脉冲1.338μm激光角膜损伤效应研究

目的:实验研究脉冲1.338μm激光的角膜损伤效应,确定其损伤阈值,并与10.6μm激光角膜损伤特点进行比较。方法:采用输出波长1.338μm、脉冲宽度5 ms的Nd:YAG激光为照射光源,角膜光斑直径1.7 mm,以不同剂量的激光照射新西兰白兔角膜,于照后1 h观察角膜损伤情况,统计损伤发生率,采用加权概率单位法计算损伤发生率为50%时所对应的激光剂量,即损伤阈值ED50。在1.5倍阈值剂量下比较该激光与10.6μm激光角膜损伤的特点。实验中注意观察晶状体和眼底是否有损伤。结果:脉冲1.338μm激光角膜损伤阈值为27.0 J/cm2(95%置信区间25.8～28.1 J/cm2)。阈值水平下,角膜损伤斑肉眼观察呈淡淡的灰白色,裂隙灯下可见一与角膜同厚的灰白色反光带,晶状体或视网膜正常;1.5倍阈值剂量下,角膜损伤斑为清晰的瓷白色,裂隙灯下可见一与角膜同厚的白色反光带,同时观察到晶状体前表面白色反光点,但视网膜无变化。与之相比,10.6μm激光角膜损伤在裂隙灯下仅观察到一很窄的亮白反光条,位于角膜表层。结论:脉冲1.338μm激光在光斑直径1.7 mm,脉冲宽度5 ms条件下的角膜损伤阈值为27.0 J/cm2。角膜损伤特点是,损伤斑呈灰白色或瓷白色,累及角膜全层,而10.6μm激光损伤仅累及角膜浅层。     

光化学反应诱导大鼠视网膜水肿模型

目的:通过静脉注射光敏剂Erythrosin B联合激光照射诱导大鼠视网膜水肿模型,并观察该模型中大鼠视网膜及血管形态改变.方法:大鼠尾静脉注射光敏剂Erythrosin B后,使用532nm Nd:YAG激光(1.95±0.05 mw)照射大鼠视网膜8分钟.分别于建模后第1、2、3、5、7及14天进行眼底照相、眼底荧光造影(FFA)及视网膜光学相干断层扫描(OCT)检查.并在OCT图像上测量大鼠视网膜厚度(RT).结果:眼底照相、FFA及OCT结果显示大鼠视网膜在激光照射后可立即出现血管损伤及视网膜厚度增加,但未发现视网膜血管栓塞.激光照射前RT为219±2 μm,激光照射后第1天RT即增加至283±6μm,并在第2天到达顶峰(302±7μm),之后开始下降,至第5天恢复到激光照射前水平(234±9 μm),到第14天时视网膜发生明显萎缩,RT较激光处理前减小(198±6μm).结论:这一通过光化学反应诱导的视网膜水肿模型具有可靠及可重复性,可被运用于视网膜水肿的病理学及动力学研究.     

脉冲1 064 nm激光视网膜损伤动物模型的建立

目的:建立脉冲1 064 nm Nd:YAG激光致视网膜出血性损伤及非出血性损伤动物模型,为治疗药物评价提供技术基础.方法:应用自由振荡脉冲及调Q脉冲1 064 nm激光照射青紫蓝灰兔视网膜,通过在光路中加人透镜获得直径200μm眼底光斑,加入衰减片改变角膜入射激光能量.照射即刻对损伤应用检眼镜进行实时观察,并用眼底相...     

地塞米松对过氧化氢体外氧化杀伤烟曲霉的影响

目的研究地塞米松对过氧化氢（H2O2）体外杀伤烟曲霉（Aspergillus fumigatus,A.fumigatus）的影响。方法用不同浓度的地塞米松（0 mg/mL,0.02 mg/mL,0.2 mg/mL）处理烟曲霉孢子,按照处理时间不同分为A（0.5 h）,B（2 h）,C（7 h）,D（16 h）4组。用测定H2O2杀伤真菌的标准方法——斑点法分别测定各组烟曲霉孢子对H2O2的氧化杀伤敏感性。结果在H2O2浓度为1.5 mmol/L下,未用地塞米松处理的孢子（阴性对照）氧化杀伤敏感性为5×101（生长良好）。A（0.5 h）组：地塞米松0.02 mg/mL处理后孢子的氧化杀伤敏感性为5×10^3;地塞米松0.2 mg/mL处理后孢子的氧化杀伤敏感性为5×10^4。B（2 h）组：地塞米松0.02 mg/mL和0.2 mg/mL处理后孢子的氧化杀伤敏感性均为5×10^3。C（7 h）和D（16 h）组：不同浓度地塞米松处理后氧化杀伤敏感性与阴性对照没有差别（均为5×10^1）。结论地塞米松使H2O2在体外杀伤烟曲霉的能力增强,这种作用仅发生在地塞米松接触烟曲霉孢子的早期（〈2 h）。     

不同剂量熊果酸干预糖尿病小鼠视网膜病变的作用及机制研究

目的:探究不同剂量熊果酸(UA)干预糖尿病小鼠视网膜病变的作用及机制。方法:选取雄性健康C57BL/6小鼠60只,其中50只按50 mg/kg的剂量一次性往小鼠尾静脉注射新鲜配置的四氯嘧啶生理盐水溶液构建小鼠糖尿病视网膜病变模型,随机分为5组,每组10只,分别为模型组、阳性对照组(小鼠玻璃体注射3μL 40 mg/m L的曲安奈德),低剂量UA干扰组(小鼠玻璃体注射3μL剂量为0.5μg/μL的UA)、中剂量UA干扰组(小鼠玻璃体注射3μL剂量为1.0μg/μL的UA),高剂量UA干扰组(小鼠玻璃体注射3μL剂量为2.0μg/μL的UA),余下10只小鼠作为正常对照组。观察各组小鼠对胰岛素敏感性、视网膜内糖代谢情况、小鼠视网膜神经节细胞(RGCs)凋亡情况,比较各组小鼠视网膜组织中血管内皮生长因子(VEGF)、环氧化酶-2(COX-2)、基质金属蛋白酶2(MMP-2)蛋白及其mRNA的表达情况。结果:建模后,正常对照组胰岛素抵抗指数(HOMA-IR)、视网膜含糖量、葡萄糖转运体-1(GLUT-1)与葡萄糖转运体-3(GLUT-3)含量、RGCs凋亡率、视网膜组织中VEGF、COX-2、MMP-2蛋白及其mRNA的表达量低于模型组(P0.05);经干扰后,阳性对照组、不同剂量UA干扰组HOMA-IR、视网膜含糖量、GLUT-1、GLUT-3的含量、RGCs凋亡率、视网膜组织中VEGF、COX-2、MMP-2蛋白及其mRNA的表达量低于模型组(P0.05),且随UA干扰剂量的升高而降低(P0.05)。结论:UA能够降低HOMA-IR和视网膜糖代谢能力,抑制RGCs的凋亡,对VEGF、COX-2、MMP-2蛋白及其mRNA的表达具有一定的抑制作用,高剂量UA对糖尿病小鼠视网膜病预防治疗效果较好。     

低能量氦氖激光眼损伤的治疗研究

探讨谷氨酸受体拮抗剂MK-801对激光视网膜损伤的治疗作用。建立氦氖激光的大鼠眼损伤模型,通过病理染色、免疫组化以及原位杂交等方法,观察照后即刻肌注MK-801(2 mg/kg)对视网膜损伤的保护作用。实验结果表明治疗组视网膜的形态结构均较对照组更完整,感光细胞层的厚度也多于对照组,同时,照后给予MK-801还可明显地减少视网膜损伤区域内NMDAR的表达。该实验结果对低能量激光视网膜损伤后的治疗具有参考意义。     

软骨细胞联合BMP/bFGF移植对关节软骨损伤的修复作用

目的：探讨同种异体软骨细胞移植联合骨形态发生蛋白（BMP）/碱性成纤维细胞生长因子（bFGF）对关节软骨损伤的修复作用。方法：取24只14周龄成年大白兔,随机分为A、B、C、D组,每组6只,于双侧膝关节软骨处制作软骨缺损模型,A组采用软骨细胞移植联合应用BMP/bFGF处理,B组采用单纯软骨细胞移植,C组采用单纯BMP/bFGF修复,D组采用磷酸盐缓冲液（PBS）作为阴性对照,于处理后8、12、24周行形态学、电镜观察及组织学评分。结果：8周时,A组关节修复面与周围结合紧密,可见大量软骨细胞出现,电镜下有软骨基质形成;B、C组仅有少量软骨细胞;D组未见修复。12周时,A组关节修复面与周围组织界限模糊,软骨细胞增殖活跃,电镜下可见成熟软骨基质;B、C组修复块周围有肉芽组织生成,电镜下可见未成熟的软骨基质出现;D组可见肉芽组织形成。24周时,A组修复面周围组织融合,电镜下软骨细胞纵行排列;B、C组关节面修复不完全,电镜下软骨细胞分布不均;D组见大量肉芽组织形成。24周时,A组组织学评分（1.87±0.65）,明显低于B组（3.49±0.71）、C组（3.43±0.83）组和D组（13.45±0.97）,差异均有统计学意义（P〈0.05）,B、C组均明显低于D组,差异有统计学意义（P〈0.05）,B、C组之间比较无明显差异。结论：软骨细胞联合BMP/bFGF移植能够促进软骨生长,提高软骨损伤的修复质量。     

吸入糖皮质激素对大鼠肺纤维化的干预作用及bFGF表达的影响

目的:研究吸入糖皮质激素对大鼠肺纤维化模型的干预作用及可能的机制。方法:雌性Wistar大鼠40只,体重180～250g,按照随机数字表法将大鼠随机分为4组(n=10):①对照组(C组);②模型组(M组);③布地奈德组(B组);④地塞米松组(D组)。M组、B组、D组给大鼠气管内吸入博莱霉素(5mg/kgbw,8mg)复制肺纤维化模型,C组气管内吸入同等剂量的生理盐水作对照,B组于次日给予雾化吸入等效剂量布地奈德,D组于次日腹腔内注射地塞米松。上述各组均于注药后第1、4周各宰杀5只。通过苏木素-伊红染色观察肺泡炎、Masson胶原染色观察肺纤维化、用免疫组化及酶联免疫吸附测定(ELISA)法检测bFGF蛋白在大鼠肺组织,血清及肺泡灌洗液(BALF)的表达。结果:1、4周时M组表现为肺泡炎及肺间质炎症,B组、D组肺泡炎及肺纤维化程度较M组减轻。1、4周时血清、肺组织、BALF中M组的bFGF表达高于C组(P0.01),B、D组低于M组(P0.01)。结论:吸入糖皮质激素可减轻博莱霉素诱导的肺纤维化,其抗纤维化作用的机制与抑制bFGF表达有关。     

维生素C对万古霉素诱导大鼠肾损伤自噬的作用

摘要 目的：探讨维生素C对万古霉素诱导肾损伤自噬水平的影响。方法：将20只雄性SD大鼠随机分为：对照组、万古霉素组、万古霉素+维生素C组和维生素C组。万古霉素组：连续每天腹腔注射400 mg/kg万古霉素;万古霉素+维生素C组：注射万古霉素之前30 min腹腔注射200 mg/kg维生素C;对照组和维生素C组分别单独注射同体积的生理盐水和200 mg/kg维生素C。连续给药7 d后,通过苏木精-伊红染色（HE）观察大鼠肾组织病理损伤;免疫组化和免疫荧光检测肾组织中LC3B和Beclin 1的表达情况,比较各组之间的表达差异。结果：相对于对照组,万古霉素诱导大鼠肾损伤模型组肾组织出现明显的病理改变,包括肾间质水肿,肾小管细胞质空泡性变化,细胞凋亡坏死等;同时观察到肾组织中LC3B光密度明显升高和Beclin 1的荧光强度显著增强。维生素C处理组,肾组织的病理损伤显著改善并且自噬相关蛋白LC3B和Beclin 1的表达显著降低。相对于对照组,维生素C单独处理组肾组织损伤和自噬相关蛋白的表达无明显变化。结论：维生素C可降低自噬相关蛋白LC3B和Beclin 1的表达,缓解万古霉素诱导的大鼠肾损伤。     

血清25-羟维生素D3水平与2型糖尿病视网膜病变的关系研究

目的:探讨血清25-羟维生素D3[25(OH)D3]水平与2型糖尿病(T2DM)视网膜病变的关系。方法:选取T2DM患者150例,对每位患者进行一般临床资料收集,Hb A1c、PTH、血清25(OH)D3水平检测;根据维生素D水平由低到高按三分位法将患者分为25(OH)D3低(A组)、中(B组)、高(C组)3组,比较3组患者DR的发生情况。结果:A组患者的视网膜病变的患病率显著高于B组、C组患者,差异有统计学意义(P0.05);按25(OH)D3水平由低到高的3组患者的DR的患病率也逐渐降低,分别为:48.0%、30.0%和14.0%。结论:随着血清25(OH)D3水平的降低,T2DM视网膜病变的发生率逐渐增高,血清25(OH)D3在糖尿病视网膜病变的的发生发展中起重要作用。     

Basic fibroblast growth factor-induced protection from light damage in the mouse retina in vivo

Basic fibroblast growth factor (bFGF) has proven neuroprotective efficacy in the rodent retina against a diverse array of injurious stimuli. However, there is no consensus to date as to the molecular mechanisms underlying this neuroprotection. The study presented herein demonstrates increased expression of endogenous bFGF in the albino mouse retina in response to acute exposure to sublethal levels of light stress. The increased expression correlates with significant photoreceptor protection from light damage. The neuroprotection is likely to be mediated by bFGF as we demonstrate that a shorter exposure to bright light stress that does not up-regulate bFGF fails to protect photoreceptors from light damage. Furthermore, intravitreal bFGF injection into the retina of mice 3 h prior to light damage affords almost complete photoreceptor protection from light-induced degeneration. In addition, injected bFGF induces the activation of protein kinase B and extracellular signal-regulated kinase 1/2 signalling which correlate directly with the pathways we find to be activated in response to light stress and up-regulated bFGF. Moreover, we demonstrate that both bright light pre-conditioning and intravitreal bFGF injection result in dramatic increases in levels of inactive glycogen synthase kinase 3β and cyclic AMP response element binding protein phosphorylation indicating a potential mechanism by which bFGF promotes survival of photoreceptors in vivo .     

Enhancement of Apoptosis in Developing Chick Neural Retina Cells by Basic Fibroblast Growth Factor

Abstract: To evaluate the role of various growth factors in naturally occurring cell death during development of the neural retina, we examined the effects of such factors on the nuclear morphology and the size of DNA in cultured chick embryonic neural retina cells. Basic fibroblast growth factor (bFGF) increased internucleosomal cleavage of DNA and nuclear fragmentation in a time- and dose-dependent manner. The effect was inhibited by anti-bFGF antibody, suramin, and cycloheximide. Epidermal growth factor, platelet-derived growth factor, nerve growth factor, tumor necrosis factor-α, and dexamethasone had no effect. These results provide evidence that bFGF may eventually act as a lethal factor inducing apoptotic cell death during the development of the neural retina in chick embryo.     

Effect of growth hormone in an experimental model of protein hypercatabolism induced by glucocorticoids.

OBJECTIVE: The aims of the study were to evaluate whether growth hormone could be beneficial in a model of hypercatabolism induced by glucocorticoids and to examine its effects on ACTH, corticosterone and IGF-1 levels. The effects of growth hormone on the expression of both glucocorticoid receptor and tyrosine aminotransferase were also evaluated. METHODS: Fifty Wistar rats were divided into five groups and treated as follows: (A) daily subcutaneous injection of growth hormone (4.8 IU/kg/day) and oral placebo, (B) daily injection of placebo and oral dexamethasone (3 mg/kg/day), (C) daily injection of growth hormone and oral dexamethasone, (D) daily injection of placebo and oral placebo, and (E) no treatment. The animals were decapitated seven days after initiating treatment. RESULTS: Growth hormone did not modify the weight loss induced by dexamethasone. Glucocorticoid receptor expression was significantly lower in group A than in group E. An increase in tyrosine aminotransferase was observed in group C. CONCLUSION: Growth hormone did not exert any beneficial effect in this model of hypercatabolism. Growth hormone decreased glucocorticoid receptor expression. This fact could explain its beneficial effect when protein hypercatabolism is not the predominant phenomenon. Growth hormone induced the hyperexpression of tyrosine aminotransferase, thus suggesting an amplifying effect on the glucocorticoid action.     

Ethanol Inhibits Basic Fibroblast Growth Factor-Mediated Proliferation of C6 Astrocytoma Cells

Abstract: Early ethanol exposure alters the proliferative activity of glial and neuronal precursors in the developing CNS. The present study tests the hypothesis that ethanol-induced alterations in cell proliferation result from interference with growth factors. An in vitro model of astroglia (C6 astrocytoma cells) was used to study the effects of ethanol on proliferation mediated by basic fibroblast growth factor (bFGF). bFGF stimulated the proliferation of C6 cells. This bFGF-enhanced proliferation was evident by increases in total cell number, DNA synthesis (as measured by [³H]thymidine incorporation), and the number of cells that took up bromodeoxyuridine. A synthetic peptide that specifically blocked the binding of bFGF to its high-affinity receptor completely abolished the proliferation-promoting effect of bFGF. The action of another mitogen for C6 cells, insulin-like growth factor-1, was not affected by this peptide. Therefore, the bFGF-stimulated proliferation was mediated through a specific bFGF receptor. Ethanol inhibited bFGF-mediated proliferation in a concentration-dependent manner. Ethanol concentrations of 100 and 200 mg/dl partially inhibited bFGF-mediated proliferation (by 58 and 74%, respectively), whereas concentrations of ≥400 mg/dl completely abolished the growth-stimulating effect of bFGF. Our data show that ethanol alters proliferative activity of C6 cells by disrupting the action of bFGF. The target of ethanol neurotoxicity is a receptor-mediated activity. bFGF can affect cell proliferation by a non-receptor-mediated intracellular pathway, but ethanol does not have an impact on this pathway.     

Opposite Regulation of Basic Fibroblast Growth Factor and Nerve Growth Factor Gene Expression in Rat Cortical Astrocytes Following Dexamethasone Treatment

Abstract: Growth factors are peptides that exert different activities in the CNS, supporting the survival of different cell populations and playing an important role in the maintenance of cell homeostasis. Much evidence has suggested that these molecules can protect neurons from degeneration induced by mechanical injury or excitotoxic stimuli. Different factors can contribute to the regulation of neurotrophic factor expression in the brain. Such mechanisms may therefore be important in the manipulation of the levels of these peptides in specific brain areas as a therapeutic intervention in acute and chronic neurodegenerative diseases. We have used a primary culture of rat cortical astrocytes to investigate the regulation of basic fibroblast growth factor (bFGF) gene expression in comparison with other neurotrophic molecules. Our results indicate that the glucocorticoid analogue dexamethasone markedly elevates bFGF mRNA levels but reduces the expression of nerve growth factor. The induction of bFGF was transient, as it peaked after 6 h and returned to basal levels within 24 h and was not blocked by coincubation of cycloheximide, thus indicating that it did not require de novo protein synthesis. This effect was also observed in vivo, as systemic injection of dexamethasone (1 or 10 mg/kg) produced a significant increase in the amount of bFGF mRNA in cerebral cortex and hippocampus. The effect we describe can contribute to the regulation of bFGF expression in the brain and may be important in relation to the protective effect exerted by this growth factor in different models of neuronal injury.     

Effects of Dexamethasone and Insulin Alone or in Combination on Energy and Protein Metabolism Indicators and Milk Production in Dairy Cows in Early Lactation – A Randomized Controlled Trial

Objectives

This study investigated the effects of dexamethasone and insulin, when administered at 3^rd or 10^th day of lactation on energy and protein metabolism in dairy cows.

Materials and Methods

Two hundred Holstein cows were enrolled in a randomized controlled clinical trial. The cows were randomly assigned to receive 1 of 4 treatments at 3 or 10 days in milk: control group, 10-mL i.m. injection of sterile water, group insulin, s.c. injection of 100 units of insulin, group dexamethasone, i.m. injection of 20 mg of dexamethasone, group insulin plus dexamethasone, i.m. injection of 20 mg of dexamethasone and 100 units of insulin. The cows randomly assigned to receive the treatments on 3 or 10 days of lactation. Serum samples obtained at the time of enrollment, time of treatment and at 2, 4, 7 and 14 days after intervention. The sera were analyzed for β-hydroxybutyrate (BHBA), nonesterified fatty acids (NEFA), glucose, cholesterol, albumin, urea, and aspartate amino transferase (AST). Data were analyzed using a repeated measures mixed model that accounted for the effects of parity, body condition score, dystocia, retained placenta, metritis and the random effect of cow.

Results

There was no significant interaction of group of treatment and time of intervention (day 3 or 10 post-partum) on serum components. Cows that received insulin or dexamethasone alone or in combination, had lower BHBA 2 days after treatment compared with control cows, whereas concentrations of NEFA, were unaffected suggesting that glucocorticoids lipolytic effects do not appear to be important in healthy cows. AST activities significantly reduced in cows that received dexamethasone with or without insulin at 2 and 4 days after treatment. Albumin and urea concentrations 2 days after treatment were higher for cows that received dexamethasone only or dexamethasone plus insulin compared with control and Ins received cows. There were no treatment effects on test-day milk production, milk fat and protein percentages.

Conclusions

The results suggested that administration of glucocorticoids in early lactation resulted in short-term improvement of metabolism in postpartum dairy cows in biochemical terms.     

Fibroblast growth factor stimulates protein kinase C in quiescent 3T3 cells without Ca2+ mobilization or inositol phosphate accumulation

To elucidate the transmembrane signalling processes initiated by fibroblast growth factor (FGF), we have studied the effect of recombinant basic FGF (bFGF) on various early events associated with mitogenesis in Swiss 3T3 fibroblasts. bFGF, at mitogenic concentrations, neither induced Ca2+ mobilization from intracellular stores nor increased the accumulation of inositol phosphates. In contrast, bFGF stimulated the phosphorylation of the Mr 80,000 (80K) cellular protein which is a major substrate of protein kinase C. This effect was potentiated by the diacylglycerol kinase inhibitor R59022. Two-dimensional polyacrylamide gel electrophoresis and phosphopeptide mapping showed that the 80K phosphoproteins generated in response to bFGF, bombesin, and phorbol 12,13-dibutyrate were indistinguishable. Down-regulation of protein kinase C prevented bFGF stimulation of 80K phosphorylation. Other protein kinase C-dependent early events such as transmodulation of the epidermal growth factor receptor, cytoplasmic alkalinization, inhibition of vasopressin induced increase in cytosolic [Ca2+], and enhancement of cAMP accumulation in response to forskolin were also induced by bFGF. Similar results were obtained when bFGF was added to quiescent cultures of tertiary mouse embryo fibroblasts. We conclude that bFGF stimulates protein kinase C through a signal transduction pathway distinct from inositol phospholipid turnover and Ca2+ mobilization.     

Basic fibroblast growth factor inhibits osteoclast formation induced by 1alpha,25-dihydroxyvitamin D(3) through suppressing the production of osteoclast differentiation factor.

Basic fibroblast growth factor (bFGF) inhibited osteoclast-like cell (OCL) formation in cocultures of mouse spleen cells with either osteoblasts or a stromal cell line, ST2, in the presence of 1alpha, 25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)]. bFGF directly acted on osteoblasts/stromal cells, but not osteoclast progenitors, to inhibit 1,25(OH)(2)D(3)-induced OCL formation. bFGF suppressed the mRNA expression of osteoclast differentiation factor (ODF) but did not affect that of osteoclastogenesis inhibitory factor (OCIF) in ST2 cells treated with 1,25(OH)(2)D(3) and dexamethasone. Enzyme-linked immunosorbent assay showed that bFGF hardly affected OCIF production in the treated ST2 cells. A genetically engineered soluble form of ODF, but not anti-OCIF neutralizing antibody, abolished bFGF-mediated inhibition of OCL formation. bFGF suppressed the binding of (125)I-labeled OCIF to both ST2 cells and osteoblasts treated with 1,25(OH)(2)D(3). These findings indicate that bFGF inhibits 1,25(OH)(2)D(3)-induced OCL formation via suppression of ODF production by osteoblasts/stromal cells.     

静脉与硬膜外注射地塞米松对吗啡硬膜外术后镇痛的影响

目的:比较两种不同途径注射地塞米松磷酸钠对吗啡硬膜外术后镇痛的影响。方法:选择200例(ASAⅠ-Ⅱ)在腰硬联合麻醉下行腹式子宫切除术的患者,随机分为A、B、C、D四组(n=50),各组均给以硬膜外注射2.5 mg吗啡作为术后镇痛治疗的同时,A组静脉注射安慰剂(生理盐水),B组静脉注射地塞米松磷酸钠10 mg,C组静脉注射地塞米松磷酸钠5 mg,D组硬膜外注射地塞米松磷酸钠5 mg及静脉注射安慰剂(生理盐水),以上均以5 mL作为注射容积。观察和比较术后24 h内各组恶心和呕吐(PONV)、皮肤瘙痒、补救镇痛、呼吸抑制的发生率、排气时间和补救镇痛时间。结果:B、C、D三组的PONV总发生率显著低于A组(P0.0083),而B、C、D三组之间比较无显著差异(P0.0083);A、B、C、D四组间恶心的发生率无显著差异(P0.05),而D组呕吐的发生率明显低于A组(P0.0083);B组皮肤瘙痒的发生率明显低于A组(P0.0083);四组患者的VAS评分比较无显著差异,均达到满意的镇痛效果(P0.05)。四组患者补救镇痛的发生率、补救镇痛药量和排气时间比较无明显差异(P0.05),而C、D组的补救镇痛时间明显比A组延长(P0.0083),四组患者均未出现呼吸抑制。结论:地塞米松磷酸钠可降低吗啡硬膜外术后恶心和呕吐的发生率,延长补救镇痛时间;硬膜外注射地塞米松磷酸钠对降低呕吐的发生率更有效;静脉注射地塞米松磷酸钠10 mg可降低瘙痒的发生率,且无明显的不良反应。     

The effect of diphenylhydantoin on the frequency of micronuclei in bone-marrow polychromatic erythrocytes of mice

Using the micronucleus test to evaluate the mutagenic effect of 5,5-diphenylhydantoin (DPH) on bone marrow polychromatic erythrocytes, male Balb-C mice were treated with the drug in single and multiple injection tests. A significant increase in the frequency of micronucleated polychromatic erythrocytes (MPE), P less than 0.05, was found when the mice received a single injection of DPH at doses of 0.5 and 1.0 mg/kg, and this frequency did not increase at higher doses. When mice were treated 3 times, at 24-h intervals, with 1.0 mg/kg of DPH, a significant increase in MPE was also observed (P less than 0.05) but this was lower than when they received a single injection of the same dose. A cytotoxic effect of NaOH, 0.1 N, which was used as solvent, was also observed either when alone or when DPH (1.0 mg/kg) was injected 3 times. This effect was comparable to the one produced by mitomycin C (MMC) at a dose of 0.5 mg/kg.