醒后脑卒中患者临床特点及短期预后分析

【】： 目的：初步了解探讨醒后脑卒中(WUS)的临床特点,提高对醒后脑卒中的认识。方法：采用回顾性研究,收集住院急性期脑梗死患者184例,按照WUS定义对所有入组患者分为WUS组和非醒后脑卒中(NWUS)组,登记脑血管病危险因素及相关实验室指标,并以入院时NHISS评分和发病2周时mRS评分评价疾病严重程度及短期预后,比较WUS与NWUS的临床特点、脑血管危险因素及短期预后的异同。 结果：WUS组有TIA病史者9例(22.0%),高于NWUS组(10例,7.0%,P<0.05),WUS组入院时NHISS评分高于NWUS组{7[4,9] Vs. 5[3,8],P＜0.05}。发病2周时mRS评分,WUS组高于NWUS组﹛3[2,4]Vs.2[2,4],P<0.05﹜。结论：WUS病前TIA发作史及血脂代谢异常者较多,其他脑血管病危险因素与NWUS无明显差异；WUS相对病情较重,短期预后较差。     

缺血与出血性脑卒中相关因素多项反应模型

目的通过建立多项反应Logit模型探讨缺血与出血性脑卒中发生的相关因素。方法纳入187例缺血性脑卒中和106例出血性脑卒中患者,同时选择100例健康体检者作为正常对照,调查人口学因素、生活事件、实验室检查结果等流行病学资料。采用x2检验和多项反应Logit模型进行统计学处理。结果（1）与2种类型脑卒中的发生密切相关的公共因素是高血压病史、心脏病、BMI、TG、纤维蛋白原、收缩压、舒张压（P〈0．05或P〈0．01）。（2）仅与缺血性脑卒中发生有统计意义的因素是HDL—C、糖尿病、载脂蛋白B（ApoB）及年龄;仅与出血性脑卒中发生有统计意义的因素是吸烟。（3）相对于缺血性脑卒中而言,男性、高血压病史、BMI、舒张压和年龄发生出血性卒中的OR值分别是2．927、3．016、1．429、1．709和0．640（P〈0．05或P〈O．01）。结论缺血性和出血性脑卒中既有共同的危险因素,又不完全等同,相对于脑缺血,出血性脑卒中更为危险的因素是男性、高血压病史、高BMI和高舒张压,年龄为保护因素。     

急性脑卒中患者糖代谢异常及其预后的前瞻性研究

目的 观察急性脑卒中患者糖代谢异常的情况,探讨其对预后的影响.方法 采用前瞻性研究的方法,将我院自2009年1月至2011年1月收治的急性脑卒中患者,入组研究病例268例,对其急性期糖代谢异常在年龄、卒中类型、既往病史等分布情况进行分析,观察急性脑卒中患者在住院后1周内及出院后3个月时的糖代谢状况.结果 年龄≥65岁、女性、出血性卒中、美国国立卫生研究院卒中量表(NIHSS)评分≥7分、体质指数≥30 kg/m2、高脂血症的脑卒中患者糖代谢异常的发生率显著高于年龄<65岁、男性、缺血性卒中、NIHSS评分<7分、体质指数<30 kg/m2、无高脂血症的脑卒中患者,具有统计学意义(P<0.05).通过口服葡萄糖耐量试验(OGTT)试验,268例患者入院 1周时正常糖耐量(IGT)检出率为(116/268)56.72%,空腹血糖受损检出率为(72/268)26.87%,糖耐量受损(80/268)29.85%;患者出院3个月时IGT检出率为(108/268)40.30%,空腹血糖受损检出率为(68/268)25.37%,糖耐量受损(92/268)34.33%.住院1周时和出院3个月时糖耐量糖代谢异常患者检出率比较,差异无统计学意义(P>0.05).结论 年龄≥65岁、女性、出血性卒中、高脂血症的脑卒中患者急性期糖代谢异常的发生率较高;对急性脑卒中患者进行早期监测血糖,并及早对异常的糖代谢状态进行干预,对改善脑卒中患者的预后有重要意义.     

老年人进展性缺血性脑卒中危险因素的病例对照研究

目的了解老年人进展性缺血性脑卒中的危险因素,为预防其发生提供依据。方法采用成组病例对照研究,以住院进展性脑卒中患者为病例组,同期非进展性脑卒中病人为对照组,比较两组相关因素。结果单因素分析结果显示,两组间是否有高血压病史、入院时NIHSS评分是否≥10分、是否存在感染（包括呼吸、泌尿道等）、糖尿病史、住院期间是否发热等因素差异具有统计学意义（P〈0．01）。非条件Logisitc回归分析结果显示,有高血压病史、NIHSS评分≥10分、是否存在感染和糖尿病史有统计学意义（P〈0．05）。结论脑卒中患者在有高血压、糖尿病、感染和病情较重的的情况下,发生进展性脑卒中的风险较大,应及早采取临床措施,以改善病人的预后。     

荆门市某社区居民脑卒中高危人群筛查及危险因素分析

目的:分析了解荆门市某社区脑卒中危险因素分布情况,为社区脑卒中高危人群的干预提供依据。方法:对荆门市某社区538例居民进行脑卒中高危人群筛查,高危人群判定标准为高血压、糖尿病、血脂升高(甘油三酯≥2.26 mmol/L)、房颤、肥胖、缺乏锻炼、吸烟、脑卒中家族史8项中满足3项及以上;或脑血管功能检测评分在75分以下。分析该地区脑卒中发病危险因素的分布情况。结果:538例中,共筛查出244例脑卒中高危者,其中脑血管功能检测评分75分198例(36.8%)。所占比例较高的危险因素依次为高血压(170例,69.67%)、超重或肥胖(113例,46.31%)、血脂升高(53例,21.72%)、吸烟(51例,20.90%)、家族史(44例,18.03%)、糖尿病(42例,17.21%)。结论:荆门市某社区脑卒中发病危险因素主要为高血压、肥胖、吸烟、血脂升高和糖尿病。     

2型糖尿病并脑血管病变的临床特点及危险因素分析

目的探讨2型糖尿病合并脑血管病变的临床特点及危险因素。方法对我院住院的646例2型糖尿病患者中合并脑血管病变的124例临床资料进行回顾性分析,分析其临床特点及危险因素。结果在124例脑卒中患者中,男性稍多于女性,但均以60岁以上的高龄多见,共有93例(75%)。脑卒中以缺血性脑病灶为主(88.7%),与出血性脑病灶相比有显著性差异(P<0.05)。2型糖尿病并脑卒中患者中高血压和肥胖的发生比例较高(分别为69.4%和77%),而2型糖尿病无合并脑卒中组高血压的发生比例为42.3%,二者相比有显著性差异(P<0.05)。124例脑卒中患者当中,有7例死亡(占5.6%),有26例为再发(20.9%)。Logistic回归分析结果显示收缩压、年龄、低密度脂蛋白胆固醇、糖化血红白蛋白是2型糖尿病合并脑血管病变的危险因素。结论收缩压、年龄、低密度脂蛋白胆固醇、糖化血红白蛋白是2型糖尿病合并脑血管病变的危险因素。2型糖尿病伴有高血压及/或肥胖者易发生脑卒中,多发生在60岁以上的老年患者,临床特点为以缺血性病变为主,且脑卒中再发率高。     

急性脑卒中院内死亡患者危险因素的临床研究

目的探讨急性脑卒中患者院内死亡的危险因素,有针对性地提出防临床治措施。方法选择2007年5月至2013年5月间于我院就诊的急性脑卒中院内死亡病例为病例组,按照病例对照研究1∶1匹配的方法,选择同期在我院就诊的急性脑卒中存活病例为对照组,采用回顾性分析的方法,分析急性脑卒中院内死亡患者的相关危险因素。结果共有87例死亡病例进入病例组,87例存活进入对照组。Logistic回归分析结果显示,发病与入院的时间间隔、高血压史、糖尿病史、卒中史、入院神经功能损害评分、意识障碍、心电图异常为急性脑卒中院内死亡患者的危险因素,调整年龄和性别因素后,发病与入院的时间间隔、糖尿病史、肾病史、入院神经功能损害评分仍为院内死亡的危险因素,差异有统计学意义(P<0.05)。结论发病与入院时间间隔长、高血压病史、糖尿病史、卒中史、入院神经功能损害评分、意识障碍、心电图异常是急性脑卒中院内死亡的高危人群,其中发病与入院的时间间隔、糖尿病史、肾病史、入院神经功能损害评分是急性脑卒中院内死亡的独立危险因素。     

青年脑卒中临床特点及相关危险因素分析

目的探讨青年脑卒中的临床特点及相关危险因素。方法收集2000年1月至2010年12月期间我院住院的73例青年脑卒中患者,另随机选取同期收治的中老年脑卒中患者75例作比较,对比分析两组患者的临床特征及危险因素。结果青年脑卒中以男性患者为主,多数于活动状态下发病;青年组最危险因素是高血压病史、高血脂症、吸烟,其他为酗酒、家族史、糖尿病史、颅内血管畸形、心脏病史等,其中在高血压病史、高血脂症、酗酒、糖尿病史及心脏病史方面与中老年人比较差异有统计学意义(P<0.05)。结论青年脑卒中患者与性别、高血压、高血脂、吸烟、酗酒等因素密切相关,应加强对高危人群的危险因素进行早期干预,以改善患者预后。     

缺血性脑卒中及其TOAST分型相关危险因素分析

目的 探讨缺血性脑卒中及其急性卒中治疗低分子肝素试验(TOAST)分型与相关危险因素的关系.方法 收集缺血性脑卒中病例841例(病例组),根据TOAST分型标准分为5个亚型;选择同期入院的739例非脑卒中患者作为对照组.分析缺血性脑卒中及各亚型的患病危险因素.结果 与对照组比较,卒中组及各亚型在年龄增大、性别(男性)、肥胖、脑卒中家族史、疾病史(高血压、糖尿病等)、入院血压、白细胞计数、血脂水平等方面差异有统计学意义;多因素Logistic回归分析显示影响缺血性脑卒中及各亚型发病风险的危险因素不完全相同.结论对不同病因引起的缺血性脑卒中应采取不同的预防和治疗措施.     

多模式MRI指导下醒后缺血性脑卒中静脉溶栓有效性研究

目的研究多模式MRI指导下醒后缺血性脑卒中静脉溶栓有效性。方法回顾性分析我院2017年3月至2020年3月收治的醒后缺血性脑卒中患者80例,按照随机数字表法分为对照组和溶栓组,对照组为38例拒绝静脉溶栓后常规治疗急性缺血性脑卒中(AIS)患者,溶栓组为42例重组组织型纤溶酶原激活剂(rt-PA)静脉溶栓AIS患者,观察两组美国国立卫生研究院卒中量表(NIHSS)评分、改良Rankin评分量表(mRS)、脑出血发生率。结果入院时两组患者NIHSS评分比较,差异无统计学意义(P 0.05),溶栓组出院时NIHSS评分低于对照组,溶栓组出院后3、6个月m RS评分低于对照组,溶栓组脑出血发生率为2.38%,低于对照组的13.16%,差异有统计学意义(P 0.05)。结论多模式MRI对醒后缺血性脑卒中静脉溶栓具有重要指导意义,为早期再灌注治疗提供合理有效的影像学依据,在MRI指导下能够改善患者神经情况,降低脑出血发生率。     

他汀类药物与出血性卒中

他汀类药物目前广泛应用于冠状动脉粥样硬化性心脏病和缺血性卒中的预防,但也有研究发现该类药物可能增加出血性卒中的风险.发生机制可能与血胆固醇水平、微出血及他汀类药物自身药理作用有关.他汀类药物所引起的出血性卒中主要表现为颅内出血,包括脑叶出血和深部出血.既往用药史是判断相关性的重要依据.治疗措施包括停药、降低颅内压、控制血压及对症治疗.     

Rodent models of hemorrhagic stroke

Both intracerebral and subarachnoid hemorrhages are associated with high mortality and most survivors are burdened with severe disability. Currently, there is no approved treatment for intracerebral hemorrhage and surgical evacuation was not proven beneficial. Regarding subarachnoid hemorrhage, existing therapies need substantial improvement. Detailed pathophysiologic mechanisms need to be understood in order to develop novel therapeutic strategies. Hemorrhagic stroke models can help achieve both these goals and answer those questions that cannot be addressed in the clinical setting. There are several animal models of intracerebral and subarachnoid hemorrhage, each mimicking fairly reliably different aspects of the condition studied. The similarities and differences among the existing rodent models, model modifications, and some aspects concerning the choice of relevant model are discussed.     

PPA与出血性中风相关性

背景PPA(phenylpropanolamine,苯丙醇胺)常见于食欲抑制药和咳嗽感冒药中,以往病例报告表明含PPA的药物与出血性中风有关,通常发生在首次使用后.为阐明二者相关性,我们设计了一项病例对照研究.方法18～49岁的男、女性研究病例来自美国43所医院,其合格标准包括在参与项目前30天内发生蛛网膜下腔出血或颅内出血,而既往并无确诊的脑损伤史.采用随机电话拨号,为每个病例安排2例对照进行面访.结果调查人群包括702名病例和1376名对照.女性服用含PPA食欲抑制药和出血性中风危险之间相关联的调整比值比为16.58(95%可信区间1.51～182.21,P=0.02);女性首次服用含PPA药物与出血性中风危险之间关联的调整比值比3.13(95%可信区间0.86～11.46,P=0.08),所有首次服用的PPA皆为咳嗽感冒药.男、女性调查人群服用含PPA药物与出血性中风危险二者关联的调整比值比为1.49(95%可信区间0.84～2.64,P=0.17);男、女性调查人群服用含PPA的咳嗽感冒药与出血性中风危险二者关联的调整比值比为1.23(95%可信区间0.68～2.24,P=0.49),服用含PPA的食欲抑制药与出血性中风危险关联的调整比值比为15.92(95%可信区间1.38～184.13,p=0.03).对男性的分析结果表明服用含PPA的咳嗽感冒药未引起出血性中风危险增加,男性无一例使用食欲抑制药.结论结果显示食欲抑制药中的PPA(咳嗽感冒药中的PPA也有可能)是女性出血性中风的一个独立的危险因素.     

缺血性与出血性脑卒中的血液流变学检测对照分析

脑卒中分为缺血性脑卒中和出血性脑卒中两种形式，一种是以血管堵塞引起大脑缺血为主要原因和病理变化的所谓缺血性脑卒中或脑梗死；另一种是以血管破裂导致脑出血的所谓出血性脑卒中或脑溢血。这两种不同形式的脑卒中在治疗上也截然不同，据此，我们应用血液流变学的检测方法对这两种不同形式的脑卒中患的血液黏度等指标进行了测定，并指导临床治疗。现将结果报告如下。     

针灸治疗急性出血性中风疗效观察

目的：探讨中西医结合针灸治疗急性出血性中风的价值。方法：随机分组,常规治疗组（对照组）和针灸结合常规治疗组（治疗组）各29例,治疗前和治疗两周后分别采用美国国立卫生研究所脑卒中评分（The United States National Institute of Health Stroke Scale, NIHSS）评定患者神经功能,CT测量血肿评价血肿吸收情况,同时参照《中风病辨证诊断标准》动态观察中医症候的改变,观察两组患者头痛、头晕、呕吐、言语謇涩、口角歪斜、吞咽困难、半身不遂、偏身感觉异常等症状、体征的改善情况。结果：两组临床疗效、中医症候疗效、血肿吸收情况比较,治疗组明显优于对照组,P＜0.01。结论：西药和针灸结合治疗对于急性出血性中风患者整体功能的恢复明显优于单纯西药治疗。     

Genetics of ischemic and hemorrhagic stroke in Chinese population

Stroke is a major cause of adult death and disability worldwide. Epidemiological and animal studies have provided strong evidence that the pathogenesis of stroke is multi-factorial and induced by a combination of environmental and genetic risk factors, but the identification of individual causative variants remains little known. Genetic influences are likely to be polygenic with small effect sizes, and stroke itself consists of a number of different subtypes which may each have different genetic profiles. In addition, various ethnic populations may have different stroke risk, such as Asian race. The reasons for high risk of stroke among the Chinese, especially hemorrhagic stroke, remain unknown. Most human studies have taken a candidate gene approach using case-control methodology. To be reliably detected, small relative risks require large sample sizes, probably 1000 patients or more. Genome-wide association (GWA) study is an unbiased and comprehensive approach to identify common risk alleles for complex diseases. Recently, a multistage GWA study has identified three loci on chromosomes 2q, 8q and 9p to be associated with intracranial aneurysm in European and Japanese populations. Another GWA finding is the identification of risk variants for cardioembolic stroke on chromosome 4q25 in European populations. In this review, we mainly focus on the results from case-control association studies on genetic factors that play a role in the risk of ischemic and hemorrhagic stroke in Chinese population. The combined effects of multiple susceptibility genes for stroke risk are also summarized.     

Advances in hemorrhagic stroke therapy: conventional and novel approaches

Treatments for spontaneous intracerebral, thrombolytic-induced and intraventricular hemorrhages (IVH) are still at the preclinical or early clinical investigational stages. There has been some renewed interest in the use of surgical evacuation surgery or thrombolytics to remove hematomas, but these techniques can be used only for specific types of brain bleeding. The STICH (Surgical Trial in Intracerebral Haemorrhage) clinical trials should provide some insight into the potential for such techniques to counteract hematoma-induced damage and subsequently, morbidity and mortality. More recently, clinical trials (ATACH [Antihypertensive Treatment in Acute Cerebral Hemorrhage] and INTERACT [Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial]) have begun testing whether or not regulating blood pressure affects the well-being of hemorrhage patients, but the findings thus far have not conclusively demonstrated a positive result. More promising trials, such as the early stage CHANT (Cerebral Hemorrhagic And NXY-059 Treatment) and the late stage FAST (Factor VIIa for Acute Hemorrhagic Stroke Treatment), have addressed whether or not manipulating oxidative stress and components of the blood coagulation cascade can achieve an improved prognosis following spontaneous hemorrhages. However, CHANT was halted prematurely because although it showed that the spin trap agent NXY-059 was safe, it also demonstrated that the drug was ineffective in treating acute ischemic stroke. In addition, the recombinant activated factor VII FAST trial recently concluded with only modestly positive results. Despite a beneficial effect on the primary end point of reducing hemorrhage volume, controlling the coagulation cascade with recombinant factor VIIa did not decrease the mortality rate. Consequently, Novo Nordisk has abandoned further development of the drug for the treatment of intracerebral hemorrhaging. Even though progress in hemorrhage therapy that successfully reduces the escalating morbidity and mortality rate associated with brain bleeding is slow, perseverance and applied translational drug development will eventually be productive. The urgent need for such therapy becomes more evident in light of concerns related to uncontrolled high blood pressure in the general population, increased use of blood thinners by the elderly (e.g., warfarin) and thrombolytics by acute ischemic stroke patients, respectively. The future of drug development for hemorrhage may require a multifaceted approach, such as combining drugs with diverse mechanisms of action. Because of the substantial benefit of factor VIIa in reducing hemorrhage volume, it should be considered as a prime drug candidate included in combination therapy as an off-label use if the FAST trial proves that the risk of thromboembolic events is not increased with drug administration. Other promising drugs that may be considered in combination include uncompetitive NMDA receptor antagonists (such as memantine), antioxidants, metalloprotease inhibitors, statins and erythropoietin analogs, all of which have been shown to reduce hemorrhage and behavioral deficits in one or more animal models.     

Advances in hemorrhagic stroke therapy: conventional and novel approaches

Treatments for spontaneous intracerebral, thrombolytic-induced and intraventricular hemorrhages (IVH) are still at the preclinical or early clinical investigational stages. There has been some renewed interest in the use of surgical evacuation surgery or thrombolytics to remove hematomas, but these techniques can be used only for specific types of brain bleeding. The STICH (Surgical Trial in Intracerebral Haemorrhage) clinical trials should provide some insight into the potential for such techniques to counteract hematoma-induced damage and subsequently, morbidity and mortality. More recently, clinical trials (ATACH [Antihypertensive Treatment in Acute Cerebral Hemorrhage] and INTERACT [Intensive Blood Pressure Reduction in Acute Cerebral Hemorrhage Trial]) have begun testing whether or not regulating blood pressure affects the well-being of hemorrhage patients, but the findings thus far have not conclusively demonstrated a positive result. More promising trials, such as the early stage CHANT (Cerebral Hemorrhagic And NXY-059 Treatment) and the late stage FAST (Factor VIIa for Acute Hemorrhagic Stroke Treatment), have addressed whether or not manipulating oxidative stress and components of the blood coagulation cascade can achieve an improved prognosis following spontaneous hemorrhages. However, CHANT was halted prematurely because although it showed that the spin trap agent NXY-059 was safe, it also demonstrated that the drug was ineffective in treating acute ischemic stroke. In addition, the recombinant activated factor VII FAST trial recently concluded with only modestly positive results. Despite a beneficial effect on the primary end point of reducing hemorrhage volume, controlling the coagulation cascade with recombinant factor VIIa did not decrease the mortality rate. Consequently, Novo Nordisk has abandoned further development of the drug for the treatment of intracerebral hemorrhaging. Even though progress in hemorrhage therapy that successfully reduces the escalating morbidity and mortality rate associated with brain bleeding is slow, perseverance and applied translational drug development will eventually be productive. The urgent need for such therapy becomes more evident in light of concerns related to uncontrolled high blood pressure in the general population, increased use of blood thinners by the elderly (e.g., warfarin) and thrombolytics by acute ischemic stroke patients, respectively. The future of drug development for hemorrhage may require a multifaceted approach, such as combining drugs with diverse mechanisms of action. Because of the substantial benefit of factor VIIa in reducing hemorrhage volume, it should be considered as a prime drug candidate included in combination therapy as an off-label use if the FAST trial proves that the risk of thromboembolic events is not increased with drug administration. Other promising drugs that may be considered in combination include uncompetitive NMDA receptor antagonists (such as memantine), antioxidants, metalloprotease inhibitors, statins and erythropoietin analogs, all of which have been shown to reduce hemorrhage and behavioral deficits in one or more animal models.     

匹诺塞林对高血糖诱导的大鼠卒中后出血转化的作用

目的研究匹诺塞林(pinocembrin)对高血糖诱导的大鼠卒中后出血转化的作用。方法实验分为假手术组、大脑中动脉堵塞(MCAO)模型组、高糖+MCAO模型组、高糖+匹诺塞林+MCAO组。MCAO模型采用线栓法造模,缺血1.5 h;高糖+MCAO模型组于造模前30 min腹腔注射50%葡萄糖;高糖+匹诺塞林+MCAO组于再灌前5 min尾静脉注射匹诺塞林10 mg·kg~(-1)。葡萄糖注射前、后30 min及MCAO术后1,2和3 h用血糖仪检测血糖。缺血24 h后,采用改良的大鼠神经功能缺损评分法进行神经学评分,TTC染色测定脑梗死体积,血红蛋白检测试剂盒检测脑组织中血红蛋白含量,伊文斯蓝渗漏实验观察对血脑屏障的影响,通过脑病理切片观察脑组织出血情况。全部实验结束后统计脑组织出血发生率和大鼠死亡率。结果MCAO模型组各时间点血糖水平与假手术组比较均无明显变化;高糖+MCAO模型组,提前30 min腹腔注射50%葡萄糖能使血糖水平从注射前4.0升至20.9 mmol·L~(-1),且各时间点血糖水平均显著高于MCAO模型组(P<0.01);匹诺塞林对高糖+MCAO模型大鼠血糖水平无影响。MCAO模型组和高糖+MCAO模型组的神经学评分(分别为9.4±1.5和10.0±0.6)无显著性差异;匹诺塞林使高糖+MCAO模型大鼠神经学评分降至7.4±1.1(P<0.01)。MCAO模型组脑梗体积为(23.3±11.3)%,高糖+MCAO模型组脑梗体积增加至(36.9±8.2)%(P<0.05),匹诺塞林使脑梗体积降至(26.9±5.8)%(P<0.05)。与MCAO模型组相比,高糖+MCAO模型组大鼠脑组织中血红蛋白含量和伊文斯蓝含量分别由(195.5±30.1)mg·L~(-1)和(74.6±46.8)μg·g~(-1)组织增加至(472.0±166.9)mg·L~(-1)(P<0.01)和(132.9±49.6)μg·g~(-1)组织(P<0.05);匹诺塞林可显著减轻高糖+MCAO模型大鼠出血损伤,使血红蛋白含量和伊文斯蓝含量降至(299.8±47.7)mg·L~(-1)(P<0.01)和(70.4±39.2)μg·g~(-1)组织(P<0.05)。MCAO模型组脑出血发生率和死亡率分别为18.2%和16.7%,高糖+MCAO模型组显著增加,分别为95.4%和57.3%;给予匹诺塞林后分别降至59.1%和18.9%。结论匹诺塞林能减轻高血糖诱导的出血转化,降低出血的发生率和死亡率,是一种具有潜力的抗出血转化药物。     

Effect of Cerebral on the immune system in experimental hemorrhagic stroke

Data on the development of three experimental models of hemorrhagic stroke in mice are reported. The models differ in the extent of damage. From the standpoint of the immunopharmacological investigation, most adequate model is provided by the light acute brain circulation disorder (LABCD). In the LABCD model, the hemorrhagic stroke is characterized by reduction in the thymus weight, inhibition of the antibody (hemolysin) synthesis, and enhancement of the delayed type hypersensitivity response. The new antistroke drug cerebral decreased (especially after intranasal administration) the level of lethality in experimental animals and improved the immunological indices.