瑞舒伐他汀与阿托伐他汀对急性脑梗死患者血脂、血清超敏C反应蛋白及颈动脉粥样硬化斑块作用的比较

目的比较瑞舒伐他汀与阿托伐他汀对急性脑梗死患者血脂、超敏C反应蛋白(hs-CRP)及颈动脉粥样硬化斑块的影响。方法在标准缺血性脑卒中治疗的基础上,瑞舒伐他汀组加用瑞舒伐他汀10mg/d,阿托伐他汀组加用阿托伐他汀片20 mg/d,治疗6个月。于治疗前及治疗后6个月,检测患者血脂、hsCRP水平,颈动脉超声检查颈动脉粥样硬化斑块情况。结果与治疗前比较,瑞舒伐他汀组与阿托伐他汀组6个月时总胆固醇(TC)、三酰甘油(TG)、低密度脂蛋白胆固醇(LDL-C)和hs-CRP水平均显著降低(均P0.05)。6个月时,瑞舒伐他汀组TC、TG、LDL-C及hs-CRP水平显著低于阿托伐他汀组及对照组(均P0.05)。3组间治疗前内-中膜厚度(IMT)差异无统计学意义;与治疗前及对照组比较,瑞舒伐他汀组与阿托伐他汀组6个月时IMT及低回声斑块比率显著降低,高回声斑块率显著增高(均P0.05)。瑞舒伐他汀组、阿托伐他汀组及对照组患者第6个月的NIHSS评分及mRS评分均显著低于治疗前(均P0.05)。治疗前及治疗后6个月时,3组间NIHSS评分及mRS评分差异无统计学意义。结论瑞舒伐他汀与阿托伐他汀能显著降低急性脑梗死患者血脂及血清hs-CRP水平,抑制动脉粥样硬化斑块的形成。瑞舒伐他汀的降脂及抗炎作用比阿托伐他汀更强。     

瑞舒伐他汀对脑梗死患者超敏C反应蛋白及颈动脉粥样硬化的影响

目的探讨瑞舒伐他汀对脑梗死患者超敏C反应蛋白及颈动脉粥样硬化的影响及疗效。方法 80例脑梗死患者随机分为观察组(常规治疗+瑞舒伐他汀)和对照组(常规治疗)各40例。比较2组的疗效以及治疗前后hs-CRP、颈动脉粥样硬化斑块情况。结果观察组治疗后的总有效率明显高于对照组(P<0.05),且治疗后观察组hs-CRP水平均有明显下降,明显低于对照组(P<0.05);同时观察组检查出的颈动脉粥样硬化斑块数明显少于对照组,组间比较差异有统计学意义(P<0.05)。结论瑞舒伐他汀对脑梗死患者除提高疗效,且还具有抗炎、逆转斑块的作用,值得临床应用。     

瑞舒伐他汀与辛伐他汀治疗缺血性脑卒中的疗效比较

目的探讨瑞舒伐他汀与辛伐他汀治疗缺血性脑卒中的疗效。方法选取我院缺血性脑卒中患者90例,随机分为2组,观察组45例在基础治疗基础上加用瑞舒伐他汀,对照组45例在基础治疗基础上加用辛伐他汀,比较治疗前与治疗3个月后患者空腹静脉血中总胆固醇(TC)、甘油三酯(TG)、低密度脂蛋白胆固醇(LDL-C)、高密度脂蛋白胆固醇(HDL-C)及超敏C反应蛋白(hs-CRP)的变化。观察2组不良反应。结果治疗后2组TC、TG、LDL-C、hs-CRP水平均显著低于治疗前,HDL-C水平显著高于治疗前,且瑞舒伐他汀组变化幅度更大,差异均有统计学意义(P<0.05)。瑞舒伐他汀组与辛伐他汀组的缺血性脑卒中复发率分别为11.11%(5/45)和24.44%(11/45),2组比较差异有统计学意义(P<0.05)。观察组不良反应较轻微,与对照组相比,差异有统计学意义(P<0.05)。结论瑞舒伐他汀与辛伐他汀对于缺血性脑卒中患者均有很好的降脂及抗炎作用,且不良反应情况类似,但瑞舒伐他汀效果更为显著且复发率更低。     

阿托伐他汀对急性脑梗死患者血清超敏C反应蛋白及一氧化氮水平的影响

目的研究阿托伐他汀对急性脑梗死(ACI)患者血清超敏C反应蛋白(hs-CRP)及一氧化氮(NO)水平的影响。方法将60例ACI患者随机分为阿托伐他汀组(30例)和常规治疗组(30例)。阿托伐他汀组在常规治疗基础上加用阿托伐他汀20mg,每日1次,连续服用14d。在治疗前后检测血清hs-CRP和NO含量,并进行神经功能缺损程度评分(NDS)评定。结果治疗14d时两组血清hs-CRP水平均较治疗前明显下降(均P<0.01),且阿托伐他汀组较常规治疗组下降明显(P<0.01);两组血清NO水平较治疗前明显升高(均P<0.01),且阿托伐他汀组较常规治疗组升高明显(P<0.05);两组NDS评分较治疗前明显下降(均P<0.01),且阿托伐他汀组较常规治疗组下降明显(P<0.05)。结论阿托伐他汀能明显降低ACI患者血清hs-CRP水平,升高NO水平;有助于ACI患者的神经功能恢复。     

氟伐他汀对脑梗死患者颈动脉粥样斑块干预治疗的临床观察

目的观察氟伐他汀对脑梗死患者血脂、炎性因子水平及颈动脉粥样硬化的影响。方法选择90例脑梗死患者,将患者随机分为3组,每组30人:A组(对照组)采用脑梗死常规治疗,氟伐他汀治疗组B组(40mg组)和C组(80mg组),B、C组在常规治疗基础上每晚分别口服氟伐他汀40mg、80mg。所有患者均于治疗前及治疗后6个月测定血脂、超敏C反应蛋白(hs-CRP)、基质金属蛋白酶-9(MMP-9)水平及颈动脉粥样硬化情况。结果经过治疗6个月后,A组TC、TG、LDL-C、HDL-C、hs-CRP、MMP-9水平及颈动脉斑块积分、不稳定斑块数量、IMT较治疗前无明显改变(P>0.05);B、C两组TC、TG、LDL-C、hs-CRP、MMP-9显著下降,HDL-C升高,与A组比较差异有统计学意义(P<0.05),其中C组TC、TG、LDL-C、hs-CRP、MMP-9水平下降更明显(P<0.05);C组治疗后颈动脉斑块积分、不稳定斑块数量、IMTP明显减少,与A组比较差异有统计学意义(P<0.05),而B组下降不明显(P>0.05);三组NDS较治疗前均明显降低(P<0.05),三组之间差异有统计学意义(P<0.05)。结论氟伐他汀能有效降低脑梗死患者血脂、炎性因子水平,改善颈动脉粥样硬化,以80mg剂量效果显著。     

瑞舒伐他汀联合普罗布考治疗老年期脑梗死对患者颈动脉粥样硬化与血脂及血浆炎性因子的影响

目的探讨瑞舒伐他汀联合普罗布考治疗老年期脑梗死对患者颈动脉粥样硬化、血脂及血浆炎性因子的影响。方法抽取我院收治的104例老年脑梗死患者,随机分为研究组与对照组各52例。对照组采用瑞舒伐他汀治疗,研究组在对照组基础上加用普罗布考治疗。比较治疗前后2组颈动脉斑块、血脂水平、血浆炎性因子水平变化情况。结果治疗前2组高回声斑块、低回声斑块比例、颈动脉斑块面积、内中膜厚度、总胆固醇、三酰甘油、低密度脂蛋白胆固醇、高密度脂蛋白胆固醇、高敏C-反应蛋白、肿瘤坏死因子α水平比较差异无统计学意义(P0.05),治疗后2组高密度脂蛋白胆固醇无明显差异,其余各指标差异均有统计学意义(P0.05)。结论瑞舒伐他汀联合普罗布考治疗老年期脑梗死疗效确切,可有效缩小、稳定颈动脉粥样硬化斑块,抗炎、降血脂功效更加显著,具有推广价值。     

分析阿托伐他汀和瑞舒伐他汀对短暂性脑缺血发作患者颈动脉斑块的影响

目的探讨阿托伐他汀和瑞舒伐他汀对短暂性脑缺血患者颈动脉斑块的影响。方法选取2014-05—2015-05在我院接受治疗的短暂性脑缺血发作患者82例,按照随机数字表分为A组(阿托伐他汀组,n=41)和B组(瑞舒伐他汀组,n=41)。A组给予阿托伐他汀(10mg/d)联合阿司匹林(100mg/d),B组给予瑞舒伐他汀(10mg/d)联合阿司匹林(100mg/d),连续治疗6个月;比较2组治疗前后颈动脉中层厚度(IMT)和粥样硬化斑块面积,甘油三酯(TG)、胆固醇(TC)、高密度脂蛋白(HDL-C)和低密度脂蛋白(LDL-C)水平,比较2组6个月内的脑血管事件发生率。结果治疗前,2组IMT和粥样硬化斑块面积差异无统计学意义(P0.05),治疗后,B组IMT和斑块面积显著小于A组(P0.05);治疗前2组TG、TC、LDL-C和HDL-C水平差异无统计学意义(P0.05),治疗后2组TG、TC、LDL-C和HDL-C水平与治疗前差异具有统计学意义(P0.05);2组患者6个月内的脑血管事件发生率差异无统计学意义(P0.05)。结论阿托伐他汀和瑞舒伐他汀均能够很好地降低短暂脑缺血发作患者的血脂水平、降低脑血管事件的发生率,治疗剂量为10mg/d瑞舒伐他汀稳定及改善颈动脉粥样硬化斑块的疗效优于10mg/d阿托伐他汀。     

阿托伐他汀对急性脑梗死患者血清抵抗素和脂联素的作用

目的探讨急性脑梗死(ACI)患者应用阿托伐他汀治疗后血清抵抗素和脂联素水平的变化。方法选择我院2010-07—2012-06收治的ACI患者76例随机分为对照组(n=38)和观察组(n=38),对照组给予常规治疗,观察组在常规治疗基础上加用阿托伐他汀治疗,均治疗2周,观察比较2组治疗前后的血脂、高敏C反应蛋白(hs-CRP)、血清抵抗素、脂联素水平变化及不良反应发生情况。结果 2组治疗后TC、TG、LDL-C、hs-CRP水平均较治疗前明显下降,差异有统计学意义(P<0.05);治疗后观察组较对照组下降更显著,差异有统计学意义(P<0.05);2组治疗后HDL-C水平比较,差异无统计学意义(P>0.05)。2组治疗后血清抵抗素明显下降,脂联素水平明显升高,2组治疗前后比较,差异有统计学意义(P<0.05);观察组治疗后比对照组改善明显,2组治疗后比较差异有统计学意义(P<0.05)。2组不良反应发生率比较,差异无统计学意义(P>0.05)。结论阿托伐他汀可有效降低ACI患者的血脂及hs-CRP,明显改善血清抵抗素和脂联素水平,防止形成动脉粥样硬化性脑梗死。     

瑞舒伐他汀对脑梗死合并颈动脉粥样硬化患者神经功能缺损及血清炎性因子水平的影响

目的观察瑞舒伐他汀对脑梗死合并颈动脉粥样硬化患者神经功能缺损及血清炎性因子水平的影响。方法 180例脑梗死合并颈动脉粥样硬化患者随机分为成瑞舒伐他汀治疗组(他汀治疗组)和常规治疗组,每组90例。两组患者均给予脑梗死常规治疗,他汀治疗组患者加用瑞舒伐他汀钙10 mg/d,连续6个月。在治疗前和治疗后6个月进行美国国立卫生研究院卒中量表(NIHSS)评分,观察不良反应;分别采用速率散射比浊法和放射免疫分析法测定血清超敏C反应蛋白(hs-CRP)、白细胞介素6(IL-6)水平。结果治疗后,他汀治疗组的NIHSS评分和血清hs-CRP、IL-6水平明显低于治疗前及常规治疗组(P0.05~0.01)。他汀治疗组治疗期间出现恶心、轻微上腹部不适4例。结论瑞舒伐他汀对脑梗死合并颈动脉粥样硬化患者有抑制炎性因子、减低神经功能缺损程度,促进神经功能恢复的作用。     

普罗布考联合阿托伐他汀对脑梗死患者血清hs-CRP、ox-LDL、MMP-9水平及颈动脉斑块的影响

目的探讨普罗布考联合阿托伐他汀对急性脑梗死患者血清高敏C反应蛋白(high sensitivity C-reactive protein,hs-CRP)、氧化型低密度脂蛋白(oxidized low-density lipoproteins,ox-LDL)及基质金属蛋白酶-9(marix metalloproteinase-9,MMP-9)水平和颈动脉斑块的影响。方法选择196例急性脑梗死患者为研究对象,入院查颈动脉彩超提示存在动脉硬化斑块,随机分为两组,常规治疗组98例,予阿托伐他汀(20 mg/d);联合治疗组98例,予阿托伐他汀(20 mg/d)、普罗布考(500 mg/d)联合治疗。两组患者分别于治疗前、治疗后1、6、12个月检测血清hs-CRP、ox-LDL及MMP-9水平和观察治疗前、治疗后12个月颈动脉内中膜厚度(IMT)、斑块面积及斑块数量变化。结果 1与治疗前比较,两组治疗后1个月、6个月、12个月血清hs-CRP和MMP-9水平明显下降,差异有统计学意义(常规组:t=10.157,13.619,16.211和t=33.684,48.563,47.951,联合组:t=14.662,23.586,28.179和t=47.023,50.239,50.774,P均0.01),ox-LDL水平在联合治疗组治疗后1个月、6个月、12个月呈显著下降,差异有统计学意义(t=4.592,5.011,5.892,P均0.01),而在常规治疗组虽呈下降趋势,但差异无统计学意义(P0.05)。治疗后相同时间点比较,hs-CRP、ox-LDL和MMP-9水平联合治疗组低于常规治疗组,差异有统计学意义(t=7.655、5.271、2.492,t=4.927、3.772、4.673和t=16.862、4.251、2.045。P0.01或P0.05)。2治疗前,两组IMT值、斑块面积和斑块数量差异无统计学意义(P0.05);治疗12个月后,与常规治疗组比,联合治疗组IMT值及斑块面积均下降,斑块数量减少,差异有统计学意义(t=6.117,3.290,2.158,P均0.05)。结论普罗布考联合阿托伐他汀可分别从降低hs-CRP、ox-LDL及MMP-9水平,具有更强的抗氧化、逆转和稳定斑块作用。     

鼠神经生长因子联合瑞舒伐他汀治疗老年糖尿病周围神经病变临床观察

目的观察和评价鼠神经生长因子(mNGF)联合瑞舒伐他汀治疗糖尿病周围神经病变(DPN)的疗效。方法67例老年DPN患者随机分为3组A组(n=23)给予甲钴胺治疗,B组(n=22)给予甲钴胺+鼠神经生长因子治疗,C组(n=22)给予甲钴胺+鼠神经生长因子+瑞舒伐他汀治疗,共4周;观察各组患者治疗前后的多伦多神经症状评分(TCSS)、神经传导速度(NCV)以及肝功能和血脂变化。结果3组治疗后均取得TCSS下降和NCV增加的显著改善(P<0.05),其中C组较A、B组改善程度更优,差异具有统计学意义(P<0.05)。结论联合使用mNGF和瑞舒伐他汀治疗老年DPN可能获得显著疗效。     

普罗布考对脑梗死患者急性期血清MMP-9水平的影响

目的 观察普罗布考对脑梗死患者急性期血清基质金属蛋白酶9（matrix metalloproteinases9，MMP-9）水平的影响。方法 采用自身对照和组间对照，将62例急性期脑梗死患者分为2组，其中普罗布考组（32例），常规治疗组（30例），用酶谱法分别测定治疗前后血清MMP-9水平的变化。结果 （1）普罗布考组治疗2周后血清MMP-9水平较治疗前明显降低（P〈0．05），而常规治疗组治疗前后血清MMP-9水平无明显差异（P〉0．05）；（2）治疗2周后普罗布考组血清MMP-9水平较常规治疗组明显降低（P〈0．05）。结论 普罗布考能降低脑梗死患者急性期血清MMP-9水平，可能因此抑制了血-脑屏障的早期开放和脑水肿，从而减轻缺血性脑损伤，防止脑梗死出血转化和再发。     

Cerebral density and perfusion measured among heart disease patients with and without stroke

Abstract

This' investigation was designed to clarify the chronic effects of cardiogenic emboli on cerebral perfusion and tissue densities within remaining noninfarcted brain. Local cerebral perfusion and tissue densities were measured by xenon-contrasted CT scanning and compared by cross-sectional designs among normal volunteers without heart disease (Group C, n - 44), normal volunteers with heart disease (Group N, n =20), patients with heart disease and lacunar infarctions (Group L, n = 31) and patients with heart disease associated with cardiogenic cerebral embolism (Group E, n = 12). In Group E, remaining cortical and subcortical gray and white matter perfusion were reduced compared to Groups C and N (p = 0.01), but did not differ from Group L, who had similar profiles of risk factor for stroke. In Group E, perfusion was reduced within the thalamus ipsilateral to cortical infarctions (p <0.05). There were no differences in remaining tissue densities between Groups E and L. It is concluded that reduced cerebral perfusion in noninfarcted regions among patients with cardiogenic emboli appears to be related to atherosclerosis of small cerebral vessels in a similar manner to patients with lacunes, but thalamo-cortical disconnections also contribute to cerebral hypoperfusion. [Neurol Res 1995; 17: 377-383]     

First night effect in children and adolescents undergoing polysomnography for sleep-disordered breathing.

OBJECTIVE: To establish whether there is a first night effect (FNE) in children and adolescents with suspected obstructive sleep apnoea undergoing polysomnography (PSG) and whether this affects sleep and breathing, furthermore, to determine the extent to which age may influence the sleep and cardiorespiratory parameters. METHODS: One hundred and thirty-one children and adolescents (age classes-A: 2-6 years n=37; B: 7-12 years n=60; C: 13-17 years n=34) underwent PSG on 2 consecutive nights (I and II) under identical conditions for suspected sleep-related respiratory disorders. One hundred and five patients including 3 patients with obstructive sleep apnoea syndrome (OSAS) treated by adenotonsillectomy and 18 OSAS patients receiving nCPAP-therapy had no PSG-abnormalities (Group 1-A: n=28; B: n=53; C: n=24). A further 26 patients (Group 2) had clinically and polysomnographically confirmed untreated OSAS (A: n=9; B: n=12; C: n=5). RESULTS: There were no statistically significant differences between children with no PSG-abnormalities (Group 1) and those with OSAS (Group 2) in terms of sleep parameters (arousal indices excluded), oxygen saturation (SaO(2)) and heart rate (HR), and these parameters have, therefore, been pooled for the entire group (n=131) in the 3 age classes A, B and C. In the second and third age classes, sleep efficiency on the first night was reduced. In all age classes, there was significantly more wakefulness during the first night. In the second and third age ranges, the proportion of NREM 1 in the first night was significantly higher, with a correspondingly reduced proportion of NREM 4 in the third age group. In all age classes, REM sleep was significantly less during the first night, but REM latency was comparable on both nights. On the first night, the mean HR was higher.There were significant differences in apnoea/hypopnoea-index (AHI), electroencephalogram (EEG)-arousal-index (AI) and motoric arousal index (jerk index, JI) between Groups 1 and 2. In neither group, were there any significant differences in AHI, mean SaO(2) or number of EEG-arousals between nights 1 and 2. Only in the age class A, in Group 2 (n=9) was the number of motoric arousals significantly higher on the first night.Comparison of the age classes A, B, and C revealed that most polysomnographic parameters were age-dependent. Increasing age was found to correlate with a higher proportion of NREM 1, especially on the first night. Also, there was an age-dependent increase in NREM 2 on both nights, a decrease in NREM 3 on the first night, and a decrease in NREM 4 on both nights. In older children, we also found a lower proportion of REM sleep on the first night and a lower HR on both nights. In Group 1, we found a lowered AHI, AI and JI (for JI significant only on the first night) in older patients. No such age dependence of AHI, AI and JI was seen in OSAS patients (Group 2). CONCLUSIONS: In children and adolescents, there is an FNE comparable with that described in adults. In OSAS children and also in children with no PSG-abnormalities, there is night-to-night-variability in sleep parameters, but not in respiratory parameters. An adaptation night is, therefore, necessary when sleep architecture is to be studied, but not when only the nocturnal respiratory pattern is investigated. Sleep parameters, HR and arousal indices are all age-dependent.     

急性脑梗死患者血清HMGB1、OPG和MIF水平的变化及PAS三联疗法的干预作用

目的 探讨急性脑梗死患者血清高迁移率族蛋白BI( HMGB1)、骨保护素(OPG)及巨噬细胞移动抑制因子(MIF)水平的变化以及普罗布考、阿司匹林、他汀类药物(PAS)三联疗法对其干预作用.方法 选择150例急性脑梗死患者,根据颈动脉超声检查结果分为颈动脉稳定斑块组(50例)和颈动脉易损斑块组(100例).将稳定斑块组作为对照组,易损斑块组抽血检查后按随机数字法分为AS组50例(阿司匹林100 mg/d,阿托伐他汀20 mg/d,口服)和PAS组50例(阿司匹林100 mg/d,阿托伐他汀20 mg/d,普罗布考0.25/次,2次／d,口服).比较治疗前和治疗后4周血清HMGB1、OPG和MIF水平.结果 治疗前,易损斑块组中两亚组血清HMGB1、OPG和MIF含量均明显高于稳定斑块组,差异有显著统计学意义(均P＜0.01);两亚组中血清HMGB1、OPG和MIF含量差异无统计学意义(均P＞0.05).治疗后4周,PAS组中血清HMGB1,OPG和MIF含量均明显低于AS组,且各指标下降幅度均高于AS组,差异有显著统计学意义(均P＜0.01).结论 血清HMGB1、OPG和MIF均参与脑梗死患者动脉粥样硬化的进程,可作为评估颈动脉粥样硬化斑块不稳定性的预测因子,PAS三联疗法可有效降低其血清浓度,具有更强的抗炎作用,可提高易损斑块的稳定性.     

普罗布考对急性期缺血性卒中患者血清MMP-9抑制作用的相关研究

目的 探讨普罗布考对缺血性卒中患者急性期血清基质金属蛋白酶-9（matrix metalloproteinases-9,MMP-9）水平的影响。方法 采用自身对照和组间对照,随机将82例急性期缺血性卒中患者分为两组：普罗布考组（42例）和常规治疗组（40例）,采用酶联免疫吸附双抗夹心测定法分别测定治疗前后血清MMP-9水平的变化。结果 （1）普罗布考组治疗前血清MMP-9水平为399±85ng/ml,治疗两周后血清MMP-9水平为174±56ng/ml,较治疗前明显降低（P<0.05）;而常规治疗组治疗前血清MMP-9水平为401±62ng/ml,治疗两周后血清MMP-9水平为353±90ng/ml,治疗前后无统计学差异（P>0.05）;（2）治疗两周后普罗布考组血清MMP-9水平较常规治疗组明显降低（P<0.05）。结论 普罗布考能降低急性期缺血性卒中患者血清MMP-9水平,从而减轻缺血性脑损伤,防止缺血性卒中出血转化和再发。     

阿司匹林抵抗的危险因素分析和临床干预

目的探讨脑梗死患者阿司匹林抵抗的危险因素,研究阿司匹林抵抗者抗血小板药物调整后阿司匹林抵抗的发生情况及预后。方法选取269例新发脑梗死患者,口服阿司匹林100 mg/d,经血栓弹力图筛选出阿司匹林抵抗者90例,分析其危险因素,并将其随机分为3组:A组口服阿司匹林200 mg/d;B组口服阿司匹林100 mg/d+氯吡格雷75 mg/d;C组口服阿司匹林100 mg/d。1 m后复测血栓弹力图,比较血小板抑制率的变化。随访12 m观察血管事件和死亡的发生情况。结果阿司匹林抵抗的发生率为33.5%。单因素分析显示,阿司匹林抵抗组(AR)与阿司匹林敏感组(AS)年龄比较差异有统计学意义(P=0.029);Logistic回归分析显示,年龄是脑梗死患者阿司匹林抵抗的危险因素(OR=1.026,95%CI 1.002 1.049,P=0.030)。A组和B组患者AA诱导的血小板抑制率明显升高(P0.05),且B组患者血小板抑制率升高更明显;C组患者AA诱导的血小板抑制率较前无明显改变(P0.05)。随访12 m后3组患者总体缺血性事件发生率比较差异有统计学意义(P=0.002),C组总体缺血性事件发生率明显高于A组和B组;3组患者出血性事件发生率比较差异无统计学意义(P0.05)。结论年龄是脑梗死患者阿司匹林抵抗的危险因素;阿司匹林加量或联合氯吡格雷治疗可以有效改善阿司匹林抵抗现象,并可减少或避免缺血性事件发生。     

The association of hyperglycemia with cerebral edema in stroke

A retrospective review of stroke patients admitted to our hospital revealed 39 patients diagnosed as suffering an acute completed ischemic stroke who also had had fasting (AC) serum glucose determinations and sequential computer tomography (CT) studies. The patients were divided into three groups on the basis of mean AC serum glucose: Group 1 (n = 12) mean serum AC glucose greater than 150 mg/dl; Group 2 (n = 13) mean serum AC glucose 100-150 mg/dl; and Group 3 (n = 14) mean serum AC glucose less than 100 mg/dl. CT scans performed on each patient were studied for the presence of midline shift and/or ventricular compression, which were interpreted as evidence of cerebral edema. The three groups were comparable with respect to mean age, average mean arterial blood pressure and initial infarct size. Our results show that in Group 1, 42% of the patients died within the first week following their CVA with clinical evidence of transtentorial herniation confirmed by CT or autopsy. In contrast, none of the Group 3 patients died and only one showed radiological evidence for cerebral edema. Group 2 patients showed intermediate mortality and evidence of cerebral edema. These trends were statistically significant at p less than 0.005. In addition, the combined hyperglycemic group (1 and 2) had a significantly higher rate of development of hypodensity on CT (p less than 0.05) than the normoglycemic group. Our findings suggest that patients with hyperglycemia in association with their CVA develop more pronounced cerebral edema and have a worse clinical outcome. Possible pathophysiological mechanisms that may underlie this observation are discussed.     

Hemorrhagic transformation following tissue plasminogen activator in experimental cerebral infarction

The effect of an intravenous infusion of recombinant tissue plasminogen activator on hemorrhagic transformation early after middle cerebral artery territory ischemia was studied in an established awake nonhuman primate (baboon) model. Following 3 hours' occlusion of the middle cerebral artery and 30 minutes' reperfusion in each of 30 baboons, a 60-minute infusion of recombinant tissue plasminogen activator (at three doses: Group A, 0.3 mg/kg, n = 6; Group B, 1.5 mg/kg, n = 6; Group C, 10 mg/kg, n = 6) or normal saline (n = 12) was undertaken. The frequency and volume of intracerebral hemorrhage, the volume of infarction, and clinical alterations were determined by computed tomography at 24 hours and 10 days, neuropathology at 14 days, and serial daily neurologic evaluations, respectively. Peripheral (nonintracranial) hemorrhage (Group A, p = 0.46; Group B, p = 0.015; Group C, p = 0.002) and peak plasma tissue plasminogen activator levels varied directly with the dose of recombinant tissue plasminogen activator. Petechial hemorrhagic infarction was a common finding among the 30 baboons. No significant differences in the incidences or volumes of infarction-related hemorrhage were apparent in any group compared with the respective saline-treated baboons. In pooled data, no significant relation between the volume of hemorrhage and the volume of infarction could be established. We conclude that the incidence and severity of hemorrhagic transformation are not related to infarction size and that recombinant tissue plasminogen activator does not increase the incidence or severity (volume) of hemorrhage when given early (less than or equal to 3.5 hours) after the onset of focal cerebral ischemia in this model.     

PAS三联疗法对急性脑梗死患者血脂、血清sCD40L及MMP-9水平及颈动脉易损斑块稳定性的影响

目的 探讨普罗布考、阿司匹林、他汀类药物(PAS)三联疗法对急性脑梗死患者血脂、血清超敏C-反应蛋白(hs-CRP)、可溶性CD40配体(sCD40L)及基质金属蛋白酶-9(MMP-9)水平的影响,观察其对颈动脉易损斑块稳定性的影响.方法 根据颈动脉超声检查结果分为颈动脉稳定斑块组(n=45)和颈动脉易损斑块组(n=90).将稳定斑块组作为对照组,按随机数字法将易损斑块组分为AS组(n=45,阿司匹林100mg/d,阿托伐他汀20mg/d,口服)和PAS组(n=45,AS基础上加用普罗布考片,0.25/次,2次/日,口服).比较治疗前后血脂、血清hs-CRP、sCD40L和MMP-9水平;观察治疗前后颈动脉内-中膜厚度(IMT值)、斑块Crous积分及斑块回声变化.结果 治疗后4w,两组中TG、TC、LDL-C、血清hs-CRP、sCD40L和MMP-9水平均下降,PAS组中各项指标下降幅度均大于AS组,差异具有显著性(P均＜0.01);治疗后12个月,两组IMT值和斑块Crous积分较治疗前减少,且PAS组两项指标低于AS组,PAS组低回声斑块回声增强例数高于AS组(P均＜0.01).结论 PAS三联疗法是一种安全有效的治疗方法,具有更强的降脂抗炎作用,可逆转和稳定斑块.