干细胞经脑脊液移植后在损伤脊髓的早期变化观察

目的观察神经干细胞经脑室注射后在损伤脊髓的早期动态变化。方法取转录有绿色荧光蛋白（GFP）基因的孕16天SD鼠胚脑海马组织，培养成神经干细胞球，注射到损伤脊髓鼠第四脑室（实验组），观察其在脊髓的存活、分化状况。结果移植细胞在脊髓表面形成细胞团。分布于损伤区头侧。细胞团的面积背侧小于腹侧；数目背侧多于腹侧。这种分布和增殖形式见于损伤脊髓正常部分和无损伤脊髓（对照组）。1周时细胞侵入损伤区，GFAP表达呈阳性。2～3周时与宿主细胞良好整合。结论移植细胞通过脑脊液能广泛分布于脊髓表面。保持黏附、增殖和分化能力。并可迁移、整合到损伤脊髓组织中。     

兔坐骨神经挤压伤的MRI与SEP对比研究

目的:探讨磁共振成像和体感诱发电位以及两者结合在坐骨神经急性挤压伤中的诊断价值。方法:24只兔按钳夹力的不同随机分为A、B两组,左后肢为损伤侧,右后肢为对照侧,建立坐骨神经急性挤压伤模型,于伤后1、2、4、8周行MR扫描,同时行双侧体感诱发电位检查。结果:损伤侧24条神经,有23条MR显示异常,诊断正确率95.8%,假阴性率4.17%(1/24);24条损伤侧坐骨神经,有22条SEP显示异常,诊断正确率91.6%,假阴性率8.3%(2/24)。MRI与SEP对神经损伤的正确诊断率无统计学差异(P>0.05)。MRI与SEP结合起来,24条损伤神经均显示异常,诊断正确率100%。结论:MR与SEP检查可无创、准确地判断神经损伤,两者结合可明显提高神经损伤的正确诊断率,重复性好,可作为神经损伤的较好诊断手段。     

The Hemodynamic Mechanisms of Lung Injury and Systemic Inflammatory Response Following Brain Death in the Transplant Donor

Brain-dead donors are the major source of lungs for transplantation. Brain death is characterized by two hemodynamic phases. Initially, massive sympathetic discharge results in a hypertensive crisis. This is followed by neurogenic hypotension. Up-regulation of pro-inflammatory mediators occurs in all organs and lung injury develops; this can adversely affect graft function post-transplantation. The mechanisms of the systemic and lung inflammation are unknown. We hypothesized that the hemodynamic changes are responsible for these inflammatory phenomena. Brain death was induced by intra-cranial balloon inflation in rats. This resulted in hypertensive crisis, followed by hypotension. There was a significant increase in blood neutrophil CD11b/CD18 expression and pro-inflammatory cytokine levels in serum and bronchoalveolar lavage, compared with control animals. Rupture of the capillary-alveolar membrane was demonstrated by electron microscopy. Elimination of the hypertensive response by α-adrenergic antagonist pre-treatment prevented inflammatory lung injury, reduced the systemic inflammatory markers and preserved capillary-alveolar membrane integrity. Correction of the neurogenic hypotension with noradrenaline ameliorated the systemic inflammatory response and improved oxygenation. We conclude that the sympathetic discharge triggers systemic and lung inflammation, which can be further enhanced by neurogenic hypotension. Management of the brain-dead donor with early anti-inflammatory treatment and vasoconstrictors is warranted.     

Pretreatment with Tongxinluo protects porcine myocardium from ischaemia/reperfusion injury through a nitric oxide related mechanism

Background The traditional Chinese medicine Tongxinluo can protect myocardium against ischaemia/reperfusion injury, but the mechanism of its action is not well documented. We examined the involvement of nitric oxide in the protective role of Tongxinluo. Methods Miniswine were randomized to four groups of seven: sham, control, Tongxinluo and Tongxinluo coadministration with a nitric oxide synthase inhibitor Nω-nitro-L-arginine (L-NNA, 10 mg/kg i.v.). Three hours after administration of Tongxinluo, the animals were anaesthetised and the left anterior descending coronary artery ligated and maintained in situ for 90 minutes followed by 3 hours of reperfusion before death. Area of no reflow and necrosis and risk region were determined pathologically by planimetry. The degree of neutrophil accumulation in myocardium was obtained by measuring myeloperoxidase activity and histological analysis. Myocardial endothelial nitric oxide synthase activity and vascular endothelial cadherin content were measured by colorimetric method and immunoblotting analysis respectively.Results Tongxinluo significantly increased the local blood flow and limited the infarct and size of no reflow. Tongxinluo also attenuated myeloperoxidase activity and neutrophil accumulation in histological sections and maintained the level of vascular endothelial cadherin and endothelial nitric oxide synthase activity in the reflow region when compared with control group. The protection of Tongxinluo was counteracted by coadministration with L-NNA. Conclusions Tongxinluo may limit myocardial ischaemia and protect the heart against reperfusion injury. Tongxinluo regulates synthesis of nitric oxide by altering activity of endothelial nitric oxide synthase.     

临床护士锐器伤调查与预防

目的探讨护士预防锐器伤的对策。方法对某所综合性医院193名护士在2004年1月~2005年6月发生的锐器伤进行问卷调查。结果46.1%护士发生锐器伤,人均1.6次;发生锐器伤的锐器主要是注射器针头(36.7%),其次是玻璃(32.4%);护士主要在掰安瓿(29.5%)、使用后处理锐器(22.3%)、安装调整针头(15.8%)、医护配合传递锐器(10.1%)等环节容易发生锐器伤;有79.1%护士发生锐器伤时未戴手套。结论护士面临锐器伤职业危险,各方应当采取对策,预防和控制锐器伤。     

TCD观察动脉瘤性SAH后脑血管痉挛的血流动力学改变

目的探讨动脉瘤性蛛网膜下腔出血(SAH)后脑血管痉挛的血流动力学改变。方法经CT、DSA证实为动脉瘤性SAH患者179例,床旁经颅超声多谱勒(TCD)在术前、术后1~3d、5~7d、9~11d、12~14d记录并分析大脑中动脉(M CA)的血流参数及频谱改变。结果M CA平均血流速度(Vm)于SAH后1~3d开始升高,5~7d、9~11d达到高峰;L I(血管痉挛指数)为3~6时预后良好;>6时可以出现神经系统功能损害,颅内压增高且有脑血管痉挛(CV S)者预后较差。结论TCD能无创、实时评价SAH后CV S的动态变化,可以推断SAH后CV S的严重程度及临床转归。     

细胞内游离Ca2+在发育中大鼠皮层神经元无镁诱导惊厥性损伤中的作用

目的: 观察细胞内游离Ca2+([Ca2+]i)在培养的不同发育阶段皮层神经元无镁诱导惊厥性损伤中的作用,探讨惊厥性脑损伤年龄依赖性的可能机制.方法:体外培养6 d、17 d的胚胎大鼠皮层神经元用无镁细胞外液处理3 h,或于无镁处理前用NMDA(N-甲基-D-门冬氨酸)受体拮抗剂或Ca2+通道阻滞剂预处理,用MTT代谢率测定的方法检测神经元损伤,以Fluo-3作标记用激光共聚焦显微镜扫描的方法检测[Ca2+]i.结果:体外培养6 d、17 d的神经元单纯无镁组MTT代谢率较同期对照组降低.应用MK-801 10 μmol*L-1、AP-5 50 μmol*L-1、尼莫地平10 μmol*L-1预处理后再给无镁处理,培养6 d、17 d的神经元MTT代谢率均不同程度高于同期单纯无镁组.培养6 d、17 d的神经元相对荧光强度之间差异有显著性,两者与基线荧光强度比较差异亦有显著性.应用上述各种拮抗剂后,[Ca2+]i改变的峰值均明显低于同期单纯无镁组.结论: 在体外不同发育阶段的神经元,短暂无镁处理诱导惊厥样放电所引起的神经元线粒体功能损伤以及[Ca2+]i改变程度不同.这种[Ca2+]i改变的年龄依赖性可能是惊厥导致神经元损伤的年龄依赖性的机制之一.NMDA受体-Ca2+通道激活是导致这种[Ca2+]i改变及神经元损伤的关键环节.     

岛状皮瓣静脉淤血再通后对大鼠全身情况的影响

目的：探讨岛状皮瓣静脉淤血再通后对全身多脏器的影响。方法：按静脉淤血时间的不同将大鼠分为4组。观察耳部微循环的改变，测量术后肿瘤坏死因子α(TNFα），白细胞介素10（IL－10）的动态变化，观察心，肺，肝，肾，小肠及耳部血管等组织结构及中性粒细胞浸润数目。结果：皮瓣原位缝合组及静脉淤血2h组，耳部微循环、TNFα、IL-10浓度基本保持不变，各脏器结构改变较轻，中性粒细胞浸润数目少。静脉淤血6、10h组，微循环，肺，小肠，血管则有明显组织学改变，大量中性粒细胞浸润其中，但心，肝，肾组织学改变较轻。TNFα浓度再灌注1h达到高峰，其后逐渐下降，IL－10浓度3h达到最低，然后逐渐上升。结论：皮瓣静脉淤血再通后可造成肺、小肠及血管器官损伤，静脉淤血时间越长，再通后则损伤程度越重。全身微循环的改变，中性粒细胞在肺、小肠中的浸润，与血管内皮细胞的粘附及细胞因子TNFα与IL－10的浓度失衡是重要的操作原因。     

尿激酶溶栓对大鼠局灶性脑缺血基质金属蛋白酶-9表达的影响

目的研究大鼠局灶性脑缺血后应用尿激酶(urokinase,UK)溶栓对基质金属蛋白酶-9(Matrix metalloproteinase-9,MMP-9)表达的影响,探讨MMP-9在UK溶栓引起的再灌注损伤及出血性转化中的作用。方法将实验动物随机分成3组进行研究(1)UK溶栓组;(2)缺血对照组;(3)假手术组。分别用免疫组织化学方法分析3组缺血后24hMMP-9的表达,对比研究两组MMP-9表达的差异性。结果缺血后24h前两组均有MMP-9的表达,但是UK溶栓组表达的程度明显高于缺血对照组;假手术组无MMP-9的表达。结论(1)缺血能导致MMP- 9的表达。(2)UK溶栓引起MMP-9表达的上调。