CAROTID SINUS HYPERSENSITIVITY IN PATIENTS REFERRED WITH POSSIBLE EPILEPSY

SUMMARY Four patients with recurrent transient loss of consciousness, all of whom had previously undergone extensive non-invasive cardiological investigations, were referred for neurological opinion. All were found to exhibit a resting bradycardia and a cardioinhibitory response to carotid sinus stimulation. All were referred for cardiological opinion but only two patients were considered by their respective cardiologists to warrant pacemaker implantation. Those who did not receive a pacemaker continue to suffer from their symptoms. The clinical management of these patients highlights an apparent divergence of opinion amongst cardiologists on the treatment of carotid sinus hypersensitivity and emphasises that, unless the ECG and blood pressure responses to carotid sinus stimulation are observed in patients with histories of unexplained episodes of altered consciousness, carotid sinus hypersensitivity will be missed as a possible cause of symptoms. The presence of unexplained bradycardia may suggest carotid sinus hypersensitivity.     

三尖杉酯碱和高三尖杉酯碱诱导人早幼粒白血病细胞的程序性死亡

体外实验证明2×1O^-7 mol·L^-1 三尖杉酯碱和 1O^-7 mol·L^-1高三尖杉酯碱与HL-60细胞作用 4 h，可诱导该细胞产生程序性死亡。提取细胞DNA进行琼脂糖凝胶电泳呈现典型的DNA 梯，同时出现细胞核染色体断裂、核固缩及细胞空泡样变等形态变化。并且在一定范围内具有作用时间和浓度依赖性，二者诱导HL-60细胞程序性死亡作用的强弱与其细胞毒作用平行。     

动脉血压改变对大鼠下丘脑后部GABA释放的影响

用推～挽灌流技术，定位灌流大鼠下丘脑后部，同时ｉｖ给予去氧肾上腺素（１５μｇ·ｋｇ·ｍｉｎ－１）和静脉输血（３ｍｌ／１００ｇ，ｗｔ）引起血压升高时，下丘脑后部γ－氨基丁酸（ＧＡＢＡ）的释放率增加，而ｉｖ给予硝普钠、氯化四氯吲哚铵和控制性失血导致血压下降时，ＧＡＢＡ的释放率减少。进一步证明下丘脑ＧＡＢＡ能神经系统参与外周动脉血压的调节，且有降压作用。     

腰椎静脉丛三维增强MR静脉成像初步研究

目的 探讨正常人腰椎静脉系统在三维增强MR静脉造影(MRV)的显示率,初步确定正常人腰椎椎管内前静脉(AIVV)的宽度范围。观察腰椎静脉系统在各种疾病情况下的表现。方法89例MR增强扫描受检者行MRV检查,其中62例为正常志愿者。分别观察不同年龄组各个腰椎节段的椎管内、外静脉显示情况。测量AIVV的宽度。观察各种疾病时椎管内、外静脉的表现。结果除L1和L2水平的左右吻合静脉外,其他各个节段41岁以上组的静脉显示率均低于40岁以下组(P<0.05)。AIVV平均宽度从L1-5逐渐增粗;年龄、性别、左右侧差异无统计学意义。AIVV全部显示的42例正常志愿者中,AIVV的平均宽度L1-L5逐渐增粗,范围在(3.9±0.6)mm-(7.9±1.2)mm;各种疾病时,AIVV可表现为正常、受压、移位或扩张。结论 三维增强MR静脉造影能满意地显示AIVV各分支及椎管外静脉的全貌,能够显示各种病变时椎静脉相应改变,对于指导临床治疗、研究椎静脉的临床意义具有潜在价值。     

uPA纤溶途径与肝纤维化

细胞外基质(extracellular matrix,ECM)过度沉积是肝纤维化的特征性表现,纤溶系统尤其是尿激酶型纤溶酶原激活剂(urokinase- plasminogen activator,uPA)所介导的纤溶途径与肝纤维化关系密切,其主要成分包括纤溶酶原、纤溶酶、纤溶酶原激活剂及其抑制剂．uPA纤溶途径位于ECM降解酶系的顶端,肝纤维化时通过uPA-纤溶酶-基质金属蛋白酶(matrix metalloproteinases,MMPs)-ECM级联机制下调ECM降解,促进ECM在肝内沉积,而且可能在肝星状细胞(hepatic stellate cell,HSC)增殖、迁移以及肝细胞再生等过程中起到重要作用．