碘杂环化合物对离体豚鼠心乳头肌动作电位和收缩力的作用

采用细胞内微电极记录技术,同步观察了3,6-[二甲氨基]-二苯并碘因甲酸盐(IHC-64)对豚鼠心乳头肌细胞动作电位和收缩力的作用。50μmol/L IHC-64抑制心肌收缩力,而不影响快反应动作电位。增加IHC-64浓度,动作电位0相最大峰值(APA)、除极速率(dp/dt_(max))和复极50％和90％时程(APD_(50)、APD_(90))被明显抑制。IHC-64抑制慢反应动作电位,提高细胞外钙浓度可拮抗这种抑制。结果提示,IHC-64主要抑制慢Ca~(2+)内流,同时也部分抑制快Na~+内流,它可能是一种新型B类钙通道阻滞剂。     

Differential antagonism of the behavioral depressant and hypothermic effects of 5'-(N-ethylcarboxamide) adenosine by theobromine

The methylxanthine, theobromine (3,7-dimethylxanthine), was tested in mice, to determine whether theobromine could function in vivo as an adenosine receptor antagonist, in keeping with its reported in vitro effects as a blocker of agonist binding to the adenosine A-1 receptor. Theobromine doses, which themselves had no direct effects on spontaneous locomotor activity, completely blocked N6-cyclohexyladenosine-induced suppression of locomotor activity but were without effect on 5'-N-ethylcarboxamide adenosine (NECA)-induced decreases in motor activity. In contrast to the specific antagonism, theobromine blocked the hypothermia induced by both of these adenosine analogs. These results demonstrate that theobromine is an active in vivo adenosine receptor antagonist and that the antagonism of N6-cyclohexyladenosine sensitive systems occurs even though theobromine does not stimulate spontaneous locomotor activity. Thus, the behavioral stimulant effects of methylxanthines may be more related to effects on NECA-sensitive systems, which are not blocked by theobromine. The use of in vivo differences in the effects xanthine may provide a useful tool in the development of compounds to probe the mechanisms of caffeine induced CNS effects.     

潘生丁增强氨甲蝶呤的抗肿瘤作用

外源性核苷能抵消抗代谢药对肿瘤细胞的杀伤作用;核苷转运抑制剂潘生丁则能阻断核苷的这种抵消作用,从而增强抗代谢药的细胞毒性。本研究证明,胸苷和次黄嘌呤可明显抵消氨甲蝶呤对L1210细胞的杀伤作用,潘生丁则能有效地阻断核苷的抵消作用;潘生丁和两性霉素B合用可明显增强氨甲蝶呤对小鼠S180肉瘤的抑制作用,但不增强氨甲蝶呤对动物的毒性。提示潘生丁有可能应用于肿瘤联合化疗。     

尿流改道及膀胱重建术的现状与展望

膀胱全切术后尿液的贮存与排出一直是未能满意解决的问题。自从1852年Simon报道输尿管乙状结肠吻合以来，经过一个多世纪的不断改进与创新，特别是1982年Kock用去管重建法制作贮尿囊的可控膀胱以来，尿流改道与膀胱重建术有了跨时代的进步和发展，显地提高了患术后生活质量。     

The correlation between TNF-α, IL-6 in cervical mucous during follicular development and ovulation stimulation in different protocols

Objective To investigate the correlation between TNF-α and IL-6 levels in cervical mucous during follicular development and ovulation stimulation in different protocols.Methods 36 infertile women were set up as experimental groups,divided into CC, HMG, IVF-ET group,each group consisted of 12 infertile women and 15 women with normal menstrual cycles were choiced as control group.Cervical mucous during follicular phase, luteal phase and ovulation phase were collected.TNF-α, IL-6 levels in cervical mucous were measured by radioimmunology assay (RIA).Follicular development were monitored by transvaginal ultrasonagraphy.Results (1) TNF-α levels in cervical mucous of experimental groups and control group were periodically various among the reproductive cycle.It increased during follicular phase, reached to peak during ovulation phase, and decreased during luteal phase (P＜0.05).IL-6 levels had no obvious periodical changes.(2) Compared with CC and control group, levels of TNF-α,IL-6 in HMG and IVF-ET group were significantly higher (P＜0.05).(3) Levels of TNF-α and IL-6 in cervical mucous were positively correlated with the dominant follicle diameter (r=0.261, r=0.192 respectively,P＜0.05).(4) TNF-α and IL-6 showed positive correlation in the reproductive cycle (r=0.782,P＜0.05).Conclusions (1) TNF-α level shows a cyclic change in the reproductive cycle and peaks during ovulation,whereas IL-6 level does not.(2) TNF-α and IL-6 may play a certain role in the process of follicular development and ovulation.(3)The levels of TNF-α and IL-6 are up-regulated by gonadotrophic hormone.(4) TNF-α and IL-6 may have coordination properties and participate in the same biological effects.     

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。     

活性炭纤维在地方性氟中毒方面的应用展望

介绍了活性炭纤维（ＡＣＦｓ）的制造，特性及其应用。它具有优异的结耕与性能特征。含碳量高，比表面积大，微孔丰富，从而吸附力强，而且活性炭纤维还可制成纱、布、毡等形状，它可用于去除燃煤氟中毒区室内空气中氟化氢、二氧化硫、氧化氮、氨等污染物，利用它的高吸附性能还可较好的去除饮水中的氟化物及其他有害物质。活性炭纤维是一种新型高效吸附材料。在氟中毒防治方面有广阔的前途。     

173例支气管哮喘特异性脱敏治疗的进一步评价

对173例支气管哮喘特异性脱敏治疗的疗效及影响疗效的因素进行了分析。结果表明:显效为30.6%(53/173).有效为56.1%(97/173),无效为13.3%(23/173)。影响疗效的因素与病情的程度有关,而与年龄、病程、皮试阳性反应强弱及脱敏治疗前4个疗程内是否应用曲安缩松等无关。并对特异性脱敏治疗支气管哮喘的优缺点进行讨论。