Ligustrazine inhibits high voltage-gated Ca~(2+) and TTX-resistant Na~+ channels of primary sensory neuron and thermal nociception in the rat:a study on peripheral mechanism

Objective Ligustrazine, also named as tetramethylpyrazine, is a compound purified from Ligusticum chuanxiong hort and has ever been testified to be a calcium antagonist. The present investigation was to determine the antinoci-ceptive effect of ligustrazine and, if any, the peripheral ionic mechanism involved. Methods Paw withdrawal Latency ( PWL) to noxious heating was measured in vivo and whole-cell patch recording was performed on small dorsal root ganglion (DRG) neurons. Results Intraplantar injection of ligustrazine (0.5 mg in 25μl) significantly prolonged the withdrawal latency of ipsilateral hindpaw to noxious heating in the rat. Ligustrazine not only reversibly inhibited high-voltage gated calcium current of dorsal root ganglion (DRG) neuron in dose-dependent manner with IC50 of 1.89 mmol/L, but also decreased tetrodotoxin (TTX) -resistant sodium current in relatively selective and dose-dependent manner with IC50 of 2.49 mmol/L. Conclusion The results suggested that ligustrazine could elevate the threshold of thermal nociception through inhibiting the high-voltage gated calcium current and TTX-resistant sodium current of DRG neuron in the rat.     

神经降压素的肝细胞保护作用与Ca~（2＋）的关系

观察了神经降压素（ＮＴ）的肝细胞保护作用与Ｃａ２＋的关系。结果显示，醋氨酚使肝细胞Ｃａ２＋内流和肝脏钙含量增加，但对于线粒体Ｃａ２＋摄取及其钙含量无明显影响，表明细胞可能出现胞质Ｃａ２＋超载。若在醋氨酚之前给予ＮＴ则使肝细胞Ｃａ２＋内流明显减少，肝脏Ｃａ２＋含量有降低趋势，但线粒体钙含量显著增加。这些结果提示，ＮＴ通过减少Ｃａ２＋内流，增强线粒体贮存Ｃａ２＋的能力，部分缓解醋氨酚所致胞质Ｃａ２＋超载从而减轻细胞损伤。     

周围性面神经损伤患者对侧神经支配的研究

目的　通过测定面神经损伤患者组及大学生志愿者组面神经各分支对侧神经支配率 ,探讨周围性面肌瘫痪恢复过程中面神经对侧代偿支配的问题。方法　分别测定大学生志愿者 2 2例( 2 2侧 )及 10 8例面神经损伤患者的面神经电图对其对侧神经支配率进行分析其中损伤组又按发病原因不同 ,分为医源性损伤组、Bell氏面瘫组和创伤性损伤组 ,测试损伤支数为Ⅰ支 76支 ,Ⅱ支 81支 ,Ⅲ支 88支 ,Ⅳ支 6 6支。结果　①损伤组 3组间对侧支配率差异无显著性 (P >0 0 5 ) ;②损伤组Ⅰ、Ⅱ支对侧支配率明显高于志愿者组 (P <0 0 0 1) ;③损伤组Ⅰ支对侧支配率明显高于Ⅱ支(P <0 0 0 1)。结论　面神经损伤后 ,存在对侧神经支配功能增强的表现     

马桑内酯所致癫痫发作大鼠红细胞免疫粘附功能的研究

作者用红细胞Ｃ＿３ｂ受体花环试验和红细胞免疫复合物花环试验对马桑内酯所致癫痫发作大鼠红细胞免疫粘附功能的变化进行了观察，结果表明，癫痫组动物红细胞Ｃ＿３ｂ受体花环率明显低于对照组，而红细胞免疫复合物花环率相差不显著．提示癫痫发作可导致大鼠红细胞免疫粘附功能降低，因此在癫痫治疗中注意调整和增强患者的红细胞免疫功能具有重要意义。     

家兔化学裸露心肌标本制备及其张力-pCa关系

家兔右室乳头肌在含3mM EDTA、5mM Na_2ATP、10mM Tris、140 mM KCl的溶液中浸浴150min,其Ca~(2+)通透性显著增高。Ca~(2+)浓度为10~(-7)M时,便可产生张力,10~(-4.6)M时,张力达到最大。相对张力-pCa(Ca~(2+)浓度的负对数)关系近似一S形曲线,产生50％最大张力的Ca~(2+)(pCa_(50))约为10~(-6.6)M。同法制备的大鼠乳头肌Ca~(2+)通透性未见增高。     

急性心脑血管血栓性疾病患者血浆FⅦ：C、FⅧ：C、凝血酶原及纤维蛋白原的变化

目的检测凝血因子Ⅶ、Ⅷ、Ⅱ、Ⅰ的活性,研究其在急性心脑血管血栓性疾病中的变化.方法分别采用凝血活酶时间、部分凝血活酶时间、发色底物法及凝血酶时间法测定了急性心肌梗死(AMI)和急性缺血性脑卒中(AIS)病人血浆FⅦC、FⅧC、凝血酶原及纤维蛋白原相对活性.结果AMI病人血浆FⅦC为98.3%±36.7%,与青年组的104.0%±29.4%和老年组的114.9%±23.6%比较无明显差异(P值均＞0.05),而AIS病人为152.9%±30.3%,较青年组和老年组显著升高(P值均＜0.001).AMI病人血浆FⅧC为234.2%±57.9%,明显高出青年组的101.2%±32.6%和老年组的116.4%±35.7%(P值均＜0.001).但AIS病人FⅧC±为85.5%±32.6%,低于老年组(P＜0.05).AMI和AIS病人血浆凝血酶原活性分别为130.2%±¨.7%和128.0%±29.4%,高于青年组的108.0%±7.7%(P＜0.001和0.01)和老年组的106.1%±19.4%(P值均＜0.001).AMI和AIS病人血浆纤维蛋白原活性分别为207.2%±53.0%和174.3%±28.5%,二者均显著高于正常青年组的103.3%±¨.6%(P值均＜0.001)和老年组的143.8%±16.8%(P＜0.001和0.01).结论AMI病人FⅧC增高,AIS病人FⅧC增高;二者血浆凝血酶原和纤维蛋白原活性均高于正常水平.     

褐云玛瑙螺中枢内支配大触角肌肉神经元的分布

实验用荧光素Ｂｂ逆行追踪方法，研究了褐云玛瑙螺支配大触角肌肉活动的神经元在中枢的分布，结果表明，Ｂｂ标记神经元大多分布于同侧脑节，少量分布于侧脑节，同侧口球节，足节和侧节，Ｂｂ标记神经元大多为中小型神经元，个别属于大型神经元。     

骨髓内皮细胞无血清条件培养液对CFU-E和BFU-E生成的影响

利用本室建立的小鼠骨髓内皮细胞株作传代培养 ,收集其无血清条件培养液 ,离心超滤 ,观察分子量(MW) >1 0 0 0 0组分及分子量 <1 0 0 0 0组分对红系生成的影响。结果表明 :分子量 >1 0 0 0 0组分对CFU E和BFU E有明显刺激作用 ,且在 2 %～ 6% (V/V ,下同 )范围内集落产率随浓度增加而增加 ;而分子量 <1 0 0 0 0组分对CFU E ,BFU E有明显抑制作用 ,且在 1 0 %～ 40 %范围内集落产率随浓度增加而降低     

川芎嗪抗缺氧致脑细胞损伤作用的实验研究

目的:观察川芎嗪对缺氧状态下离体大脑皮层细胞脂质过氧化物(LRO)含量及超氧化物歧化酶(SOD)活性的影响。方法:将4～5日龄 Wistar 大鼠大脑皮层分离并制成细胞悬液(5×10~6个细胞/ml),在 CO_2培养箱内孵育2h 之后观测单纯缺氧1h(细胞悬液通以95％N_2加5％CO_2),以及预先向细胞悬液加入磷酸川芎嗪(分10~(-5)、10~(-4)和10~(-3)mol/L3个剂量组),再缺氧1h 细胞 LPO 含量与 SOD 活性的改变。结果:缺氧可使 LPO 显著增加、SOD 活性明显降低;预先加入川芎嗪能有效防止缺氧所致的 LPO 升高和 SOD 活性降低。结论:川芎嗪对缺氧致细胞脂质过氧化损伤具有保护作用,其机制可能是通过增强内源性 SOD 活性、清除氧自由基,进而降低了细胞脂质过氧化程度。     

Effects of testosterone and estradiol on anxiety and depressive-like behavior via a non-genomic pathway

Besides their known slow genomic effects, testosterone and estradiol have rapid effects in the brain. However, their impact on mood-related behavior is not clear. The aim of this study was to investigate the non-genomic pathway of testosterone and estradiol in the amygdala in relation to anxiety and depressive-like behavior. Sham-operated and gonadectomized male rats(GDX) supplemented with testosterone propionate, estradiol, or olive oil were used. Five minutes after administration, anxiety and depression-like behavior were tested. Estradiol increased anxiolytic behavior in the open-field test compared to the GDX group, but administration of testosterone had no significant effect. Besides, c-Fos expression in the medial nucleus of the amygdala significantly increased after testosterone treatment compared to the GDX group, while no significant difference was observed in the central and the basolateral nuclei of the amygdala in the testosterone-treated group compared to the GDX group. In conclusion, estradiol had an anxiolytic effect via a rapid pathway, but no rapid effect of testosterone on anxiety was found. Further studies elucidating whether the rapid effect is mediated by a non-genomic pathway are needed.