首页 | 本学科首页   官方微博 | 高级检索  
相似文献
 共查询到20条相似文献,搜索用时 187 毫秒
1.
目的 探讨脑出血患者血浆β-内啡肽(β-EP)、强啡肽A1-13(DynA1-13)和亮氨酸脑啡肽(L-ENK)的含量变化及纳络酮对其影响.方法 将60例脑出血患者随机分为对照组(n=30)和纳络酮组(n=30).对照组采用常规治疗,纳络酮组在常规治疗基础上加用纳络酮3.0mg/d静脉滴注,两组均治疗14d.采用放射免疫分析法(RIA),检测60例脑出血患者发病当天(治疗前)和治疗3d、7d、10d、14d血浆β-EP、DynA1-13、L-ENK的含量变化,并与正常组比较.观察纳络酮对上述3项指标的影响.结果 (1)脑出血患者发病后血浆β-EP,DynA1-13含量即明显增高,与正常组比较差异有显著性(均P<0.01);L-ENK含量与正常组比较差异无显著性(P>0.05);(2)脑出血患者血浆β-EP、DynA1-13和L-ENK含量在发病7d达高峰,14d基本接近正常,治疗结束后两组比较差异有显著性(P<0.05或P<0.01).结论 (1)脑出血后血浆β-EP、DynA1-13、L-ENK含量异常升高;(2)纳络酮能拮抗β-EP、DynA1-1 3、L-ENK的异常升高,具有脑保护作用.  相似文献   

2.
目的探讨脑出血患者血浆和脑脊液(CSF)阿片肽———β内啡肽(βEP)、强啡肽A113(DynA113)的含量变化及纳络酮的干预作用。方法将60例脑出血患者随机分为纳络酮组和对照组;两组在脑出血常规治疗的基础上,纳络酮组加用纳络酮3.0mg静脉滴注,每日1次,连用14d。采用放射免疫分析法(RIA)检测两组患者治疗前和治疗7d、14d血浆和CSF中βEP、DynA113的含量,分析脑出血部位及出血量与上述指标变化的关系并与正常组(正常血浆组及正常CSF组)比较;对两组脑出血患者治疗前后格拉斯哥昏迷评分(GCS)和神经功能缺损程度评分(NDS)进行比较。结果(1)脑出血患者血浆和CSF中βEP、DynA113含量与两正常组比较明显增高(均P<0.01);不同出血部位患者的血浆和CSF中βEP、DynA113含量的差异无显著性;脑出血量与血浆和CSF中βEP、DynA113含量呈显著正相关(r=0.663、0.480、0.645、0.380,均P<0.01);(2)治疗后纳络酮组血浆和CSF中βEP、DynA113含量明显低于对照组(P<0.05~0.01);GCS、NDS较对照组明显改善(均P<0.05)。结论脑出血后血浆和CSF中阿片肽含量异常升高;纳络酮治疗能明显降低血浆及CSF中阿片肽含量,显著改善脑出血患者的神经功能缺损。  相似文献   

3.
依达拉奉联合纳络酮治疗急性脑梗死的疗效   总被引:1,自引:0,他引:1  
目的 探讨依达拉奉联合纳络酮治疗急性脑梗死的疗效.方法 120例进展型脑梗死随机分为纳络酮组(对照组)和依达拉奉联合纳络酮治疗组(治疗组).分别对两组治疗前、治疗14 d后的神经功能缺损及临床疗效进行评价.结果 两组治疗后14 d的神经功能缺损较治疗前均有显著改善P<0.01,治疗组与对照组比较有显著性差异P<0.01.治疗14 d后临床疗效评价治疗组总有效率(85%)较对照组(71.67%)有显著性差异P<0.01.结论 依达拉奉联合纳络酮治疗急性脑梗死能保护脑细胞,有效改善神经功能.  相似文献   

4.
早期大剂量纳络酮治疗高血压脑出血的临床研究   总被引:4,自引:0,他引:4  
目的 观察早期应用大剂量纳络酮 ,对高血压脑出血的治疗作用。方法  47例高血压脑出血患者随机分成纳络酮治疗组 (n =2 5)和对照组 (n =2 2 ) ,观察早期血压的变化 ,1 0d时患者的颅内压、脑水肿带、GCS、及远期疗效 ,并进行统计分析。结果 治疗早期两组血压变化无明显差异 (P >0 .0 5) ,纳络酮治疗组颅内压明显增高和重度脑水肿者比对照组显著减少 (P <0 .0 1 ) ,治疗 1 0天后 ,治疗组意识恢复清醒率 (48.0 % )高于对照组 (2 7.3 % )(P <0 .0 5) ,3个月恢复良好率明显高于对照组 ,且重残率明显减少 (P <0 .0 5)。结论 早期大剂量纳络酮治疗高血压脑出血 ,能降低颅内压上升的幅度、减轻脑水肿 ,并且具有促醒、减少致残率 ,促进神经功能恢复的作用  相似文献   

5.
非特异性阿片受体拮抗剂-纳络酮能减轻脑损伤后颅内压、脑水肿,但应用纳络酮在临床上治疗颅脑损伤的效果少有报导.我科自1996年7月~1999年1月收治重型颅脑损伤55例,GCS 评分≤8分.其中30例患者常规综合治疗,另25例患者加用纳络酮等综合治疗,取得良好的效果.  相似文献   

6.
纳络酮血肿腔内注射治疗高血压脑出血的临床观察   总被引:1,自引:0,他引:1  
目的 比较纳络酮血肿腔内注射与静脉注射对高血压脑出血的疗效。方法 40例高血压脑出血患者随机分为A、B两组。两组均采取锥颅血肿穿刺置管抽吸和脑室外引流治疗。A组血肿腔内局部注射纳络酮,B组静脉滴注纳络酮。比较两组患者治疗前后颅内压、GCS评分、脑脊液内皮素-1(ET-1)水平。对患者进行三月以上的随访。结果 40例脑出血患者发病后48hET-1平均水平明显高于非脑出血患者。A组发病后第3天、第7天ET-1峰值较B组明显低(P〈0.01);A组术后颅内压较B组降低更明显(P〈0.01);连续GCS评分较B组明显高(P〈0.01),平均清醒天数缩短;A组治疗有效率明显高于B组(P〈0.05)。结论 纳络酮血肿腔内注射较静脉注射可明显提高脑出血患者疗效,改善预后。  相似文献   

7.
盐酸纳络酮是阿片受体纯拮抗剂,能拮抗应激时机体释放大量内源性阿片肽所致的广泛病理生理效应。根据纳络酮的药理功效及特点,我科一年来将纳络酮应用于颅脑损伤等术后恢复期及脑出血后缓解症状,取得了明显的临床疗效。1临床资料1.1一般资料本组共22例,男性13例,女性9例,年龄18~67岁,平均29岁。颅脑损伤13例,脑出血7例,颅内肿瘤术后2例。1.2方法本组在入院抢救及术前均未使用纳络酮,14例手术病人在5~10d因意识恢复较慢或伴剧烈头痛在应用大剂量脱水、利尿药无效后使用纳络酮1.6~3.2mg/d静滴,保守治疗的8例颅脑损伤、脑出血患者在伤(病)后…  相似文献   

8.
目的探讨血浆阿片肽与重症脑血管病患者关系及大剂量盐酸纳络酮对阿片肽的影响和临床疗效.方法选择重症脑出血患者78例和脑梗死患者70例随机分成纳络酮组和常规药物组,治疗前后分别测定血浆β-内啡肽、强啡肽的含量并进行神经系统功能缺损评分.结果β-内啡肽值在发病后显著升高(P<0.01),治疗后均有下降,纳络酮组显著于常规药物组(P<0.01);强啡肽值在脑出血组有类似变化(P<0.05),但在脑梗死组中无变化(P>0.05).纳络酮组的疗效明显优于常规药物组,24小时内用药疗效优于24小时后(P<0.05).结论两种阿片肽均参与重症脑血管病病理生理过程,并有相异的作用;大剂量纳络酮早期应用有催醒,促进神经功能恢复,减少致残率的作用.  相似文献   

9.
目的 动态检测颅脑损伤后血液及腩脊液中体液免疫指标,分析颅脑损伤后体液免疫与疾病发展和恢复的关系,探讨纳络酮干预治疗的临床疗效.方法 前瞻性研究南海人民医院神经外科自2008年1月至12月收治的100例中重型颅脑损伤患者.按随机数字表法分为治疗组和对照组,每组50例,其中对照组仅给予常规治疗,治疗组除常规治疗外加用纳络酮治疗.伤后第4、14、21天检测患者血液和脑脊液IgG、IgA、IgM、补体C3、白蛋白(Alb)含量的变化,比较2组患者上述免疫指标、临床感染率和残疾等级评分(RDS)的差异.结果与对照组同一时间点比较.治疗组患者血液中各项免疫指标、脑脊液IgM含量差异无统计学意义(P>0.05),但脑脊液IgG、IgA、Alb含量,临床感染率和RDS评分均较低,差异有统计学意义(P<0.05);治疗组患者伤后第4天脑脊液C3阳性率(20/50)低于对照组(27/50),差异有统计学意义(P<0.05).结论 脑损伤后早期应用盐酸纳络酮,可以调节免疫、促进神经功能恢复和降低感染率,从而改善患者的预后.  相似文献   

10.
目的 动态检测颅脑损伤后血液及腩脊液中体液免疫指标,分析颅脑损伤后体液免疫与疾病发展和恢复的关系,探讨纳络酮干预治疗的临床疗效.方法 前瞻性研究南海人民医院神经外科自2008年1月至12月收治的100例中重型颅脑损伤患者.按随机数字表法分为治疗组和对照组,每组50例,其中对照组仅给予常规治疗,治疗组除常规治疗外加用纳络酮治疗.伤后第4、14、21天检测患者血液和脑脊液IgG、IgA、IgM、补体C3、白蛋白(Alb)含量的变化,比较2组患者上述免疫指标、临床感染率和残疾等级评分(RDS)的差异.结果与对照组同一时间点比较.治疗组患者血液中各项免疫指标、脑脊液IgM含量差异无统计学意义(P>0.05),但脑脊液IgG、IgA、Alb含量,临床感染率和RDS评分均较低,差异有统计学意义(P<0.05);治疗组患者伤后第4天脑脊液C3阳性率(20/50)低于对照组(27/50),差异有统计学意义(P<0.05).结论 脑损伤后早期应用盐酸纳络酮,可以调节免疫、促进神经功能恢复和降低感染率,从而改善患者的预后.  相似文献   

11.
Restoration of normal perfusion pressure after resection of cerebral arteriovenous malformations (AVMs) is sometimes complicated by unexplained postoperative brain swelling and/or intracranial hemorrhage, which has been termed normal perfusion pressure breakthrough (NPPB). The precise mechanism of NPPB is still unclear. In this study, we investigated the time courses of blood-brain barrier (BBB) disruption, water content, neuronal apoptosis, myeloperoxidase (MPO) activity and superoxide dismutase (SOD) activity in the brain during restoration of normal perfusion pressure in a new rat model of chronic cerebral hypoperfusion associated with AVMs. Male Sprague-Dawley rats were randomly divided into either a sham-operated group, a control group, or a model group with reperfusion assessed at 1, 12, 24 and 72 h after restoration of normal perfusion pressure. BBB disruption was judged by extravasation of Evans blue (EB) dye. We observed that EB and water content in rat brains of the model group with reperfusion were significantly increased compared with the other groups. The most predominant increase occurred at 1 h after reperfusion, and the next at 24 h after reperfusion, representing biphasic changes which are similar to the pathological processes of acute cerebral ischemia/reperfusion injury. There was no difference of the percentage of apoptotic cells in rat brains between the sham-operated group and the control group using flow cytometry. No prominent apoptotic cells were found in the model group with reperfusion at 1 h. However, the percentage of apoptotic cells increased significantly in rat brains of the model group with reperfusion at 12 h, peaked at 24 h, and decreased at 72 h after reperfusion. Apoptotic cells were confirmed with electron microscopy and terminal deoxynuleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL). A significant enhancement of MPO activity in combination with reduction of SOD activity was seen at 12, 24 and 72 h in rat brains of the model group with reperfusion. Our data indicates that reperfusion after restoration of normal perfusion pressure with chronic cerebral hypoperfusion lead to secondary neuronal damage which may associate with cerebral ischemia/reperfusion injury.  相似文献   

12.
目的观察大鼠脑出血后脑组织中内质网蛋白29(ERp29)的表达变化,进而探讨其在脑出血继发性脑损伤中的作用。 方法将60只SD大鼠按随机数字表法分为2组:对照组(10只,不做处理)和实验组(50只,在脑立体定位仪下采用自体血注入尾状核法制备脑出血模型)。实验组再分为术后6h、12h、18h、24 h、48 h5个时相点,对各个时相点的模型鼠分别采用RT-PCR和Western blotting方法检测脑组织中ERp29和内质网伴侣蛋白Bip/GRp78 mRNA及蛋白的表达。结果在脑出血大鼠模型中,BiP/GRp78 mRNA及蛋白表达在术后12h开始升高,并随着时间的推移在术后18h、24h、48 h继续逐渐升高,于术后48 h达顶峰,与对照组比较差异均有统计学意义(P<0.05)。ERp29 mRNA及蛋白表达在术后6h、12h无明显变化,与对照组比较差异无统计学意义(P>0.05);而在术后18h、24h、48h ERp29 mRNA及蛋白表达明显升高,与对照组比较差异均有统计学意义(P<0.05)。 结论大鼠脑出血后18h时血肿周围脑组织细胞中发生了内质网应激反应,而ERp29在此过程中表达升高,推测其有可能作为一种保护因子并以与BiP/GRp78相互作用形成复合物的形式来抵抗细胞内质网应激反应,进而减轻血肿对周围脑组织造成的损害。  相似文献   

13.
目的 建立一种微创、重复性好的大鼠蛛网膜下腔出血后早期脑损伤动物模型.方法 采用视交叉前池注血法建立蛛网膜下腔出血( SAH)后早期脑损伤(EBI)动物模型.在脑立体定位仪引导下将导管插入视交叉前池,注入300μl自体动脉血建立SAH后EBI模型.进行神经功能学评分,采用激光多普勒血流量仪(LDF)测定局部脑血流量(rCBF),解剖观察前循环周围血液分布情况,应用透射电子显微镜观察海马区神经细胞超微结构变化.结果 大部分大鼠在SAH后有神经行为学异常,48 h后逐渐恢复正常.SAH后不同时间点的rCBF均低于对照组.模型组大鼠颅脑解剖发现前循环蛛网膜下腔有大量的血液和血凝块.透射电子显微镜观察:与对照组比较,SAH组神经细胞线粒体和内质网肿胀,核染色质凝聚、趋边.结论 此动物模型稳定可靠,重复性高,适合进行临床前循环动脉瘤性蛛网膜下腔出血后早期脑损伤病理生理研究.  相似文献   

14.
目的探讨不同部位脑出血(基底节区出血、脑干出血)患者肠黏膜屏障变化。方法选取脑出血患者共66例,其中脑干出血32例,基底节区出血34例,分别于患病后24h、72h、2w、4w采集静脉血,同时选取健康体检者30例作为对照,抽取外周血,采用双抗体夹心ELISA法测定血清二胺氧化酶(DAO)、D-乳酸(D-LAC)含量。结果无论基底节区出血还是脑干出血,患者在患病后很快出现肠黏膜屏障功能的改变,在患病24h达较高水平,随后的72h、1w及2w血清D-LAC及DAO持续高水平,两组患者于2w后呈降低趋势,两组在发病后4w明显降低,但仍高于对照组;结论不论基底节区出血还是脑干出血患者患病后24h内即可出现黏膜屏障功能损伤,两组患者肠黏膜屏障功能损伤可持续4w或更长时间。  相似文献   

15.
目的动态观察实验性脑出血大鼠脑内血肿周围神经细胞凋亡情况和Caspas-3蛋白及mRNA表达水平的变化,探讨脑H{血后血肿周围神经细胞损伤机制。方法健康雄性Wistar大鼠随机分为生理盐水对照组、假手术组和脑出血模型组,分为术后3h,6h,12h,24h,48h,3d,5d,7d共8个时相点,采用尾状核注射自体非抗凝动脉血复制大鼠脑出血模型,术后制作冰冻切片,对切片进行TUNEL染色,以及Caspase-5免疫组化和原位杂交染色,之后利用图像分析仪,观察阳性细胞数。结果脑出血后3h血肿周围尚无凋亡细胞出现,6h有凋亡发生,以后逐渐增多,3d达高峰后逐渐下降,生理盐水对照组仅有少量TUNEL阳性细胞。假手术组及生理盐水对照组3h无Caspase-3蛋白和mRNA表达,生理盐水对照组6h以后有少量表达,脑出血模型组在6hCaspase-3蛋白和mRNA开始表达,3d时Caspase-3的蛋白达到高峰,5d以后逐渐下降,24hCaspase-3mRNA表达达高峰,5d以后逐渐下降。脑出血后血肿周围脑组织Caspase-3蛋白的表达与TUNEL阳性细胞数呈正相关(r=0.515,P〈0.05);Caspase-3蛋白表达与mRNA表达呈正相关(r=0.625,P〈0.05)。结论脑出血后血肿周围神经细胞损伤有凋亡机制参与,在出血后6h发生凋亡,第3天达高峰。Caspase-3的表达在Caspase-5蛋白水平变化趋势与脑m血后细胞凋亡的趋势一致,Caspase-3的mRNA水平的表达高峰时间先于Caspase-3蛋白的表达及凋亡的发生,提示Caspase-3的表达决定脑出血后细胞凋亡的发生,在脑出血后细胞凋亡中起促进作用。  相似文献   

16.
目的 探索嗅鞘细胞脑出血大鼠脑内移植后运动神经功能及形态学改变.方法 差速贴壁法培养出较高纯度的嗅鞘细胞,用PI和P75荧光双染鉴定细胞,制作30只脑出血大鼠模型,分A、B、C 3组.A组10只为单纯脑出血组;B组10只为培养液移植组;C组10只为嗅鞘细胞移植组.3组大鼠分别在术前1h,术后7d、14d、21d、28d进行运动功能学评分,并于细胞移植后第4周、第8周取脑组织做冰冻切片,通过免疫荧光检测移植细胞在大鼠脑内形态学改变.结果 试验中分离、培养的嗅鞘细胞经标记移植入大鼠脑内后,经免疫荧光检测证实能在血肿腔边缘分化为成熟神经元细胞和星形胶质细胞.对3组大鼠术后进行评分,细胞移植组从第21天起其功能恢复明显优于其它两组(P<0.001).结论 嗅鞘细胞在脑出血大鼠脑内能存活并分化为成熟神经元及星形胶质细胞,能促进运动神经功能恢复.
Abstract:
Objective The olfactory ensheathing cells ( OECs) transplanted into cerebral hemorrhage mode to alter motor nerve function and the study of morphology. Methods Get high purification of olfactory ensheathing cells by using the method of the differing rates of attachment of the various cells type, use the technology of fluoresceinstain identificated the OECs by both PI and P75 ,make 30 rats of cerebral hemorrhage mode,and separate 3 groups. Ten rats in the A group are the blank group;Ten rats in the B group are the DPBS transplanting group;Ten rats in the C group are the OECs transplanting group. The three groups are all scored in 1 hour before operation and 7 days, 14 days,21 days and 28 days after operation by Rosenberg GA method. Evaluate the contribution of OECs transplanting curing rat cerebral hemorrhage by statistics method. And get brain of rat to make frozen section in 4weeks,8weeks after operation. Detection the morphology of transplanting cells by immunofluorescence technique. Results We get in experiment transplantd in cerebral hemorrhage rats brain. We found these OECs differentiating to riped neuron cell and horizontal cell unround cavity of blood tumor by immunofluorescence way. After scoring the three groups by Rosenberg GA method and statisticing them. We found that olfactory ensheathing cells injected significantly reduced motor deficits compared with control groups which cerebral hemorrhage after 21 days (P <0.001). Conclusions The OECs survival in the brain of rat cerebral hemorrhage, then differentiating to ripe neuron cell and horizontal cell. The treatment of OECs transplanting for rat cerebral hemorrhage could promote recovery of motor nerve function.  相似文献   

17.
Gong C  Hoff JT  Keep RF 《Brain research》2000,871(1):1781-65
Previous studies on intracerebral hemorrhage (ICH) indicate that brain edema increases progressively in the first 24 h and remains elevated for several days. The cause of secondary brain injury and edema formation is uncertain. We hypothesized that inflammatory mediators released from the blood after cerebral hemorrhage might cause secondary brain injury and edema formation. This study investigates if, when and where inflammation occurs after ICH in rat. Immunocytochemistry for polymorphonuclear leukocyte marker (myeloperoxidase, MPO), microglia marker (OX42) and intracellular adhesion molecule-1 (ICAM-1) was performed in control, and 1, 3, 7 and 10 days after the injection of 100 microliter autologous blood in the right basal ganglia. Double labeling immunohistochemistry was used to identify ICAM-1 positive cells. The results show that an inflammatory response occurred in and around the blood clot after ICH, characterized by the infiltration of neutrophils and macrophages as well as activation of microglia. ICAM-1 immunoreactivity was observed in blood vessels adjacent to the clot, as well as in activated microglia and neurons in the ipsilateral hemisphere. The present study demonstrates there is an inflammatory response in the brain after ICH. Infiltrating leukocytes and activated microglia may release cytotoxic mediators contributing to secondary brain injury.  相似文献   

18.
急性脑卒中后就医时间与预后的关系   总被引:6,自引:0,他引:6  
目的:探讨急性脑卒中发病后至就医时间与临床疗效的关系。方法:对1092例急性脑卒中患者按病因分成四类型,每类型按就医时间分为≤24h或>24h二组。并分析就医时间与临床疗效的关系。结果:动脉血栓性脑梗死,脑栓塞和脑出血>24h组,总有效率明显低于≤24h组,差异有显著性(P<0.05);脑栓塞和脑出血无变化者出明显增多,有显著性差异(P<0.05),而动脉血栓性脑梗死无变化者两组差异不显著(P>0.05);血栓性脑梗死>24h组病死率明显高于≤24h组,有显著性差异(P<0.05),而脑栓塞和脑出血两组病死率虽有差异,但不显著(P>0.05),蛛网膜下腔出血两组对比后,其总有效率和无变化者虽无显著性差异(P>0.05),但≤24h组病死率明显低于>24h组,并有显著性差异(P<05),结论:及早发现和及早治疗急性脑卒中是提高疗效和降低病死率的重要措施。  相似文献   

19.
目的研究血浆神经元特异性烯醇化酶(NSE)在脑出血急性期的变化及意义。方法采用随机方法分实验组、对照组.实验组制造免脑出血模型检测脑组织水含量及不同时点血浆NSE浓度,与对照组比较。结果实验组免48h后脑组织水含量;6、24、48h血浆NSE浓度与对照组比较存在显著性差异(P〈0.05)。结论脑出血后血浆NSE浓度发生动态变化,在出血古24h达高峰。脑出血急性期NSE升高与脑损伤、脑水肿之间存在相关性,提示NSE可作为脑损伤的监测指标。  相似文献   

20.
Early intervention after acute ischemic stroke is essential to minimize brain cell injury. Although reperfusion of the ischemic brain is the treatment of choice for acute stroke, reperfusion itself may cause additional injury. The inflammatory cascade, characterized in part by early leukocyte interaction with endothelium, may contribute to this additional injury to blood vessels and surrounding brain tissue, extending the area of infarction. The selectin family of adhesion molecules mediates the initial, rolling and tethering of leukocytes to endothelium. P-selectin is rapidly expressed on ischemic endothelium in the brain vasculature, and L-selectin is expressed on leukocytes. Blocking the selectin-mediated tethering step may limit the inflammatory component of reperfusion injury in the brain. Fucoidin (FCN), a competitive inhibitor of P- and L-selectin, has been reported to decrease leukocyte accumulation during reperfusion of other organs. The effect of both leukocyte and endothelial selectin inhibition after cerebral ischemia and reperfusion has not been previously examined. The purpose of this study was to determine the effects of selectin adhesion molecule blockade on cerebral infarction size and neurological function after middle cerebral artery occlusion and reperfusion (MCAO-R) in the rat. MCAO was induced using the filament method. All animals were subjected to 4 h of MCAO and 24 h of reperfusion. After 24 h, brains were analyzed for size of infarction. Neurological function was assessed during stroke and 24 h after reperfusion. Two groups were studied, an untreated control group (n = 9) and a group treated with the selectin inhibitor, fucoidin (25 mg kg(-1)) (n = 9). We found that selectin blockade significantly reduced cerebral infarction size by 50% (p < 0.05) and improved neurological function (p < 0.05). In addition, a trend toward decreased cerebral edema was demonstrated with selectin inhibition. These results indicate that treatment of the blood and the endothelium with a selectin anti-inflammatory agent is protective after focal stroke and reperfusion in the rat.  相似文献   

设为首页 | 免责声明 | 关于勤云 | 加入收藏

Copyright©北京勤云科技发展有限公司  京ICP备09084417号