Cerebral autoregulation is preserved in multiple system atrophy: A transcranial Doppler study.

Patients with multiple system atrophy (MSA) present large changes in blood pressure (BP) due to autonomic disturbances. We analyzed how this change may influence dynamic cerebral autoregulation (DCA). Simultaneous recordings of arterial BP (Finapres) and middle cerebral artery (MCA) blood flow velocity (BFV) (transcranial Doppler) were performed in 10 patients with MSA (61 +/- 12 yr of age) and 12 healthy volunteers (61 +/- 11 yr of age): cerebral BFV response to oscillations in mean BP was studied in the supine position by cross-spectral analysis of mean BP and mean MCA BFV. The DCA was also studied during the decrease in BP the first seconds when standing up from a sitting position by the assessment of the cerebrovascular resistance index (CR; mean BP/mean MCA BFV ratio). The MCA BFV/BP cross-spectral analysis showed a phase for the mid-frequency band (0.07-0.2 Hz) significantly larger in MSA, suggesting more active autoregulation in response to larger changes in BP. Changes in CR reflecting the rate of autoregulation, when standing did not differ between the two groups. These data suggest that dynamic cerebral autoregulation is preserved in MSA.     

创伤性迟发性颅内血肿的诊断和治疗

目的 探讨创伤性、迟发性颅内血肿的早期诊断和治疗的临床效果。方法 对22例病人的发病年龄、性别、伤因、早期诊断和治疗效果进行了回顾性分析。经过2—6个月，按GOS评定治疗效果。结果 良好者12例，中残者5例，重残者1例，植物生存者1例，死亡者3例，死亡率为14％。结论 早期诊断和治疗本病对于提高治愈率和降低死亡率至关重要，早期手术治疗本病，乃是多数病人首选的治疗方法。     

急性脑梗死超早期重组组织型纤溶酶原激活物溶栓治疗的临床研究

目的:探讨发病6h内急性脑梗死给予重组组织型纤溶酶原激活物(rt-PA)溶栓治疗的疗效及并发症,并分析预后相关因素。方法:共收集本院2001-2005年70例溶栓治疗的急性脑梗死病例,其中52例静脉溶栓,18例动脉溶栓,分析比较两组病例溶栓前后及3个月随访的ESS评分及Barthel指数结果;同时分析与预后相关的因素。结果:静脉和动脉溶栓组溶栓前及溶栓30min后ESS评分及Barthel指数迅速增加,溶栓前后分值有显著差异。1个月内颅内出血率为5.77%(静脉组)和16.67%(动脉组)。3个月时ESS评分及Barthel指数较溶栓后30min的评分有显著改善。结论:6h内动脉、静脉溶栓治疗均安全有效。     

Responses of CDKs and p53 in Delayed Ischemic Neuronal Death

Stroke is a debilitating disease that affects millions each year.While in many cases cerebral ischemic in jury can be limited by effectivw resuscitation or thrombolytic treatment,the injured neurons wither in a process known as delayed neuronal death(DND).Mounting evidence indicates that DND is not simply necrosis played out in slow motion but apoptosis is triggered.Of particular interest are two groups of signal proteins that participate in apoptosis-cyclin dependent kinases(CDKs) and p53-among a myriad of signaling events after an ischemic insult.Recent investigations have shown that CDKs,a family of enzymes initially known for their role in cell cycle regulation,are activated in injured neurons in DND.As for p53,new reports suggest that its up-regulation may represent a failed attempt to rescue in jured neurons,although its up-regulation was previously considered an indication of apoptosis.These observations thus rekindle an old quest to identify new neuroprotective targets to minimize the stroke damage.In this review,the author will examine the evidence that indicates the participation of CDKs and p53 in DND and then introduce pre-clinical data to explore CDK inhibition as a potential neuroprotective target.Finally,using CDK inhibition as an example,this paper will discuss the pertinent criteria for a viable neuroprotective strategy for ischemic in jury.     

小鼠不完全性脑缺血、再灌注时脑膜血流量的变化及尼莫地平的作用

目的：观察双侧颈总动脉阻断后脑血流的变化。方法：结扎双侧颈总动脉观察小鼠不完全性脑缺血及其再灌注时脑膜血流量的变化。结果：结扎颈总动脉后小鼠脑膜血流量在几秒钟内骤然下降，血流量较结扎前降低约８５．９％±６．４５％。同时血管中红细胞运动近停滞状态，血管再通时脑血流处于低灌注状态，血流量下降３４．４７％±１１．６９％，此时脑缺血再灌后脑组织实际上处于一种慢性缺血状态。再灌注１０ｄ后，小鼠脑海马ＣＡ１区神经细胞数明显减少。尼莫地平可以解除再灌注时的脑血流低灌状态。并防止由此所引起的脑海马ＣＡ１区神经细胞的缺失。结论：缺血后及时给予尼莫地平具有积极的治疗意义。     

心肌造影超声心动图评估心肌缺血程度的实验研究

本实验制作不同程度心肌缺血的动物模型，以声处理５％人血白蛋白为超声造影剂进行心肌灌注造影，探讨ＭＣＥ时间－强度曲线各指标与心肌缺血程度间的关系。结果表明：心肌显影的峰值强度和曲线下面积均与缺血程度呈显著负相关（相关系数分别为ｒ＝－０．９８，Ｐ值＜０．００５；ｒ＝－０．９４，Ｐ值＜０．０５），且能区分轻度、中度和重度三种程度的心肌缺血；而三项时间指标与心肌缺血程度间未发现显著性差异。本实验的初步结果表明，ＭＣＥ是一项活体评估局部心肌血流灌注的有效方法。     

羧乙基锗倍半氧化物对大鼠脑缺血再灌注损伤的保护作用

采用结扎双侧颈总动脉后再通的方法复制大鼠脑缺血再灌注损伤模型，通过测定再灌注后大鼠海马组织中脂质过氧化产物丙二醛（ＭＤＡ），超氧化物歧化酶（ＳＯＤ）与谷胱甘肽过氧化物酶（ＧＳＨ—Ｐｘ）及ＡＴＰａｓｅ的活性，观察了有机锗─羧乙基锗倍半氧化物（ＣＧＳ）对大鼠脑缺血再灌注后大鼠海马组织中ＭＤＡ水平，明显保护ＳＯＤ、ＧＳＨ─Ｐｘ、Ｎａ＋Ｋ＋─ＡＴＰａｓｅ及Ｃａ２＋─ＡＴ─Ｐａｓｅ活性。表明ＣＧＳ对大鼠脑缺血再灌注损伤具有保护作用。     

大鼠小肠缺血再灌注后血中NO,SOD浓度及肺中Bax,Bcl-2表达的改变

目的：研究大鼠小肠缺血再灌注后后血中一氧化氮（NO），超氧化物歧化酶（SOD）的浓度变化以及肺组织中Bax,Bcl-2的表达，探讨小肠缺血再灌注后对肺组织的损伤，方法：建立小肠缺血再灌注模型，分对照 ，再灌注后0，30min，1，2h,1,3,7d共8组，于各时点检测血中Bax,Bcl-2的表达情况。结果：大鼠小肠缺血再灌注后NO浓度0min明显升高，2h时降低，随后升高，7d时达高峰，SOD浓度0min明显下降，2h 时升高，随后下降，7d时达最低，Bax,Bcl-2免疫阳性细胞主要位于肺组织中血管内皮细胞和肺泡上皮细胞，再灌注0min,Bax,Bcl-2阳性细胞率增多，30min时Bax,Bcl-2阳性细胞率均升高分别为17．1％和78．1％，Bcl-2表达高于Bax，两者差别显著（P＜0．01），2h时降低，其后升高，7d时阳性细胞率达高峰分别为94．1％和83．4％，Bax表达明显高于Bcl-2，两者差异显著（P＜0．01）。结论：大鼠小肠缺血再灌注后可引起血中NO，SOD的浓度变化和Bax及Bcl-2阳性细胞在肺组织中的表达改变并可能引起肺组织细胞凋亡和损伤。