沙土鼠短暂性全脑缺血后海马CA1区星形细胞反应及亚低温的影响

目的 研究沙土鼠短暂性全脑缺血后海马ＣＡＩ区星形细胞反应及亚低温的影响。方法 阻断沙土鼠双侧颈总动脉２０分钟造成完全性脑缺血模型。实验动物被随机分为假手术组,缺血再灌流组、亚低温治疗组。免疫组化法用来标记星形胶质细胞。结果 缺血后再灌注１～３天,海马ＣＡＩ区ＧＦＡＰ阳性的星形细胞逐渐增加,至再灌注第７天仍明显高于假手术组。在低温处理的动物,星形细胞反应受到显著抑制。结论 在缺血性脑损伤的发展过程中     

亚低温干预联合青皮升压对局灶性脑缺血再灌注损伤的保护作用及相关机制探讨

目的观察中药青皮联合亚低温干预对大鼠局灶性脑缺血再灌注模型的保护作用及对脑梗死灶周边葡萄糖利用率（LCGU）的影响，同时探讨其相关的脑保护机制。方法将64只实验大鼠随机分为对照组、青皮升压组、亚低温组及亚低温＋升压组。将上述4组大鼠制成局灶性脑缺血再灌注模型，其中青皮升压组于缺血再灌注后给予升压干预，亚低温组于缺血再灌注后给予亚低温治疗，亚低温＋升压组于缺血再灌注后同时给予升压及亚低温处理，对照组则未给予特殊处理。观察各组实验大鼠神经功能缺损评分、脑梗死灶体积及缺血侧大脑半球梗死灶周边区LCGU水平的变化情况。结果青皮升压组、亚低温组及亚低温＋升压组大鼠神经功能缺损评分、脑梗死灶体积、LCGU水平均明显低于对照组（均P〈0．05）；亚低温＋升压组大鼠脑梗死体积、LCGU水平明显低于青皮升压组及亚低温组（均P〈0．05）。结论升压及亚低温干预措施均对局灶性脑缺血再灌注损伤具有明显脑保护作用，两者联用具有协同功效，能进一步提高疗效，其相关治疗机制可能包括升压及亚低温协同治疗能改善缺血半暗带区局部脑血流量与LCGU不匹配的现象。     

Erythropoietin and the brain: from neurodevelopment to neuroprotection

It is now widely known that erythropoietin (Epo) does not only affect the haematopoietic system, but it can be considered a multifunctional trophic factor with an effect on the general homoeostasis of the entire organism. The recent discovery of a specific Epo/Epo-receptor system in the central nervous system (CNS) and cerebrospinal fluid, independently of the haematopoietic system, has further paved the way for new studies aimed at investigating the different sites of cerebral expression of Epo and its receptor, the regulation of their expression and, finally, the effects that this hormone has on the development and maturation of the brain. A further aim has been to investigate how it influences CNS homoeostasis and neurotransmission in adult brain. Attention has also been focused on the neurotrophic and neuroprotective function of Epo in different conditions of neuronal damage, such as hypoxia, cerebral ischaemia and subarachnoid haemorrhage, and therefore on the possibility that human recombinant Epo therapy could soon be used in clinical practice, also to limit neuronal damage induced by these diseases.     

沙土鼠短暂性脑缺血后海马CA1区细胞凋亡及亚低温的影响

目的：研究沙土鼠短暂性脑缺血后海马ＣＡ１区细胞凋亡及亚低温的治疗作用。方法：阻断沙土鼠双侧颈总动脉２０分钟造成前脑缺血模型。实验动物被随机分为假手术组、缺血－再灌注组、亚低温治疗组。海马ＣＡ１区的迟发性神经元死亡（ＤＮＤ）过程通过序列光镜观察进行研究,原位末端标记（ＴＵＮＥＬ）法用来检测死凶的ＤＮＡ片断。结果：短暂性脑缺血后,海马ＣＡ１区锥体神经元于再灌注后２～７日死亡。死亡锥体神经元的序列光镜观察没有发现早期的凋亡样改变,ＤＮＡ 断化也发生在ＤＮＤ出现之后。亚低温处理动物再灌注后２～７日,海马ＣＡ１区缺血性神经元死亡较常温处理动物显著减轻,再灌注后３～７日,海马ＣＡ１区ＤＮＡ片断化也显著减少。结论：缺血后的亚低温治疗产生了神经保护作用,而抑制神经元ＤＮＡ片断化的出现可能是其保护机制之一。     

Enhanced neuroprotective effects of basic fibroblast growth factor in regional brain ischemia after conjugation to a blood-brain barrier delivery vector

Basic fibroblast growth factor (bFGF) has minimal pharmacological effects in the central nervous system in the absence of blood-brain barrier (BBB) disruption. BBB transport of bFGF occurs via an absorptive-mediated transcytosis mechanism, which is relatively inefficient. To enhance the BBB transport of bFGF, this neurotrophin was reformulated to enable receptor-mediated transport across the BBB via the transferrin receptor. bFGF was monobiotinylated and coupled to a BBB drug-delivery vector comprised of streptavidin (SA) and the OX26 monoclonal antibody to the rat transferrin receptor. The entire conjugate of biotinylated bFGF bound to the OX26-SA is designated bio-bFGF/OX26-SA. The bFGF retains receptor-binding affinity and has increased brain uptake following conjugation to OX26-SA. The bio-bFGF/OX26-SA conjugate protects cortical cell cultures against hypoxia/reoxygenation insult in a dose-dependent manner in vitro. A single intravenous injection of bio-bFGF/OX26-SA, equivalent to a dose of 25 microg/kg bFGF, produces an 80% reduction in infarct volume in the brain of rats subjected to permanent occlusion of the middle cerebral artery in parallel with a significant improvement of neurologic deficit. The neuroprotection is time-dependent, and there is a 67% reduction in stroke volume if the conjugate is administered at 60 min after arterial occlusion, whereas no significant reduction in stroke volume is observed if treatment is delayed 2 h. In conclusion, neuroprotection in regional brain ischemia is possible following the delayed intravenous injection of low doses of bFGF providing the neurotrophin is conjugated to a BBB drug-targeting system.     

复温速度对重症颅脑外伤亚低温神经保护的初步研究

目的探讨不同复温速度对重症颅脑外伤亚低温神经保护作用的影响。方法将39例亚低温治疗的重症颅脑外伤患者随机分为Ⅰ组(n=13,复温速度0.1℃/h)、Ⅱ组(n=13,复温速度0.2℃/h)及Ⅲ组(n=13,复温速度0.3℃/h)。治疗过程中动态监测颅内压、心率、血压、脉氧饱和度,每日测定血糖、血细胞分析、血气分析、凝血功能、肝肾功能、电解质,每日进行GCS评分,并于伤后3个月根据格拉斯哥预后分级(GOS)评定疗效。结果复温达36.5℃时及达标后24 hⅢ组颅内压监测(ICP)明显高于Ⅰ组,有统计学意义(P<0.05);复温达标后72 h GCSⅠ组、Ⅱ组均高于Ⅲ组,有统计学意义(P<0.05),Ⅰ组高于Ⅱ组,但无统计学意义;3个月时Ⅰ组、Ⅱ组GOS明显优于Ⅲ组(P<0.05),Ⅰ组与Ⅱ组间比较无明显差异;复温达36.5℃时及达标后24 hⅢ组血糖明显高于Ⅰ组和Ⅱ组,差异有统计学意义(P<0.05)。结论较慢的复温速度可改善脑灌注,减轻脑水肿,有效保护神经功能并改善预后。     

麻黄碱对脑缺血大鼠运动功能恢复的影响及分子机制研究

目的：研究麻黄碱对大鼠大脑中动脉闭塞(MCAO)后运动功能康复的影响，并探讨其加速神经康复的分子机制。方法：体重为220—250g的雄性SD大鼠56只，随机分为假手术组，自然恢复组和治疗组。应用Koizumi线栓法建立单侧MCAO模型。术后1周，2周，3周，4周应用横木行走试验评定运动功能改善，免疫组织化学方法检测缺血周围区生长相关蛋白(GAP-43)、突触素(SVP）表达的变化。结果：横木行走试验评分显示治疗组康复速度明显高于自然恢复组；在1，2，3周时，免疫组化光密度定量测定显示治疗组GAP-43和SYP的表达水平高于自然恢复组。结论：麻黄碱可加速脑缺血后动物的运动功能恢复速度，其机制与促进脑内神经重塑和结构重建的分子表达有关。     

对海风藤酮治疗实验性缺血再灌注脑损伤的磁共振波谱分析

目的 探讨血小板活化因子(platelet activiting factor，PAF)受体拮抗剂海风藤酮对活体实验性脑梗死大鼠脑组织氮-乙酰天门冬氨酸(NAA)及乳酸(Lactic Acid，Lac)等代谢产物的影响。方法 建立活体动物大脑中动脉栓塞再灌模型，采用磁共振波谱技术，分别对缺血再灌注组及海风藤酮、银杏苦内酯治疗组鼠脑组织NAA及Lac等代谢产物变化进行观察和比较。结果 在缺血60min再灌注1h、3h、6h海风藤酮均能有效减少脑缺血后Lac／(PCr Cr)比值的上升和NAA／(PCr Cr)比值的下降，与银杏苦内酯治疗组比较无差异。结论 海风藤酮与传统的PAF受体挂号抗剂银杏苦内酯均具有显著的缺血后脑保护作用。     

Characterization of neuroprotective effects of biphalin, an opioid receptor agonist, in a model of focal brain ischemia

Approximately 795,000 people experience a new or recurrent stroke in the United States annually. The purpose of this study was to assess the protective effect of a nonselective opioid receptor agonist, biphalin, in brain edema and infarct damage by using both in vitro and in vivo models of stroke. In an in vivo model of ischemia, biphalin significantly decreased edema (66.6 and 58.3%) and infarct (52.2 and 56.4%) ratios in mouse transient (60-min occlusion/24-h reperfusion) and permanent (6 h) middle cerebral artery occlusion models, respectively. Biphalin administration also showed decreased neurodegeneration in hippocampal, cortical, and striatal brain tissue after ischemia, evidenced by reduced Fluoro-Jade C staining. In addition, biphalin improved neurological function after stroke injury evidenced by neurological score and locomotor activity evaluation. Biphalin significantly decreased penumbral expression of Na(+), K(+), 2Cl(-) cotransporter (NKCC) and the translocation of the conventional isoforms of protein kinase C (PKC). It also reversed the activation of PKC-induced cell volume increase during ischemia in primary neuronal cell cultures exposed to 1 h of oxygen glucose deprivation. These data suggest that opioid receptor activation provides neuroprotection during stroke, and a possible explanation of this mechanism could be the inhibition of NKCC function via the regulation of PKC-dependent cell signaling.     

血清神经元特异性烯醇化酶和乳酸检测对局部亚低温脑保护作用的评价

目的　探讨血清神经元特异性烯醇化酶 (NSE)和乳酸检测对局部亚低温脑保护作用评价的意义。方法　将 4 0例脑出血患者按 1∶1配对分为治疗组 ( 2 0例 )和对照组 ( 2 0例 ) ,观察两组间神经功能缺损差异 ,检测和比较两组血清NSE和乳酸水平差异。结果　入院时两组之间欧洲卒中评分、血清NSE和乳酸检测水平比较 ,差异均无显著意义 (P >0 0 5 ) ;治疗 1周、2周时欧洲卒中评分治疗组为6 2 1± 10 8分和 70 3± 10 7分 ,对照组为 5 2 8± 10 9分和 6 0 5± 10 9分 (P <0 0 5 ) ;治疗 3、7d时血清NSE治疗组为 19 5± 3 8μg/L和 11 9± 3 4 μg/L ,对照组为 2 3 6± 3 7μg/L和 18 8± 5 5 μg/L(P <0 0 5 ) ;治疗 3、7d时两组之间血清乳酸水平差异无显著性意义 (P >0 0 5 )。结论　血清NSE检测对评价局部亚低温脑保护作用具有重要意义 ,血清乳酸对亚低温脑保护作用评价意义不明确     

脑立体定位微透析检测全脑缺血-再灌注模型羟自由基水平

目的：探讨两种供氧方式对于全脑缺血-再灌注模型脑内羟自由基水平影响。方法雄性长爪沙鼠16只,脑立体定位于右侧海马 CA1区植入微透析探针,阻断再开放双侧颈总动脉（BCAO）建立全脑缺血-再灌注模型,气管插管机械通气,随机（随机数字法）分为常压常氧治疗组（NO）和常压纯氧治疗组（HO）,每组各8只。通过微透析探针连续灌注含水杨酸钠的人工脑脊液并采样,高效液相色谱-电化学法检测微透析液中二羟基苯甲酸（DHBAs：2,3-DHBA 和2,5-DHBA）含量。结果全脑缺血阶段,DHBAs 浓度保持稳定;再灌注早期,NO 及 HO 组微透析液中 DHBAs 水平均较基础水平显著升高（P ＜0.05）,且 HO 组较 NO 组升高更为显著（P ＜0.05）,维持更长时间。结论全脑缺血再灌早期阶段注脑内羟自由基的生成水平与氧暴露环境呈正相关。     

雌激素对去卵巢沙土鼠脑缺血再灌注损伤后神经细胞凋亡的保护作用

目的:观察补充外源性雌激素对去卵巢沙土鼠脑缺血再灌注损伤后神经细胞凋亡的影响。方法:实验于2003-07／09在泰山医学院基础医学部机能学实验室进行。取雌性沙土鼠40只,随机分为假手术组、缺血再灌注组、去卵巢对照组和雌激素组4组,每组10只。①去卵巢对照组和雌激素组沙土鼠切除卵巢,其他两组仅打开腹腔不切除卵巢。②雌激素组沙土鼠切除卵巢 30 d后,肌肉注射雌二醇100μg/(kg·d),其余3组动物肌肉注射玉米油1 mL／(kg·d),共7 d。③末次给药30 min后,各组动物夹闭双侧颈总动脉7 min再灌注3 d制备脑缺血再灌注手术模型,假手术组不夹闭颈总动脉。④造模3 d后麻醉状态下处死动物取材,TUNEL法检测脑海马神经细胞凋亡密度,光、电镜观察脑海马CA1区神经细胞形态变化。结果:40只沙土鼠全部进入结果分析。①脑海马神经细胞凋亡细胞数: 缺血再灌注组和去卵巢对照组均高于假手术组[(59．9+2．6),(58．2±3．4), (25．5±4．1)个,P均<0．01],雌激素组低于缺血再灌注组和去卵巢对照组 [(40．6±3．5)个,P均<0．01],但仍高于假手术组。②光镜下脑海马CA1区神经细胞形态:缺血再灌注组、去卵巢对照组细胞排列稀疏、紊乱,细胞自溶,脱失明显,细胞及血管周围间隙扩大,细胞结构不清;雌激素组缺血性改变明显减轻。③电镜下脑海马CA1区神经细胞形态:缺血再灌注组、去卵巢对照组细胞外形不规则,线粒体肿胀,大部分膜崩解,嵴水肿明显;雌激素组神经细胞线粒体水肿明显变轻,但仍有部分膜崩解,核膜基本完整。结论:在缺乏雌激素的个体中补充雌激素能明显抑制细胞凋亡的发生, 对脑缺血再灌注损伤保护作用。     

雌激素对去卵巢沙土鼠脑缺血再灌注损伤后神经细胞凋亡的保护作用

目的：观察补充外源性雌激素对去卵巢沙土鼠脑缺血再灌注损伤后神经细胞凋亡的影响.方法：实验于2003-07/09在泰山医学院基础医学部机能学实验室进行.取雌性沙土鼠40只,随机分为假手术组、缺血再灌注组、去卵巢对照组和雌激素组4组,每组10只.①去卵巢对照组和雌激素组沙土鼠切除卵巢,其他两组仅打开腹腔不切除卵巢.②雌激素组沙土鼠切除卵巢30 d后,肌肉注射雌二醇100 μg/（kg&;#183;d）,其余3组动物肌肉注射玉米油1 mL/（kg&;#183;d）,共7 d.③末次给药30 min后,各组动物夹闭双侧颈总动脉7 min再灌注3 d制备脑缺血再灌注手术模型,假手术组不夹闭颈总动脉.④造模3 d后麻醉状态下处死动物取材,TUNEL法检测脑海马神经细胞凋亡密度,光、电镜观察脑海马CA1区神经细胞形态变化.结果：40只沙土鼠全部进入结果分析.①脑海马神经细胞凋亡细胞数：缺血再灌注组和去卵巢对照组均高于假手术组[（59.9&;#177;2.6）,（58.2&;#177;3.4）,（25.5&;#177;4.1）个,P均＜0.01],雌激素组低于缺血再灌注组和去卵巢对照组[（40.6&;#177;3.5）个,P均＜0.01],但仍高于假手术组.②光镜下脑海马CA1区神经细胞形态：缺血再灌注组、去卵巢对照组细胞排列稀疏、紊乱,细胞自溶,脱失明显,细胞及血管周围间隙扩大,细胞结构不清;雌激素组缺血性改变明显减轻.③电镜下脑海马CA1区神经细胞形态：缺血再灌注组、去卵巢对照组细胞外形不规则,线粒体肿胀,大部分膜崩解,嵴水肿明显;雌激素组神经细胞线粒体水肿明显变轻,但仍有部分膜崩解,核膜基本完整.结论：在缺乏雌激素的个体中补充雌激素能明显抑制细胞凋亡的发生,对脑缺血再灌注损伤保护作用.     

亚低温对局灶性脑缺血大鼠血管新生的影响

目的探讨亚低温对局灶性脑缺血大鼠血管新生的影响。方法采用改良的线栓法制作大鼠永久性大脑中动脉闭塞模型，将造模成功的大鼠分为常温组和亚低温组。造模后14d通过股静脉注射异硫氰酸荧光素右旋糖酐（FITC-dextran）标记微血管，结合共聚焦显微镜和3DDoctor3．5版软件分析梗死灶周围区微血管的直径、面积及血管分支数目，并采用TTC染色观察脑梗死灶体积的变化。结果脑梗死后14d，梗死侧微血管直径明显小于对侧，但是血管分支数目及面积较对侧增加，且亚低温组梗死侧微血管直径、面积及分支数目明显大于常温组梗死侧；亚低温组梗死体积也明显小于常温组，差异均具有统计学意义（P〈0.05）。结论亚低温治疗能减小脑梗死灶体积并促进脑梗死后血管新生：     

亚低温对缺血大鼠的脑保护作用与一氧化氮表达的相关性

目的:研究在尿激酶溶解脑血栓治疗过程中,亚低温对大鼠一氧化氮和一氧化氮合酶表达的影响。方法:以肾血管性高血压大鼠(renovascularhypertensivestroke-prone,RHRSP)为研究对象,用光化学法制成一侧大脑中动脉闭塞(middlecere-bralarteryocclusion,MCAO)模型,在血栓形成后应用尿激酶静脉溶栓结合亚低温治疗,以观察溶栓治疗时,亚低温对一氧化氮和一氧化氮合酶影响及对缺血半影区的保护作用。结果:亚低温治疗能明显降低MCAO大鼠溶栓治疗后脑组织中一氧化氮合酶的高表达(t=6.37,P<0.01);实验组脑组织一氧化氮合酶mRNA浓度(28±4)个/mm2与对照组(17±2)个/mm2比较(t=13.02,P<0.01)差异有非常显著性意义,降低血清(t=16.96,P<0.01)和脑组织(t=12.75,P<0.01)中一氧化氮的含量,实验组脑梗死面积(24±3)%与对照组(38±4)%比较,差异有非常显著性意义(t=6.26,P<0.001)。结论:亚低温对缺血性脑卒中的保护作用可能是通过影响一氧化氮和一氧化氮合酶的表达而实现的。     

Development and evaluation of assays for the determination of total and pancreatic amylase at 37 degrees C according to the principle recommended by the IFCC

OBJECTIVES: The aim of our study was a) to optimize assays for measurement of total (T-) and pancreatic (P-)amylase at 37 degrees C based on the principle recommended by the IFCC at 30 degrees C, b) to evaluate the analytical performance of these assays in a multicentric study and c) to establish reference intervals for serum and urine for either method. METHODS: Optimized conditions for 37 degrees C were elaborated with regard to substrate concentration, pH, inorganic additives and glucosidase activity. The cleavage pattern of the EPS substrate was studied by HPLC. Liquid ready-to-use reagents for T- and P-amylase were provided to six European laboratories. RESULTS: The assays showed good performance characteristics (median intraassay CVs 1.0% for T- and 1.3% for P-amylase, median interassay CVs 3.0% for either assay, dynamic range 15-fold URL for T- and 30-fold for P-amylase), high correlation with the previous EPS methods (r > 0.996, slope 0.43, intercept < 5 U/L) in serum, heparin plasma and urine and good analytical specificity of the P-amylase assay (residual S-amylase activity 2.4%). Serum reference ranges were found to be 28 to 100 U/L for T- and 13 to 53 U/L for P-amylase (n = 775); URLs in urine were estimated as 490 U/L or 280 U/g creatinine for males and 450 U/L or 380 U/g creatinine for females with total amylase. CONCLUSION: We believe that these assays based on the 30 degrees C IFCC recommendation represent a further improvement in amylase methodology at 37 degrees C and merit broad application in clinical routine.     

亚低温对犬心脏骤停后脑水肿及血脑屏障的影响

目的观察亚低温干预对犬心脏骤停后脑水肿及血脑屏障的影响。方法共选取16只成年健康杂种犬，将其随机分为亚低温组（n=8）和对照组（n=8），采用诱发室颤的方法导致上述2组动物心跳、呼吸骤停，随后施行脑复苏程序；亚低温组动物在心跳骤停期间给予亚低温干预。采用双抗夹心酶联免疫吸附技术测定各组动物血清S100B蛋白含量，同时观察其脑组织含水量及病理学改变。结果亚低温组动物经亚低温干预后，发现其血清S100B蛋白含量显著低于对照组（P〈0．05），脑组织含水量也显著低于对照组（P〈0．05）；2组实验动物脑标本经病理学检测后发现，亚低温组动物脑组织缺氧损伤程度明显轻于对照组。结论亚低温干预能减轻心跳骤停实验犬的脑水肿程度，改善其血脑屏障功能，从而发挥脑保护效应。     

1H磁共振波谱对局灶性脑缺血大鼠脑内代谢物变化的定量评估

背景:脑缺血后脑内代谢物会出现异常变化.目的:通过1H磁共振波谱动态观察局灶性脑缺血大鼠脑内一系列生化代谢的改变,客观反映脑缺血恢复期脑内代谢产物的变化规律.设计:随机对照实验.单位:重庆医科大学附属第一医院的神经内科和放射科.材料:实验于2004-04/07在重庆医科大学附属第一医院放射科完成,选择成年Wistar清结级大鼠24只.随机分为对照组,假手术组和脑缺血组,每组8只.方法:脑缺血组以右侧颈内动脉栓塞制作局灶性脑缺血模型.假手术组栓塞线仅插入颈内动脉未深及大脑中动脉的起始处,对照组麻醉后不作任何处理.应用GE signa Highspeed MRI 1.5T超导磁共振波谱仪,缺血组和假手术组于术后30 min,1,3,6,12,24 h,3,7,15 d,1,2个月对脑梗死区域和对侧半球相应区域进行代谢物的波谱分析.对照组也在上述相应的时间点进行检查.主要观察指标:脑梗死区域和对侧半球相应区域乳酸、N-乙酰天冬氨酸、胆碱及肌酸代谢物的变化.结果:参加实验的动物24只,假手术组中途因麻醉过量死亡2只,脑缺血组因脑缺血后严重脑水肿死亡4只,进入结果分析18只大鼠,正常对照组8只,假手术组6只,脑缺血组4只.①正常对照组和假手术组双侧代谢物无异常改变,分布对称.②脑缺血组梗死区N-乙酰基天冬氨酸、胆碱和肌酸均于脑缺血后30 min开始升高,3～6 h逐渐降低,但梗死区与对照区N-乙酰基天冬氨酸、胆碱和肌酸没有明显差别(P＞0.05).③6 h时患侧的N-乙酰基天冬氨酸显著降低,24 h达最低水平(45.21±0.37),胆碱和肌酸于3 d降到最低(胆碱93.80±0.56,肌酸69.33±0.44),随缺血时间的延长,N-乙酰基天冬氨酸,胆碱和肌酸逐渐增加,尤其是N-乙酰基天冬氨酸增加最明显,2个月时N-乙酰基天冬氨酸较24 h增加2.5倍(112.00±0.03,45.21±0.37,t=-3.33,P＜0.05).④患侧最早于脑缺血后10 min检测到乳酸(47.27±0.21),随缺血时间的推移,脑梗死区与对应区乳酸均持续增加到1 d以上,12 h达高峰,3 d开始减少,脑梗死区乳酸明显高于对侧(66.83±0.43,44.35±0.35,t=2.739,P＜0.05),在1,2个月时乳酸没有再次升高.结论:①1H磁共振波谱能在患侧脑缺血后10 min检测到乳酸,可及早反映动物脑缺血后脑内代谢产物的改变.②1H磁共振波谱能客观定量化反映脑缺血恢复期脑内代谢物的异常.