灌注的

Histological observation was performed. Results The peak of serum CINC concentrations occurred 3 h after reperfusion with the difference between the groups with and without ONO-5046 being significant. Expression peak of CINC mRNA in the pancreatic graft occurred 3 h after reperfusion with the expression level in the ONO-5046 treated group significantly lower than in the ONO-5046 untreated group. The activity of MPO in the treated group was obviously decreased as compared with in the untreated group.

结果 CINC于再灌注后3小时出现峰值，治疗组为(7.24±1.46)μg/L，对照组为(28.4±1.85)μg/L，差异显著；移植物中CINC mRNA于再灌注后3小时表达最强，治疗组的表达水平明显低于对照组；MPO的活性，治疗组显著低于对照组；治疗组的胰小叶间质水肿及胰小叶间质和胰小叶内的中性粒细胞浸润较轻。

In traditional Chinese medicine group the VEGF express was obriously higher than the nomal saline group at each of the time points.

缺血再灌注可上调VEGF在大脑海马区域的表达；益气活血中药治疗急性脑缺血能增强VEGF蛋白的表达，从而减少毛细血管的消失，为内皮细胞增殖、迁移、新血管再生提供基础保障，这可能是益气活血中药抵抗脑缺血再灌注损伤的机制之一。

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。

The increased expression of ICAM1 after cerebral ischemiareperfusion is signi ficantly correlated with the degree of the neutrophil infiltration in focal isc hemic brain tissue,which may be an important mechanism of ischemia reperfusion damage.

脑缺血再灌注后表达增高的ICAM1与局部缺血区中性粒细胞的浸润密切相关，这一过程是导致缺血再灌注损伤的一个重要机制。

The radiational ratio was analysed and it's changing of basing metabolizion's cerebral infarct and normal cerebral with using analysis technology of region of interest,as well as,the radiational ratio of with using same method after acupunctural metabolism.

对38例脑梗死性患者分别行基础状态下的脑灌注显像和神经穴位刺激状态下的脑灌注显像，运用感兴趣区技术测定针刺前后病灶与正常部位脑组织放射量比值及放射量比值的变化。

Methods The rat model of middle cerebral artery ischemia 2h/reperfusion 22h was established.The neurological scale, cerebral infracted volume, cerebral water content, activities of NOS and SOD were measured. ResultsThe average neurological scote,cerebral infracted volume,cerebral water content,activity of NOS,content of MDA in Naokangling Capsule group significantly decreased.

采用大鼠大脑中动脉缺血2 h/再灌注22 h模型，神经病学评分，脑梗塞范围及脑组织水含量变化，观察脑康灵胶囊抗脑缺血/再灌注损伤的效应；通过测定大鼠脑组织中一氧化氮合酶（nitric oxide synthase，NOS），超氧化物歧化酶（superoxide disumtase，SOD）活性及丙二醛（malondialdehyde，MDA）含量的变化以探讨药物作用的机制。

MethodsThe rat model of middle cerebral artery ischemia 2h/reperfusion 22h was established.The neurological scale, cerebral infracted volume, cerebral water content, activities of NOS and SOD were measured. ResultsThe average neurological scote,cerebral infracted volume,cerebral water content,activity of NOS,content of MDA in Naokangling Capsule group significantly decreased.

方法采用大鼠大脑中动脉缺血2 h/再灌注22 h模型，神经病学评分，脑梗塞范围及脑组织水含量变化，观察脑康灵胶囊抗脑缺血/再灌注损伤的效应；通过测定大鼠脑组织中一氧化氮合酶（nitric oxide synthase，NOS），超氧化物歧化酶（superoxide disumtase，SOD）活性及丙二醛（malondialdehyde，MDA）含量的变化以探讨药物作用的机制。

The main results and conclusions are as follows: 1. Culrured neurons were damaged by simulated cerebral ischemia and reperfusion in vitro: Results:(1) The activity of the darnaged neurons was decreased, the survival rate was descent.(2) The transudation rate of LDH in cultured medium increased obviously.

体外模拟脑缺血再灌注造成了培养神经元的损伤：表现为：(1)受损神经元的活性降低，细胞存活率下降；(2)细胞培养液LDH的漏出率明显提高；(3)细胞死亡率显著上升；(4)NOS染色强阳性细胞数在缺血期和再灌注早期明显增多。

Baekgroud: Spinal cord ischemia reperfusion injury is an serious secondary spinal cord injury. Trauma, arteriosclerosis, vasal abnormality, inflammation, vasal infarct, decompression after the diseases that can bring spinal cord compression, lessening the blood stream of the spinal cord temporarily ,because of clamping the aorta during the operation of aorta, all of which can engender different extent spinal cord ischemia.

背景：脊髓缺血再灌注损伤是严重的脊髓继发性损伤，创伤、动脉硬化、血管畸形、炎症、血管梗塞、各种产生脊髓压迫的疾病减压后以及在主动脉手术中，钳夹主动脉导致脊髓血液供应暂时性减少都可造成不同程度的脊髓缺血再灌注损伤。

Trauma, arteriosclerosis, vasal abnormality, inflammation, vasal infarct,decompression after the diseases that can bring spinal cord compression, lessening the blood stream of the spinal cord temporarily ,because of clamping the aorta during the operation of aorta, all of which can engender different extent spinal cord ischemia.

背景：脊髓缺血再灌注损伤是严重的脊髓继发性损伤，创伤、动脉硬化、血管畸形、炎症、血管梗塞、各种产生脊髓压迫的疾病减压后以及在主动脉手术中，钳夹主动脉导致脊髓血液供应暂时性减少都可造成不同程度的脊髓缺血再灌注损伤。

But we don't care about Battlegrounds.

但我们并不在乎沙场中的显露。

Ah! don't mention it, the butcher's shop is a horror.

啊！不用提了。提到肉，真是糟透了。