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1.
国产降纤酶对大鼠缺血/再灌注脑损伤的保护作用   总被引:3,自引:0,他引:3  
目的观察3种国产降纤酶对大鼠缺血/再灌注脑损伤的保护作用。方法采用线栓法大鼠局灶性脑缺血/再灌注模型,观察3种国产降纤酶对缺血/再灌注不同时程动物脑梗死体积、血流量、神经功能缺损评分及梗死灶内肉眼出血率的影响。结果持续缺血3h,降纤酶治疗的各组动物脑梗死体积明显小于生理盐水对照组(P<0.05);缺血3h再灌注3h和72h,降纤酶治疗的各组动物脑梗死体积与生理盐水组相比无明显变化,但缺血3h再灌注6h和24h,降纤酶治疗的各组动物脑梗死体积比生理盐水组明显减少(P<0.05)。缺血3h再灌注6h、24h和72h,降纤酶治疗组动物脑血流量比生理盐水组明显增加(P<0.05)。但治疗组动物行为学评分较生理盐水组无相应改善,梗死灶内有肉眼出血的动物较生理盐水组多,但无统计意义。结论国产降纤酶能明显减小缺血/再灌注脑损伤动物的梗死体积和增加脑血流量,改善损伤后的低灌注状态,对脑组织有一定保护作用。  相似文献   

2.
目的 建立大鼠血栓栓塞模型及探讨超早期尿激酶溶栓治疗的有效性。方法 用自体血体外制备栓子,经颈外动脉推入,栓塞大脑中动脉,半小时或4小时后分别予以尿激酶或生理盐水治疗。6小时后检查血栓的位置,测定梗死灶大小,及进行组织病理学检查。结果 生理盐水治疗组6小时后大脑中动脉起始部均见栓子存在,尿激酶治疗组栓子完全溶解;生理盐水治疗组和4小时溶栓治疗组梗死灶大小无显著性差异(P<0.05),而半小时溶栓治疗组梗死灶明显较前两组小(P<0.05),细胞坏死程度减轻。结论 本模型可复制性强,溶栓治疗后血管再通率高,梗死灶大小恒定,是进行溶栓研究的理想模型。超早期溶栓梗死灶明显减小。  相似文献   

3.
目的研究降纤酶对实验性脑梗死灶周围微血管的作用。方法用线栓法将易卒中型肾血管性高血压大鼠(stroke-pronerenovascularhypertensiverats,RHRSP)复制成一侧大脑中动脉闭塞(MCAO)模型,静脉注射降纤酶,对照组注射生理盐水,分别于缺血3、6、24h进行功能评分并处死大鼠,TTC染色计算脑梗死范围,HE染色观察梗死边缘区的病理形态,同时免疫组织化学检测尿激酶型纤溶酶原激活剂(urokinasetypeplasminogenactivator,uPA)和纤溶酶原激活剂抑制物1(plasminogenactivatorinhibitor1,PAI1)蛋白的表达。结果降纤酶能改善MCAO后神经功能评分,减少梗死灶体积,梗死灶边缘微血管损害减轻,血管内皮uPA蛋白表达减少及PAI1蛋白表达增加。结论降纤酶可能是通过抑制微血管内皮细胞uPA蛋白表达和增加PAI1蛋白表达而减轻脑梗死灶边缘微血管损害。  相似文献   

4.
目的 在改良法自体血血栓栓塞性脑卒中大鼠模型上使用尿激酶静脉溶栓 ,试图建立理想化的溶栓治疗脑卒中研究的模型体系。方法 治疗组于大脑中动脉闭塞后 0 .5h尿激酶进行静脉溶栓。 5h和2 4h后进行神经功能缺损评分 ,用TTC染色法测定梗死灶体积 ,并观察梗死后 6h的脑组织病理变化。结果 此模型可产生范围较恒定的梗死灶 ,治疗组梗死灶体积明显小于对照组 (P <0 .0 1)。但两组 5h和 2 4h神经功能缺损评分无显著性差异。结论 这种模型超早期使用尿激酶静脉溶栓疗效好 ,由于可能存在缺血性神经元顿抑 ,尽管溶栓组脑梗死体积减小 ,但早期神经功能恢复不明显。  相似文献   

5.
目的:研究不同时间窗脑血栓溶解治疗后脑电变化与梗死体积的关系。方法:应用肾血管性高血压大鼠,用光化学法制成一侧大脑中动脉闭塞模型,在血栓形成后不同时间应用尿激酶静脉溶栓,观察脑电图变化与梗死体积的大小。结果:缺血2小时之内实行溶栓治疗,可缩小梗死性。MCAO30分钟后溶栓复流后,EEG有改善,一小时后慢波减少,24小时EEG可恢复到基本正常。  相似文献   

6.
目的:探讨国产降纤酶对大鼠局灶性脑缺血/再灌注动物模型的神经行为学和脑梗死体积的影响,以证明其是否有脑保护作用。方法:采用线检法制作大鼠大脑中动脉闭塞模型,用Zea Longa 5分制评分和TTC染色法评价神经行为学和脑梗死体积。由吉林大学第一医院和复旦大学华山医院共同进行实验研究,每部分实验动物各做一半。动物随机分为缺血3h及再灌注3h,6h,24h和72h;缺血6h及再灌注3h,6h,24h;缺血24h等共10组。降纤酶采用8U/kg腹腔注射给药。结果:行为学结果:在10组中仅于缺血6h再灌注6h组Zea Longa评分有明显改善(P<0.05),其余各组与盐水对照组比较无显著性差异。梗死体积测定结果:在缺血3h各组中,只有缺血3h再灌注72h这个时间点比盐水组无明显缩小(P>0.05),其余各时间点梗死体积均明显缩小(P分别<0.05、0.01和0.001)。在缺血6h和24h组中,各时间点与盐水组比较均明显缩小(分别为P<0.01和P<0.05)。结论:国产降纤酶对大鼠局灶性脑缺血及再灌注损伤有一定的保护作用。  相似文献   

7.
尿激酶联合镁剂治疗大鼠急性脑梗死的实验研究   总被引:2,自引:0,他引:2  
目的 观察尿激酶溶栓联合硫酸镁神经保护对大鼠急性脑梗死的疗效。方法 应用光化学诱导法建立大鼠大脑中动脉闭塞(MCAO)模型,分别于术后2 h、6 h和10 h 3 个时间点进行干预,每个时间点内再分为生理盐水对照组、尿激酶溶栓组、尿激酶加硫酸镁治疗组,术后24 h观察大鼠神经功能缺损评分及脑梗死体积的变化。结果 MCAO后2 h尿激酶溶栓组神经功能显著改善,梗死体积缩小(与生理盐水对照组相比,P<0.01),尿激酶加硫酸镁治疗组效果更好;MCAO后6 h、10 h尿激酶溶栓组与生理盐水对照组相比无显著性差异(P>0.05),而尿激酶加硫酸镁治疗组的神经功能缺损评分、脑梗死体积与生理盐水对照组及尿激酶溶栓组相比有显著差异(P<0.05或P<0.01)。结论 早期脑梗死特别是2 h内的超早期脑梗死应用尿激酶溶栓有效;加用镁剂进行神经保护可对尿激酶溶栓疗效产生协同作用,并可能扩大脑梗死溶栓治疗的时间窗。  相似文献   

8.
目的 观察糖酐酯对脑栓塞大鼠白细胞浸润的抑制作用及对溶栓治疗后梗死灶体积、细胞凋亡等的影响。方法 用自体血栓子栓塞大鼠大脑中动脉 0 .5h后 ,静脉给予糖酐酯或生理盐水 ,2h或 4h后应用尿激酶溶栓治疗 ,12h或 2 4h后 ,采用TTC染色测定梗死灶大小 ,免疫组化法检测白细胞浸润和细胞间黏附分子 1(ICAM 1)表达 ,TUNEL法检测细胞凋亡 ,透射电镜观察血脑屏障 (BBB)及细胞坏死。结果 联合溶栓组与单纯溶栓组比较 ,梗死灶减小 (P <0 .0 5 ) ,缺血周边区浸润白细胞数和凋亡细胞数明显减少 (均P <0 0 1) ,BBB损伤及细胞坏死程度减轻 ,颅内出血发生例数减少。但ICAM 1表达两组比较无显著性差异 (P >0 0 5 )。结论 糖酐酯能明显抑制白细胞浸润 ,其作用机制与ICAM 1表达无关 ;抑制白细胞浸润可以增强溶栓治疗疗效、保护BBB和减少溶栓治疗后神经细胞凋亡。  相似文献   

9.
三七三醇皂苷对脑缺血再灌注大鼠的保护作用   总被引:11,自引:0,他引:11  
目的 通过对局灶性脑缺血大鼠不同再灌注时段的动态观察.探讨三七三醇皂苷(PTS)对大鼠局灶性脑缺血/再灌注动物模型的神经行为学和脑梗死体积的保护作用。方法 采用改良的线栓法制备大脑中动脉阻塞(MACO)2h、再灌注不同时间段(3h、6h、12h、24h、48h、72h、7d)的大鼠短暂局灶性脑缺血模型。动物随机分假手术组、生理盐水对照组、三七三醇皂苷(PTS)组。用Zea Longa5分制评分和TTC染色法评价神经行为学和脑梗死体积。结果 神经行为学评分除72h组有明显改善外.其余各组与生理盐水对照组比较无显著性差异。脑梗死体积除再灌注3h、6h外.其余各组与生理盐水组比较差异均有显著性意义。结论 三七三醇皂苷对大鼠局灶性脑缺血及再灌注损伤有一定的保护作用。  相似文献   

10.
大鼠局灶性脑缺血模型缺血半暗带的定位研究   总被引:4,自引:1,他引:3  
目的通过用组织病理学方法结合局部脑血流量(rCBF)测定,对大鼠局灶性脑缺血动物模型缺血半暗带的解剖定位进行初步探讨.方法用线栓法制成大鼠大脑中动脉(MCA)闭塞及再通模型、采用TTC染色法观察分组动物在MCA闭塞的不同时间再灌流48h后脑梗死灶的分布,并用氢清除法测定缺血区rCBF的变化.结果大鼠MCA闭塞1~2h,梗死灶主要位于缺血侧的外侧尾壳核和额顶叶皮质下部;MCA闭塞3h、梗死灶向周围扩大;MCA闭塞4h、梗死灶进一步扩展至大部分新皮质区,但与MCA闭塞6h时无明显区别.MCA闭塞后缺血侧的内侧尾壳核和额顶叶皮质上部rCBF下降至对照组的27%~45%.结论大鼠MCA闭塞后在2~3h的时间窗以内恢复血流,可使位于缺血边缘区的内侧尾壳核和额顶叶皮质上部脑组织被挽救,该区域可能相当于缺血半暗带的等值区.  相似文献   

11.
降纤酶治疗急性脑梗死的疗效评价   总被引:5,自引:1,他引:4  
目的 本文通过随机、对照、开放性临床研究,对海王降纤酶治疗急性脑梗死的有效性及安全性进行评价。方法 将90例急性脑梗死病人按2:1随机分为试验组和对照组,两组均以低分子右旋糖酐作为基础治疗。试验组加用降纤酶静脉给药,首剂量10 IU,其后5 IU隔日1次,共3次,总剂量20 IU。结果 与对照组比较,降纤组治疗后血浆FIB水平明显下降(P<0.001)。在降纤治疗过程中,有2例颅内出血发生,没有死亡病例,两组出血的差异无显著性。治疗后14天神经功能缺损恢复程度明显优于对照组(P<0.01)。结论 降纤酶是一种治疗急性脑梗死较为安全有效的药物。  相似文献   

12.
BACKGROUND: At present, as a therapeutic drug mainly for reducing fibrinogen (FIB) levels, the dynamic influence of defibrase on the FIB levels of patients with acute cerebral infarction has not been clearly ascertained. OBJECTIVE: To observe the dynamic changes in FIB levels of patients with acute cerebral infarction at different time points after taking defibrase. DESIGN, TIME AND SETTING: Randomized controlled clinical trial. The study was conducted in the Department of Neurology, the Second Affiliated Hospital of Jinan University, from June to November 2006. PARTICIPANTS: Sixty patients with acute cerebral infarction, who had been treated by the Neurological Department of the Second Affiliated Hospital of Jinan University from June to November 2006, were selected, including 37 males and 23 females, aged 35-75 years. All cases met the diagnostic criteria formulated by the Fourth National Cerebrovascular Disease Conference within 12 hours of onset. All the patients were confirmed with definite hemiparesis and cerebral infarction without coma, and were randomly divided into two groups: a treatment group (n =40) and a control group (n =20). Patients' families had the right to be informed and agree with the treatment, which had permission from the Hospital Ethics Committee. METHODS: Patients in the control group were given routine treatment with 30 mL fleabane and 0.75 g cytidine diphosphate added to 500 mL saline solution once a day for 14 consecutive days. Patients in the treatment group were given routine treatment and Haiwang defibrase injection (purchased from Changchu Guoao Bio-Pharmaceutical Co. Ltd., Approval document number H10983237) within 12 hours of infarction. Defibrase doses of 15, 12.5 and 10 U were given over 2 hours according to the patients' pre-treatment plasma FIB levels of ≥ 4.50 g/L, 3.50 4.49 g/L and 1.00 3.49 g/L, respectively. Plasma FIB levels in the treatment group were measured before, and once every six hours for 48 hours after administration of defib  相似文献   

13.
It has been reported that activated neutrophils are involved in the development of cerebral damage induced by ischemia. Activated neutrophils release a lot of mediators including toxic oxygen metabolites, elastase and cytokines which damage brain tissue. Therefore, we investigated roles of neutrophil elastase in the development of cerebral damage using an elastase inhibitor, ONO-5046. The rat middle cerebral artery (MCA) was occluded by a thrombus induced by photochemical reaction between green light and the photosensitizer dye, Rose Bengal. Photochemical reaction causes endothelial injury followed by formation of a platelet and fibrin-rich thrombus at the site of the irradiation. Photochemical reaction is routinely used in our laboratory to produce arterial occlusion in experimental animals. Twenty-four hours after the MCA occlusion, the size of cerebral damage was measured by histochemical technique. Water content in the brain was measured and neuronal deficits were examined 24 h after the MCA occlusion. ONO-5046 was administered at various doses as continuous infusion for 24 h, starting just after the MCA occlusion or from 3 h after. ONO-5046 at doses of 10 and 30 mg/kg/h significantly (p<0.05 and p<0.01, respectively) reduced the size of cerebral damage and water content (p<0.05, p<0.01, respectively) in different eight rats. Further, ONO-5046 at a dose of 30 mg/kg/h significantly (p=0.01) improved neuronal deficits. ONO-5046 which was administered starting from 3 h after the MCA occlusion, also reduced the size of cerebral damage. Neutropenia by anti-neutrophil antibody injection significantly (p<0. 01) reduced the size of cerebral damage. Elastase released from activated neutrophils may play a key role in the development of cerebral damage.  相似文献   

14.
目的 评价国产降纤酶治疗急性脑梗死的疗效及安全性。方法 采用前瞻性随机双盲对照方法 ,2 8例患者随机分两组。治疗中监测纤维蛋白原水平、凝血酶原时间及凝血酶原活动度。评估指标包括临床神经功能缺损程度评分、Barthel指数、安全性及治疗一年后患者卒中复发率。结果  ( 1)治疗 14d临床神经功能缺损程度评分和Barthel指数 ,降纤酶组与对照组相比有显著性差异 (P <0 0 5 ) ,1年后两组卒中复发率有显著性差异。降纤酶组没有增加出血事件及肝肾功能损害等不良反应。 ( 2 )用药后降纤酶组与同期对照组纤维蛋白原、凝血酶原时间及凝血酶原活动度有显著性差异 (P <0 0 5 )。结论 降纤酶是降解纤维蛋白原安全有效的药物 ,可改善急性期临床神经功能评分及Barthel指数  相似文献   

15.
Objective Evolutionary stroke is one common and important subgroup of acute ischemic stroke with nerve damage symptoms evolutionarily heaving. There is not effective methods clinically to stop its development. This article aims to study the feasibility and effectiveness of Defibrase therapy on evolutionary stroke through observing curative effect of evolutionary stroke treated by defibrase therapy and analyze and compare with that of treated by routine medicine. Methods Select 52 evolutionary stroke cases 8 hours to 5 days after stroke and divide them into treatment group(28 cases):treated by 250ml saline intravenous transfusion with 10u Defibrase,once per day,after 3 successive days switch to routine treatmcnt, and control group(24 cases):receive routine treatment. Both groups have not found significant difference in age and severity through X2 inspection,and are comparable both in case history and complication accumulation.The curative effect is evaluated 10 days and 20 days after treatment respectively.Results 10 days after treatment, in treatment group total efficiency is 63%,in control group that is 36%;20 days after treatment,in treatment group total efficiency is 82% and that in control group is 53%.Both have significant difference(P<0.01).No untoward effect such as hemorrhage occurs to both groups.Discussion and Conclutions In general speaking.within 6 hours after ischmic stroke is the optimum time to conduct thrombus-dissolution,but for evolutionary stroke the situation is still developing within several hours and even several days after stroke,that is to say thrombus is still developing or ischemia half dark band is changing to irreversible .Therefore evolutionary stroke itself is the indication of needing thrombus dissolution.Volume urokinase thrombus-dissolving therapy is easy to superven serious complication such as intracrainial hemorrhage. Insertion treatment is not matured enough limited to equipment,infarct position and curative effect. Defibrase is prepared sololy from serine protease which is extracted from viper venom through modem bio-engineering methods. It can promotes tPA to release from endothediocyte so as to achieve rapid and specific thrombus-dissolution. The study result reveals that Defibrase is an effective,safe medicine to cure evolutionary stroke  相似文献   

16.
GPIIb/IIIa antagonists are expected to have a beneficial effect on acute cerebral infarction, however, the occurrence of intracranial hemorrhage has not been as widely investigated. A rabbit focal thrombotic occlusion model of the middle cerebral artery was established by creating a photochemical reaction between green light and Rose Bengal. Hemorrhagic transformation was common in the area of cerebral infarction. Using this model, the effect of a GPIIb/IIIa antagonist, ME3277 (low dose, (L); 0.15 mg/kg + 0.125 mg/kg x h, middle dose, (M); 0.3 mg/kg + 0.25 mg/kg x h and high dose, (H); 0.6 mg/kg + 0.5 mg/kg x h), aspirin (20 mg/kg) and sodium ozagrel (thromboxane A2 synthase inhibitor, 1 mg/kg + 2 mg/ kg x h) were evaluated. Drugs were intravenously administrated 30 minutes after the photochemical reaction for 24 hours. Aspirin inhibited the ex vivo platelet aggregation induced by arachidonic acid and collagen but not by adenosine diphosphate (ADP), while sodium ozagrel only inhibited the arachidonic acid-induced aggregation. ME3277 dose-dependently inhibited the platelet aggregation induced by all the inducers (approximately 60% in L, 80% in M, and 90% in H). At 24 hours of middle cerebral artery (MCA) occlusion, infarct volume was significantly reduced by aspirin and each dose of ME3277. These agents improved neurologic deficits, with ME3277 being more potent than aspirin. Sodium ozagrel did not alter the infarct volume nor neurologic deficits. No drug was found to worsen hemorrhage volume despite increasing bleeding time (2-3 fold) in the skin. In this model, the occluded artery was spontaneously recanalized and re-thrombosed frequently. One mechanism by which antiplatelet agents reduced infarct volume was inhibition of rethrombosis of the MCA. These results suggest that treatment with a GPIIb/IIIa antagonist is a useful intervention for acute cerebral infarction prolonging dose bleeding time to 3 times the basal value.  相似文献   

17.
目的:评价局部动脉内溶栓和经皮腔内血管成形术(PTA)结合在治疗急性大脑中动脉栓塞中的应用。方法:7例急性大脑中动脉栓塞用局部动脉内灌注组织纤溶酶原激活物(t-PA)溶栓,6例M_1段同时存在狭窄,用PTA成功消除;所有病例均在发病6h内开始治疗。结果:7例栓塞动脉均获得完全再通,6例M_1段狭窄用FTA消除,5例偏瘫完全恢复,1例有脑出血并发症。结论:局部动脉内溶栓和PTA结合可能是治疗急性大脑中动脉栓塞的有效方法。  相似文献   

18.
rt-PA应用后MMP-2、MMP-9表达的改变及Neuroserpin的影响   总被引:5,自引:3,他引:2  
目的 观察重组组织型纤溶酶原激活剂(rt-PA)对血管再通后基质金属蛋白酶-2(MMP-2)、MMP-9表达的影响以及神经源性丝氨酸蛋白酶抑制剂(neuroserpin,NSP)的干预作用。方法 应用易卒中型肾血管性高血压大鼠复制大脑中动脉缺血模型,缺血3 h后再灌注并静脉注射rt-PA,于预组在应用rt-PA前脑内注射NSP,1天后处死,常规病理检查,并应用免疫组织化学和原位杂交的方法观察MMP-2、MMP-9在脑组织的表达。结果 缺血再灌注后MMP-2、MMP-9表达均升高;应用rt-PA后可见缺血再灌注区有灶性出血及红细胞漏出,同时使MMP-9进一步升高,但对MMP-2影响不大;应用rt-PA的同时使用NSP可以减轻缺血损伤,减少出血的发生,并使升高的MMP-9减少至接近正常水平,但NSP可以使MMP-2表达略有升高。结论 rt-PA溶栓后出血转化的发生可能与MMP-9表达增加有关,溶栓时联合应用NSP可能通过降低rt-PA所致的MMP-9表达上调而减轻溶栓治疗的出血并发症。  相似文献   

19.
基础血压对低血压诱发脑梗塞的影响   总被引:2,自引:0,他引:2  
目的探讨大鼠的基础血压和脑血管的病理改变对低血压诱发脑梗塞的影响。方法将易卒中型肾血管性高血压大鼠(RHRSP)和正常血压SD大鼠各72只急速降压后,观察脑组织的病理改变。结果SD大鼠无脑梗塞发生;38只发生脑梗塞的RHRSP中,32只的基础血压显著高于无脑梗塞的RHRSP的基础血压(P<0.05),且脑内小动脉硬化改变也较严重,另6只有脑梗塞的RHRSP(血压均降至8kPa)的基础血压及脑内小动脉硬化改变与无梗塞的RHRSP的相似。结论高血压的严重程度和持续时间是低血压诱发脑梗塞的重要因素。  相似文献   

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