达增加；半暗带区神经元、部分神经胶质细胞及血管内皮细胞等阳染细胞可能参与脑缺血后组织细胞的能量代谢、促新生细胞形成等病理生理调节过程；胰岛素受体在缺血区血管内皮细胞高表达提示其可能在缺血区血管的病理生理变化中起某种调节作用；胰岛素受体在不同细胞中表达增高可能是缺血脑组织对抗缺血缺氧损伤的自身保护机制之一。

Methods Rat models of ischemic reperfusion in vivo were established. With autoradiography, the uptake of 99Tc-HL91 was observed in myocardium in control group, ischemic reperfusion group and ischemic group.

建立大鼠心肌在体缺血再灌注模型，采用体外放射自显影检测正常对照组、缺血再灌注组及无再灌注组心肌对99Tc-HL91的摄取。

Methods: 18 healthy new-zealand rabbits were randomly divided into 3 groups (6 for each group): ischemic reperfusion group,ischemic preconditioning group and ischemic preconditioning combined with pyrrolidine dithiocarbamata group (group IPC+PDTC).

选择健康新西兰大白兔18只，随机分为缺血再灌注组(ischemic reperfusion， IR)，缺血预处理组(ischemic preconditioning ，IPC)及缺血预处理联合PDTC组，每组6只。

The concept of ischemic tolerance is established on the base that sublethal heat shock or low-dose ischemic injuries produce tolerance in cells and tissues to subsequent exposure to heat or ischemic injury.

缺血耐受的概念是在亚致死性热休克和低强度缺血损伤可以诱导受其打击的细胞或组织中产生缺血耐受的试验基础上形成的。

Methods: Single lung in situ ischemic reperfusion animal model was used. 30 rabbits were randomly divided into three groups: sham group, ischemic/reperfusion group and ischemic preconditioning group. Wet to dry ratio and injured alveoli rate were determined. Ultramicroscopic structural change was observed under electron microscope. Heat shock protein-27 was detected with immunohistochemistry.

采用在体兔单位缺血瑞灌注模型，30只日本大耳兔随机均分为三组：假手术组、缺血／再灌注组及缺血预处理组，实验检测肺组织混干重比和肺泡损伤数比值，电镜评定肺组织起微结构损伤，免疫组化检测肺组织热休克蛋白27的定位及表达。

To study genetic mutations of methylenetetrahydrofolate reductase C677T and cystathioinine-β-synthase T833C related to homocysteine metabolism in patients with ischemic stroke, the MTHFR gene C677T gene mutation and the CBS T833C gene mutation were detected by PCR-RFLP or ARMS method in 74 patients with ischemic stroke and 83 normal people for control. Results showed that the frequencies of MTHFR genet homogenetic type(2.7%), heterogenetic type(51.4%) and T allele(28.4%) in ischemic group were higher than those in control group(1.2%, 39.8% and 21.1%, respectively).

为研究同型半胱氨酸代谢相关酶亚甲基四氢叶酸还原酶基因C677T和胱硫醚-β合成酶基因T833C位点碱基突变与缺血性脑卒中的关系，对74例缺血性脑卒中患者和83例健康对照者，采用聚合酶链反应-限制性片段长度多态性技术检测MTHFR基因C677T基因型，用扩增阻滞突变体系法检测CBS基因T833C突变。

Methods To compare levels of hsCRP and SF in 30 cases of progressive ischemic stroke with those in 30 cases of nonprogressive ischemic stroke on the 1st,3rd,7th and 14th day during hospitalization respectively. The relationship of levels of hsCRP and SF with condition in patients with ischemic stroke was analyzed.

方法分别于患者入院第1天、第3天、第7天和第14天分别检测缺血性脑卒中患者hsCRP和SF血清浓度，比较进展组与非进展组的差异，分析hsCRP和SF动态水平与缺血性脑卒中患者病情的关系。

objective trimetazidine has shown anti-ischemic properties to improve exercise tolerance without haemodynamic effects and direct cyto protective effect on the myocardium.however,it is not clear whether trimetazidine has beneficially effect on severe ischemic cardiomyopathy.methods 19patients（68±9）years with postnecrotic left ventricular dysfunction（ejection fraction31.7%±5.4%）were studied to examine the benefit of adding60mg a day of trimetazidine for3months to the classical therapy.the assessment included clinical evaluation,electrocardiography and echocardiography.results after adding60mg a day of trimetazidine for3months,attack of angina was relieved and dyspnea was improved（p.05）.but heart rate,systolic blood pressure,rate pressure product,ejection fraction,left ventricular volume and global wall motion index were not changed.conclusion trimetazidine seems to improve clinical status while can not change oxygen supply-to-demand ratio without adverse effects in patients on severe ischemic carˉdiomyopathy.

目的 曲美他嗪是一种新型的抗心肌缺血的药物，能够改善患者的运动耐量和心肌的直接保护作用同时并没有血流动力学效应。但目前对于严重缺血性心肌病患者的临床治疗价值还需要进一步观察。方法 19例（68±9）岁确诊为缺血性心肌病（左心室射血分数0%）的患者在常规治疗的基础上加用每日60mg曲美他嗪治疗3个月，随诊观察患者临床情况以及超声心动图指标的变化。结果 19例患者均可耐受在常规治疗基础上加用每日60mg曲美他嗪的治疗，随诊发现患者心绞痛发作明显减少，运动耐量明显改善。同时患者心率、收缩压、心率血压乘积、左心室射血分数、左心室容量以及整体室壁运动指数无明显改变。结论缺血性心肌病的患者在常规治疗基础上加用曲美他嗪是安全的，同时其能明显改善患者的临床状态，而这种作用并不改变心肌氧的供求比值。

Hanna: That's over now, isn't it?

都结束了，对吗

You must be ill. You look so pale.

你一定是病了，你的脸色苍白。