脑卒中医学论文

Increased Blood Sugar on hemorrhagic stroke (hemorrhagic apoplexy) the occurrence and development are very important influence, not only as an important risk factor involved in the beginning of HA, resulting in increased incidence of disease, but also to HA after the occurrence of pathological process has a catalytic role to enable hematoma volume expansion, increased edema, increased impairment, affect the blood sugar involved in the mechanism of HA, are manifold, including: lipid metabolic abnormalities, carotid artery remodeling, endothelial dysfunction, platelet dysfunction, hypercoagulability, insulin resistance. Expansion of infarct size and high blood sugar and promoting the development of HA mainly caused by acid poisoning, ischemic injury in areas of apoptosis and other endothelial growth factor (VEGF) and cyclooxygenase (COX-2) and cerebral vascular disease, has attracted people's attention. Vascular endothelial growth factor induced by the prominent role of angiogenesis in vivo and improve vascular permeability; discovered in recent years it also has to stimulate the neurons, glial cells, axonal growth and survival role. COX (cyclooxygenase, COX), is catalyzed arachidonic acid (arachidonic acid, AA) synthesis of prostaglandins (prostgalandin, PG) and thromboxane (thromboxan, TX) of the rate-limiting enzyme. One COX-1 for structural type, exist in most organizations, the catalyst is generated to maintain the normal structure of the PG; COX-2 is induced in physiological conditions, COX-2 in most tissues at very low copy number expression. However, IL-1, TNF and many other inflammation-stimulating factor can induce COX-2 expression. However, current vascular endothelial growth factor and cyclooxygenase Most studies focused on the relationship between cerebral ischemia and brain edema after intracerebral hemorrhage on the dynamic changes of VEGF, COX-2 expression in correlation among recognition of hyperglycemia on cerebral hemorrhage injury in danger at the same time, control, treatment of blood glucose levels become a means of treating cerebrovascular disease, in particular, is used to reduce blood sugar levels of insulin into the acute stroke treatment guidelines. Has been found that insulin on acute cerebral hemorrhage around the brain tissue has a protective effect of ischemic injury. Possible mechanisms are: the brain has been found that the existence of insulin receptors, insulin and insulin receptor binding may reduce the brain cells of glucose uptake, thereby reducing the storage of sugar within the brain cells, reduce lactic acid produced by the substrate, fundamentally correct cellular acidosis; the same time, can also lower blood sugar, insulin concentration, increased bleeding surrounding edema and effective blood supply, resulting in relatively low perfusion state of high blood sugar, thereby improving effect of brain damage was the order to understand these two cytokines and diabetes mellitus the relationship between cerebral hemorrhage injury, this study of diabetes on the basis of the model to be adopted by autologous blood injection method to establish a stable animal model of cerebral hemorrhage in this dynamic observation of cerebral hemorrhage on the basis of After the behavioral and brain water content trends, analysis VEGF and COX-2 in the hemorrhagic brain tissue distribution and expression changes, and then explore the VEGF and COX-2 in brain tissue damage in cerebral hemorrhage the role and significance, compared to diabetes rats and normal blood sugar difference between the volume of brain edema in rats with an initial observation of the two factors in diabetic rats and normal blood sugar difference between the expression of rat brain hemorrhage, with a view to the treatment of cerebral hemorrhage provide new ways and and methods1. Experimental animals and groupingHealthy adult male Wistar rats, a total of 96, weighing 250 to 280 grams from the Experimental Animal Center of Zhengzhou University. In accordance with the principles of randomized experimental animals were divided into four groups, namely sham operation group, normal blood glucose group, high glucose group and the insulin intervention group. Prizes will be awarded 4 points each time: 6h, 24h, 72h, 7d. At each time points are located at 6 . High blood sugar and insulin production in rat model of intervention methodsPrepared by the light of STZ-induced hyperglycemia in rats. With STZ 60mg/kg, high blood sugar and insulin in the intervention group rats a single intraperitoneal injection. Value for four rats with normal blood sugar a 6mmol / L, a week after injection, blood glucose ≥ / L for a successful model for alternative use. Model of high blood sugar after the success of the intervention group I rats were normal insulin, abdominal subcutaneous injection, 3 times / d, 4U / times qd for 3 days, the measured blood sugar value of the normal range.

血糖升高对出血性脑卒中（hemorrhagic apoplexy）的发生发展有极其重要的影响，不但作为重要危险因素参与HA的起始，导致疾病发病率增高，而且对HA发生后病理过程有促进作用，使血肿体积扩大，加重水肿，加重功能损害，影响预后。Hyperglycemia has a very important impact on the occurrence and development of hemorrhagic stroke (hemorrhagic apoplexy). It not only acts as an important risk factor in the initiation of HA, but also increases the incidence of disease, and promotes the pathological process of HA, enlarges the volume of hematoma, aggravates edema, aggravates functional damage, and affects prognosis.高血糖参与HA的发生机制是多方面的，包括:脂代谢异常、颈动脉重塑、内皮功能障碍、血小板功能异常、高凝状态、胰岛素抵抗。而高血糖扩大梗死面积，促进HA发展主要与致酸中毒、缺血损伤区域细胞凋亡等机制有关。Hyperglycemia is involved in the pathogenesis of HA in many aspects, including: abnormal lipid metabolism, Carotid Remodeling, endothelial dysfunction, platelet dysfunction, hypercoagulability, insulin resistance. However, hyperglycemia can enlarge the infarct area and promote the development of HA, which is mainly related to the mechanism of acidosis and apoptosis in ischemic injury area.血管内皮生长因子（VEGF）和环氧合酶（COX-2）与脑血管病的关系，已引起人们的重视。血管内皮生长因子的突出作用是诱导体内血管形成，提高血管通透性；近年来发现它也有刺激神经元、胶质细胞、轴突的生长和成活的作用。环氧合酶(cyclooxygenase，COX)，是催化花生四烯酸(arachidonic acid，AA)合成前列腺素(prostgalandin，PG)以及血栓素(thromboxan，TX)的限速酶。其中COX-1为结构型，存在于大多数组织中，催化生成维持正常结构的PG；COX-2为诱导型，在生理状态下，COX-2在大多数组织中以极低拷贝数表达。但IL-1、TNF等许多炎症刺激因子均可诱导COX-2表达。但目前有关血管内皮生长因子和环氧合酶的研究多集中在与脑缺血的关系上，而关于脑出血后脑水肿的动态变化与VEGF、COX-2表达的相关性研究却不多。The relationship between vascular endothelial growth factor (VEGF) and cyclooxygenase (COX-2) and cerebrovascular diseases has attracted people's attention. In recent years, it has been found that vascular endothelial growth factor can stimulate the growth and survival of neurons, glial cells and axons. Cyclooxygenase (COX) is a rate limiting enzyme that catalyzes the synthesis of prostaglandin (PG) and thromboxane (TX) from arachidonic acid (AA). COX-1 is a structural type, which exists in most tissues and catalyzes the generation of PG maintaining normal structure; COX-2 is an inducible type, which is expressed in a very low copy number in most tissues under physiological conditions. But many inflammatory factors such as IL-1 and TNF can induce COX-2 expression. However, at present, the researches on VEGF and COX-2 are mostly focused on the relationship with cerebral ischemia, but few on the relationship between the dynamic changes of brain edema and the expression of VEGF and COX-2 after cerebral hemorrhage.在认识到高血糖对脑出血损伤危害性同时，控制血糖水平治疗即成为脑血管病治疗手段之一，特别是采用胰岛素降低血糖水平纳入急性脑卒中治疗指南。已有研究发现胰岛素对急性期脑出血周围脑组织的缺血性损伤有保护作用。可能机制为：现已发现脑中存在胰岛素受体，胰岛素可与胰岛素受体结合，降低脑细胞对糖的摄取，从而降低脑细胞内糖的储存，减少乳酸产生的底物，从根本上纠正细胞酸中毒；同时胰岛素还可以降低外周血糖浓度，增加出血周围水肿带的有效血供，造成相对低血糖高灌流状态，从而对脑损害产生改善作用。In recognition of the harm of hyperglycemia to cerebral hemorrhage, the control of blood glucose level has become one of the treatment methods of cerebrovascular disease, especially the use of insulin to reduce blood glucose level has been included in the treatment guidelines of acute stroke. It has been found that insulin has a protective effect on the ischemic injury of brain tissue around acute cerebral hemorrhage. The possible mechanisms are as follows: it has been found that there is insulin receptor in the brain, insulin can combine with insulin receptor, reduce the uptake of sugar by brain cells, thus reduce the storage of sugar in brain cells, reduce the substrate produced by lactic acid, fundamentally correct cell acidosis; at the same time, insulin can also reduce the concentration of peripheral blood sugar, increase the effective blood supply of edema zone around hemorrhage, resulting in relatively low blood supply Hyperperfusion of blood glucose can improve brain damage.为了解这两种细胞因子与糖尿病合并脑出血损伤的关系，本研究在糖尿病模型的基础上，拟通过自体血注入法建立稳定的大鼠脑出血的动物模型，在此基础上动态观察脑出血后行为学和脑含水量的变化趋势，分析VEGF和COX-2在出血后脑组织中的分布特点和表达变化，进而探讨VEGF和COX-2在脑出血后脑组织损伤中的作用和意义，对比糖尿病大鼠和正常血糖大鼠脑水肿体积的差别，初步观察此二因子在糖尿病大鼠和正常血糖大鼠脑出血表达的差异，以期为脑出血的治疗提供新的方法和思路。In order to understand the relationship between these two cytokines and the injury of cerebral hemorrhage in diabetes mellitus, this study is to establish a stable animal model of cerebral hemorrhage by autogenous blood injection on the basis of diabetes model. On this basis, dynamic observation of the change trend of behavior and brain water content after cerebral hemorrhage is made, and the distribution characteristics and expression changes of VEGF and COX-2 in brain tissue after hemorrhage are analyzed, Furthermore, to explore the role and significance of VEGF and COX-2 in brain tissue injury after cerebral hemorrhage, to compare the difference of brain edema volume between diabetic rats and normal glucose rats, and to preliminarily observe the difference of expression of VEGF and COX-2 in cerebral hemorrhage between diabetic rats and normal glucose rats, in order to provide new methods and ideas for the treatment of cerebral hemorrhage.材料与方法Materials and methods1. 实验动物和分组1. Experimental animals and groups健康成年雄性Wistar大鼠，共96只，体重250~280克，由郑州大学实验动物中心提供。按照随机化的原则将实验动物分为4组，即假手术组、正常血糖组、高血糖组和胰岛素干预组。每组均设4个时间点：6h、24h、72h、7d。每个时间点设6只大鼠。96 healthy adult male Wistar rats weighing 250-280 g were provided by the experimental animal center of Zhengzhou University. According to the principle of randomization, the experimental animals were divided into four groups: sham operation group, normal blood glucose group, hyperglycemia group and insulin intervention group. Each group had four time points: 6h, 24h, 72h, 7d. Six rats were set at each time . 高血糖大鼠模型制作及胰岛素干预方法2. Establishment of hyperglycemia rat model and insulin intervention参照STZ诱导法制备高血糖大鼠模型。以STZ 60mg/kg，对高血糖及胰岛素干预组大鼠单次腹腔注射。大鼠正常血糖值为4一6mmol/L，注射后一周检测血糖≥为成功模型备选用。高血糖模型成功后，予干预组大鼠普通胰岛素，腹壁皮下注射，3次/d，4U/次，连用3天，测血糖值达正常范围。The hyperglycemia rat model was established by STZ induction. STZ (60 mg / kg) was used for single intraperitoneal injection in the hyperglycemia and insulin intervention group. The normal blood glucose value of rats was 4-6mmol / L, and the blood glucose ≥ was detected one week after injection as the successful model. After the success of hyperglycemia model, rats in the intervention group were given insulin, subcutaneous injection of abdominal wall, 3 times a day, 4U a time, for 3 days, and the blood glucose value reached the normal range.（论文翻译由学术堂提供）