查询词典 ischemia

Outcome:(1) Acute ischemic damage may induce the expression of c-fos protein in Cerebral Cortex quickly. Also, the expression increases by the ischemia time delay. It may hint that ischemia injury can rise the ability of nerve cells to tolerate ischemia and anoxia. And the expression level of c-fos can be up-regulated by putting blood of 12 hand Jing Points. So we think that treated by this therapy can rise the irritability of brain to resist the development of ischemia and enhance the ability to plerosis.(2) Acute ischemic damage may induce the expression of HspVO in Cerebral Cortex quickly. Also, the expression increases by the ischemia time delay. It may hint that ischemia injury can rise the ability of nerve cells to tolerate ischemia and anoxia.

三 结果(1)急性缺血性脑损伤可快速诱导c-fos蛋白在皮层缺血区脑组织的表达，其表达有随缺血时间延长而逐渐增多的趋势，提示脑的缺血性损伤可应激性地增强神经细胞对缺血、缺氧的耐受和适应能力，而应用井穴放血的干预治疗可明显上调缺血区皮层脑组织c-fos的表达水平，进一步增强脑组织对抗缺血性损伤的应激能力，抵抗缺血性脑损害的进一步发展。

Methods By radioimmunoassay,we measured the contents of CGRP in mesencephalon and pituitary after reperfused 5 minute following 5 minute ischemia; reperfused 45 minute following 15 minute ischemia; reperfused 30 minute following 30 minute ischemia;and compared with controls(pseudo-operation, same time of ischemia and the same total time but only ischemia).

采用放射免疫测定方法，测定大鼠全脑缺血5 min再灌注5 min、缺血15 min再灌注45 min、缺血30 min再灌注30 min中脑及垂体CGRP含量变化，并与相同缺血时间组、假手术组及总时间相同但仅有缺血组相比。

At 6h after ischemia both MRI were found to indicate definite infarct foci in the caudate nucleus and the lentiform nucleus,mass effect was seen too.Histopathologic findings:At 2h after ischemia,electro microscope revealed the changes of ischemia and edema.At 4h after ischemia,the photomicroscope demonstrated the changes of ischemia edema and the electromicroscope indicated the damage to blood brain barrier.

结果 梗塞2h MRI T2加权可见尾状核头部、豆状核信号增高；6h MRI可见尾状核、豆状核形成明确梗塞，并出现占位征象。2h电镜下已有缺血水肿改变，4h光镜下出现脑缺血水肿改变，电镜下见到血脑屏障受损。

Methods: Twenty-four rabbits were randomly divided into three groups:① the control group(group C, n=8): received sternotomy only and no ischemia;② the ischemia/reperfusion group(group I/R, n=8): the left lungs of rabbits were rendered ischemia by ligating the left pulmonary hili for 60 minutes followed by 60 minutes reperfusion;③ the edaravone group(group E, n=8): the left lungs were rendered ischemia for 60 minutes followed by 60 minutes reperfusion, and 10 mg/kg edaravone was administered intravenously 5 minutes prior to ischemia. Blood MDA and SOD were measured. Protein concentrations, WBC count, and PMN percentage in broncho-alveolar lavage fluid were determined. Samples of left lung tissue were sent for determining the left lung dry-to-wet weight ratio and evaluating the pathologic changes.

采用兔肺原位热缺血再灌注损伤模型进行研究。24只大白兔随机分为三组：①对照组(C组， n=8)，开胸后不阻断肺门，静脉缓慢推注生理盐水5ml/kg；②缺血再灌注组(I/R组， n=8)，左肺接受60min的缺血，然后接受60min再灌注，于缺血前5min静脉缓慢推注生理盐水5ml/kg；③依达拉奉干预组(E组， n=8)，于缺血前5min静脉缓慢推注依达拉奉10mg/kg（5ml/kg），左肺接受60min的缺血，然后接受60min再灌注。120min实验结束时，留取各组动物血液标本，测定血浆丙二醛含量及超氧化物歧化酶活性；收集支气管肺泡灌洗液，检测支气管肺泡灌洗液中白细胞计数、中性粒细胞百分比及肺通透性指数；留取肺组织标本，测定肺组织湿、干重量，计算干／湿重比及行肺组织病理检查。

Result: The series of Muskone can improve myocardial ischemia and infarction in experimental canines, and relieve significantly the degree of myocardial ischemia determined by epicardial electrogram mapping,decrease the range of myocardial ischemia determined by epicardial electrogram mapping and decrease infarction zone determined by N-BT staining method. And it has a significant inhibition on activity of ET induced by myocardial ischemia and infarction, and increases 6-Keto-PGF1αand 6-Keto-PGF1α/TXB2 induced by myocardial ischemia.

结果：冠心苏合丸系列组方具有明显改善犬急性心肌缺血和心肌梗死的作用，明显减轻由心外膜电图标测的心肌缺血程度及范围；减小经N-BT染色所显示的梗死区；对心肌缺血及心肌梗死引起ET的活性有明显抑制作用，同时升高血浆6-Keto-PGF1α和6-Keto-PGF1α/TXB2的比值。

(1) cerebral ischemical reperfusion injury rats'limbs motor function is variable. Acupuncture could promote lims'functional recovery.(2) PCNA masc cells is visible in cerebral ischemical semidarkness region. There is cell regeneration phenomenon. Acupuncture could strengthen injury region's PCNA expression, could profit injury recovery and functional reconstruction.(3) In ischemia semidarkness region for the model group and acupuncture group, PCNA masc cells percentage of 14days group is lower than 7days group. Along with the recovery of injury, cell multiplication is weaken.(4) In cerebral ischemia semidarkness region, there is VEGF masc cells and regeneration phenomenon. Acupuncture could strengthen injury region's VEGF expression, could profit protection after injury and blood vessel regenerate.(5) In ischemia semidarkness region for the model group and acupuncture group, VEGF masc cells percentage of 14days group is lower than 7days group. Along with the recovery of semidarkness region, ischemia and anoxemia state is getting improved, and VEGF is reduce.(6) As there are PCNA and VEGF masc cells in brain injured region, we could conclude that, after brain ischemical reperfusion injury, there are blood vessel regeneration phenomenon. Acupuncture could promote blood vessel regeneration, recovery blood supply sufficiently and quickly, and promote the recovery of brain injury region.(7)The VEGF masc cells percentage of inhibitor group is lower than acupuncture group. It state that the effect of acupuncture promote VEGF is partly depend on the existing of eNOS.

实验结论：(1)脑缺血再灌注损伤后大鼠的肢体运动功能发生改变，针刺可以促进肢体功能恢复；(2)脑缺损伤区可见PCNA阳性细胞，存在细胞再生现象，针刺可以增强损伤区PCNA的表达，有利于损伤的修复和功能重建；(3)针刺组和模型组14d时缺血损伤区PCNA阳性细胞百分比低于7d组，随着损伤逐渐得到修复，细胞增殖现象减弱；(4)脑缺血损伤区可见VEGF阳性细胞，存在内皮型细胞再生现象，针刺可以增强损伤区VEGF的表达，有利于脑损伤后保护和缺血区血管再生；(5)针刺组和模型组14d时缺血损伤区VEGF阳性细胞百分比低于7d组，随着缺血损伤的修复，缺血缺氧状态得到改善，产生的VEGF减少；(6)由于脑损伤区同时出现PCNA阳性细胞和VEGF阳性细胞，前者是增殖细胞的标志，后者是促进血管再生的重要因子，可以推断，脑缺血再灌注损伤后脑内存在血管再生现象，针刺可以促进损伤区的血管再生，更迅速而充分的恢复损伤区的血供，促进脑损伤区的修复；(7)抑制剂针刺组脑损伤区VEGF阳性细胞百分比与针刺组相比有不同程度的降低，说明针刺促进缺血损伤区VEGF表达部分依赖eNOS的存在。

Results:In ischemia group, the peaks of MPO activity and CINC conentr ation were 24 hour and 6 hour respectively after ischemia, which initially incre ased at 1 hour, In ischemia reperfusion group, the peaks of MPO activity and CIN C conentration were 72 hour and 6 hour respectively after ischemia reperfusion, which initially increased at 6 hour and 1hour down to normal at 24hour respectiv ely.

结果：单纯缺血组MPO活性增高始于缺血6h并于缺血72h时达高峰，为0.15±0.01U/ml； CINC水平增高始于缺血1h，缺血6h时达高峰，为0.05±0.05ng/ml，以后逐渐下降并于缺血48h后恢复正常。缺血1小时再灌注组MPO活性增高始于再灌注1h并于再灌注24h时达高峰，为0.42 ±0.12U/ml；CINC水平增高始于再灌注1h，再灌注3h时达高峰，为0.65±0.03ng/ml，以后逐渐下降并于再灌注24h后恢复正常。

Combined with animal model of peradaptation to myocardium ischemia , the research observed the level of enzymatic dynamics of myocardium, SOD,MDA,ET and correlation peptide of calcitonin gene in peripheral blood and cardiac function, apoptic cell and expression of apoptosis regulatory gene, ultrastructure of myocardium with BIOPAC16, in situ end labeling and hybridism, optic microscope and electron microscope. The study of animal model of peradaptation to myocardium ischemia illustrated that the peradaptation and pretreatment with Wenxin capsule could be positively protective for the injury of ischemia reperfusion. The protection is mainly reflected by reduction of infarction area, correction of heart rhythm abnormality of ischemia reperfusion, melioration of the contraction and relaxation function of myocardium, recovery of the subcellular structure and themelioration of the abnormality of biochemical and bioactive substance in the myocardium.

并结合心肌缺血预适应动物模型，采用BIOPAC16导生理记录和分析处理系统处理心肌功能指标，采用原位末端标记及原位杂交技术标记凋亡细胞及凋亡相关调控基因的表达，采用光电镜技术观察心肌超微结构的变化，同时观察外周血心肌酶、超氧化物歧化酶、丙二醛、内皮素、降钙素基因相关肽等水平，结果表明心肌缺血预适应及温心胶囊预处理对心肌缺血再灌注损伤具有肯定的保护作用，其保护心脏作用主要表现在缩小心肌梗死范围、抗缺血再灌注心律失常、改善心肌收缩和舒张功能、减轻心肌超微结构损伤，调节心肌生化物质及生物活性物质的生成和释放。

This experimental study, based on the ischemia-reperfusion injury model of the isolated rabbit liver, was to investigate hepatocellular apoptosis and its mechanism during cold preservation-reperfusion of donor liver and assess the structural and functional damages of the reperfusing donor liver subsequent to rewarm ischemia. In addition, the expression and effects of ICAM-1 mRNA were mainly observed during rewarm ischemia-reperfusion of donor livers. Our experiment included three parts: The first was establishment of the isolated liver ischemia-reperfusion injury model in rabbits.

本实验在建立离体供肝缺血-再灌注损伤模型的基础上，研究供肝低温保存-再灌注过程中肝细胞凋亡现象及其相关机制；探讨作为临床肝移植中供肝的另一缺血阶段—复温缺血对再灌注后供肝结构及功能的损伤作用，并着重观察供肝复温缺血-再灌注期间组织细胞内细胞间粘附分子-1 mRNA的表达规律及其作用。

Hypoxia-ischemia for 10 minutes group , 20 minutes group: our experiment showed that at 24 hours after cerebral hypoxia-ischemia, expression of MMP-9mRNA was maximally increased, individually, in the hypoxia-ischemia for 10 minutes group, MMP-9mRNA was greatly expressed within superolateral surface cortex of cerebrum, whereas in the hypoxia-ischemia for 20 minutes group, the labeling of hybridization for MMP-9mRNA was strongly appeared within the cortexof cerebrum both the cortex in the subsequence of medial surface at the periphery of the cerebral longigudinal fissure and the cortex in superolateral surface where also there showed a few stained fibers.

3缺氧缺血10分钟、20分钟组：缺氧缺血后24小时脑内MMP9 mRNA阳性表达至最高峰，缺氧缺血10分钟组大量表达在端脑背外侧面皮质内，缺氧缺血20分钟组在端脑内侧面后份大脑纵裂旁周围皮质及背外侧面皮质内呈强阳性表达，少数纤维呈亦阳性染色。

" I' d like to get some rough idea about music in the baroque ear, please."

请简要介绍一下巴罗克时期的音乐，好吗？

The results showed that the peak latency and pattern of SEPs elicited by electrical needling in LI-l1 and MP were similar. The amplitude of SEPs elicited by electrical needling in LI-l1 was higher than that of MP. There was no obvious SEPs generation when MM was electrical needling.

结果显示，电针刺激曲池穴和其邻近桡侧伸腕长肌运动点诱发性脑电波的波形和波峰时间是类似的，只是穴位的诱发性脑电波波幅较大，而电针刺激非穴位点并没有明显的诱发性脑电位。