化疗药物性静脉炎及渗漏损伤的动物实验模型研究概况

化疗药物性静脉炎及渗漏损伤的动物实验模型是研究体内化疗药物性静脉炎及渗漏损伤的发病机制和评价各种治疗方法的重要条件。化疗药物性静脉炎及渗漏损伤的实验研究进展缓慢,其主要原因是缺乏理想的动物模型。依文献报道,化疗药物性静脉炎模型主要以大白兔耳缘静脉注射长春瑞滨等化疗药物为多见,化疗药物渗漏损伤模型主要以大鼠及大白兔背部皮下注射盐酸阿霉素等化疗药物为多见。文章就近年来常用的一些化疗药物性静脉炎及渗漏损伤的动物模型综述如下。     

乌苯美司的药物动力学及对实验性肿瘤转移的治疗作用

目的：探讨乌苯美司对小鼠药物动力学及与实验性肿瘤转移治疗活性间的关系。方法：用放射免疫法测定小鼠在不同给药途径下的乌苯美司血清药物动力学及观察乌苯美司对黑色素瘤肺转移模型的治疗活性。结果：乌苯美司ｉｖ的Ｔ１２较短，初始血药浓度较高。ｉｖ和ｉｍ给药后的曲线下面积较大；ｐｏ及ｉｐ则较小。不同给药途径对实验性肿瘤转移均有治疗作用。结论：乌苯美司的血清Ｔ１２较短，其治疗活性取决于冲击和高剂量的给药方式。     

The effects of intermittent administration of human parathyroid hormone (1–34) on streptozotocin-induced diabetic rats

Intermittent administration of low doses of human parathyroid hormone (h-PTH) has been reported to exhibit an anabolic effect on bone, increasing its mass. We investigated the effects of intermittent administration of h-PTH on bone changes in streptozotocin- (STZ-) induced diabetes mellitus (DM) rats by measuring bone mineral density and bone mineral contents and by bone histomorphometry. Wistar rats, 7–8 months old, were used. Osteoporosis was induced by diabetes mellitus, which was established by an intraperitoneal injection of STZ. Rats were separated into five groups: sham-injected, baseline control, vehicle-only-administered, and low-dose (6.0μg/kg) or high-dose (60.0μg/kg) h-PTH-administered groups. h-PTH or vehicle was injected subcutaneously six times a week for 4 weeks beginning 9 weeks after STZ administration. Bone mineral density and mineral contents were significantly lower in the baseline control and vehicle groups than in the control group. The PTH-administered groups showed higher values compared with both vehicle and baseline control groups. In bone histomorphometry, both bone volume and bone formation in the STZ group were markedly reduced. The h-PTH-administered rats showed increase in both bone volume and bone formation, which are related parameters, but administration of h-PTH did not alter the extent of eroded surface. Our results suggest that intermittent administration of h-PTH is effective in activating bone formation and in preventing further bone loss in osteoporosis developed by STZ-induced DM.     

大鼠实验性肝硬化时甲状腺激素水平及甲状腺形态学变化的研究

将Wistar大鼠分为三组：肝硬化组，给予四氯化碳等复合因素，给药组，除给CCl4等复合因素外，用赤栀黄合剂灌胃41天；正常组给以一般饮食及饮水。结果，与正常组及给药组相比，硬化组血T3、T4测定值低，甲状腺滤泡中胶质明显减少，滤泡细胞与胶质间空泡增多，滤泡上皮细胞内PAS阳性小滴数日增多。表明在实验性肝硬化期间甲状腺参与了抗疾病的代谢活动，其机理可能是肝硬化时肝细胞合成、转运T3，T4的蛋白质减少。运输中的T3，T4减少，活性甲状腺素不足，从而导致甲状腺代偿性功能活跃。赤栀黄合剂具有保肝，恢复甲状腺素水平的作用。     

Experimental study of spinal cord compression by epidural tumors using electron probe X-ray microanalysis and confocal laser scanning microscopy

Changes in the nerve fibers of the spinal cord were studied in rat experimental epidural tumor models. Light microscopy showed demyelinization in all with rats paraparesis and paraplegia. Cross-sectional views of nerve fibers stained with 3,3dipentyloxacarbo-cyanine iodide, obtained by confocal laser scanning microscopy, showed distorted, shrunken fibers with a low fluorescence intensity. Changes in the electrolyte contents of nerve fibers were studied by electron probe X-ray microanalysis. The K concentration in axons and the myelin sheath was increased in the paraparesis group, but was decreased in the paraplegia group. These findings suggest that, in the paraparesis group, compression of the spinal cord damaged cell membrane channels, which subsequently caused an increase in intracellular K, a decline in the action potential, and low-intensity fluorescence of nerve fibers. On the other hand, in the paraplegia group, destruction of cell membranes caused a decrease in intracellular K until it approached the extracellular level. This reduced both the action potential and the fluorescence intensity. As Ca and Mg concentrations in both axons and the myelin sheath increased in relation to the severity of neurologic damage, it appears that these electrolytes may also play an important role in damage to nerve fibers.     

三种泻心汤及其类方不同配伍对正常大鼠胃粘液成分的影响

目的:探讨半夏泻心汤及其类方不同配伍对正常大鼠粘液含量的影响.方法:用均匀设计法对半夏泻心汤及其类方进行组方药量变化,以胃粘液含量为药理学指标,对所得的药理实验数据进行逐步回归分析.结果:与胃粘液含量关联度最大的为黄连,可以显著降低其含量,其次对半夏、大枣和甘草的交互项,可增加胃粘液含量.药物之间存在复杂的交互作用.结论:均匀设计为研究类方配伍提供了一种可供参考的试验设计方法.     

MMP-9和TIMP-1在实验性肺气肿大鼠肺组织中的表达及其意义

目的研究基质金属蛋白酶(MMP-9)及其组织抑制因子(TIMP-1)在弹性蛋白酶所致肺气肿大鼠肺组织中的表达.方法雄性Wistar大鼠20只,随机分为两组:正常对照组和肺气肿模型组,每组10只.模型组大鼠气管内滴入弹性蛋白酶复制肺气肿模型.25d后,观察各组大鼠肺组织的病理改变,免疫组化方法观察肺组织MMP-9和TIMP-1中的蛋白表达情况.结果肺气肿模型组MMP-9和TIMP-1的表达与正常对照组相比明显增强(P＜0.01),且MMP-9/TIMP-1比值失衡.结论MMP-9/TIMP-1失衡在肺气肿形成中起重要作用.     

Analysis of gene expression in MOG-induced experimental autoimmune encephalomyelitis after treatment with a novel brain-penetrating antioxidant

Accumulating data from experimental studies indicate that oxidative stress has a major role in the pathogenesis of multiple sclerosis (MS). It has been suggested that local production of reactive oxygen species, probably by macrophages, mediates axonal damage in both MS patients and the mouse model experimental autoimmune encephalomyelitis (EAE). We have shown previously that our novel brain-penetrating antioxidant, N-acetylcysteine amide (AD4), reduces the clinical and pathological symptoms, including inflammation and axonal damage in myelin oligodendrocyte glycoprotein (MOG)-induced chronic EAE in mice. The aim of this study was to examine the molecular mechanism by which AD4 exerts protection in MOG-induced EAE mice. Therefore, we analyzed gene-expression profile in the spinal cords of MOG-induced chronic EAE mice and compared them with MOG-induced mice treated with AD4, using a cDNA microarray. We found that MOG treatment up-regulated genes encoding growth factors, cytokines, death receptors, proteases, and myelin structure proteins, whereas MOG- and AD4-treated mice demonstrated gene expression profiles similar to that seen in na?ve healthy mice. In conclusion, our study shows that chronic AD4 administration suppresses the induction of various pathological pathways that play a role in EAE and probably in MS.     

云纹技术在断裂分析中的应用

改进了传统的云纹数据处理方法,提出用曲面拟合方法处理云纹数据,提高了计算机处理云纹数据的效率与质量。又提出用云纹法测量J积分的技术,可望解决实际工程构件的J积分测量问题。     

辐射对豚鼠鼻黏膜组织结构及微血管的影响

目的：探讨辐射对豚鼠鼻黏膜结构及微血管的损伤。方法：选择健康豚鼠84只，随机分为对照组（12只）及照射组（72只）。均在同样条件下喂养。将照射组豚鼠置于直线加速器射线内照射，每周1次，每次照射5Gy，计3周，总剂量15Gy，建立辐射损伤动物模型。分别于照射后0．5、1.0、2．0、3．0、5．0、6．0个月处死动物12只，随机取6只做鼻腔黏膜微血管铸型，另6只做病理检查。对照组在假照射后6个月处死动物，随机各选6只分别做鼻黏膜微血管铸型检查和病理检查。结果：照射组豚鼠的鼻黏膜辐射后早期表现为急性炎症反应，黏膜大量坏死、脱落，电镜下见仅少部分黏膜表面还被覆着正常的纤毛结构。以后黏膜开始修复，至6个月时基本结束，但大部分黏膜失去了正常的纤毛柱状上皮结构特点，部分区域甚至代为组织转化的鳞状上皮；微血管铸型可见，早期改变为毛细血管扩张充血及血管内皮细胞肿胀，以后逐渐出现毛细血管的扭曲变形、闭塞及中断，毛细血管数量大量减少，致血液回流障碍，微静脉萎瘪。后期部分区域出现新生的毛细血管，但结构紊乱，不具备微循环的功能。结论：鼻黏膜的损伤、晚期的鳞状上皮组织转化以及鼻黏膜微循环的破坏是放疗后鼻腔功能障碍的病理学基础。