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1.
目的评价4种喹诺酮类药物(环丙沙星、左氧氟沙星、氟罗沙星、帕珠沙星)对幼龄大鼠软骨细胞的相对毒性,以及大鼠周龄、细胞培养时间对大鼠软骨细胞体外增殖和蛋白多糖分泌的影响.方法采用大鼠软骨细胞体外培养技术,将4,8,12周龄大鼠的软骨细胞在各含不同药物的培养基中培养一定时间后,以MTT法和DNB法进行测定.结果4种喹诺酮类药物对4周龄大鼠软骨细胞体外增殖和蛋白多糖分泌均有抑制作用,其顺序为环丙沙星>左氧氟沙星>氟罗沙星>帕珠沙星.环丙沙星对大鼠软骨细胞体外增殖的抑制作用随大鼠周龄的增大而减弱,随培养时间的延长而增强.结论喹诺酮类药物对大鼠软骨细胞体外培养增殖和蛋白多糖分泌具有抑制作用,且该作用与大鼠周龄、细胞培养时间相关.  相似文献   

2.
氟喹诺酮类药物应用情况分析   总被引:1,自引:0,他引:1  
目的了解氟喹诺酮类药物在广东地区医院的应用情况及其变化趋势,方法对广东地区有代表性的43家医院2001—2003年氟喹诺酮类药物的用药金额、用药频度(DDDs)、日均费用等进行统计和分析,结果与结论2002年氟喹诺酮类药物用药金额比2001年稍微下降,2003年比2002年增长13.49%.用药金额居前四位的分别是左氧氟沙星,环丙沙星,氟罗沙星,氧氟沙星。左氧氟沙星约占总金额的三分之一.DDDs居前四位的分别是左氧氟沙星,环丙沙星.司帕沙星,氧氟沙星,日均费用居前四位的分别是依诺沙星、加替沙星,氟罗沙星、莫西沙星。  相似文献   

3.
目的 了解氟喹诺酮类药物在广东地区医院的应用情况及其变化趋势。方法 对广东地区有代表性的43家医院2001-2003年氟喹诺酮类药物的用药金额、用药频度(DDDs)、日均费用等进行统计和分析。结果与结论 2002年氟喹诺酮类药物用药金额比2001年稍微下降, 2003年比2002年增长13. 49%。用药金额居前四位的分别是左氧氟沙星,环丙沙星,氟罗沙星,氧氟沙星。左氧氟沙星约占总金额的三分之一。DDDs居前四位的分别是左氧氟沙星,环丙沙星,司帕沙星,氧氟沙星。日均费用居前四位的分别是依诺沙星、加替沙星,氟罗沙星、莫西沙星。  相似文献   

4.
目的了解氟喹诺酮类药物在广东地区医院的应用情况及其变化趋势.方法对广东地区有代表性的43家医院2001-2003年氟喹诺酮类药物的用药金额、用药频度(DDDs)、日均费用等进行统计和分析.结果与结论 2002年氟喹诺酮类药物用药金额比2001年稍微下降,2003年比2002年增长13.49%.用药金额居前四位的分别是左氧氟沙星,环丙沙星,氟罗沙星,氧氟沙星.左氧氟沙星约占总金额的三分之一.DDDs居前四位的分别是左氧氟沙星,环丙沙星,司帕沙星,氧氟沙星.日均费用居前四位的分别是依诺沙星、加替沙星,氟罗沙星、莫西沙星.  相似文献   

5.
<正>氟喹诺酮类药物包括:左氧氟沙星、诺氟沙星、环丙沙星、洛美沙星、加替沙星、甲磺酸培氟沙星、依诺沙星、氟罗沙星、帕珠沙星等,这类药物在临床使用较广,只有严格掌握药物的作用于副作用,才能发挥其应有疗效。该药物为广谱抗生素,应用广泛,可以治疗多种感染性疾病,用于治疗肺炎、支气管炎、尿道、肾脏、皮肤等各种感染性疾病,通常认为是相对安全的一类药,它的抗菌谱较广,疗效  相似文献   

6.
《中国乡村医药》2013,(24):30-30
我国上市的氟喹诺酮类药品包括诺氟沙星、培氟沙星、氧氟沙星、左氧氟沙星、莫西沙星、、环丙沙星、洛美沙星、氟罗沙星、依诺沙星、司帕沙星、克林沙星、加替沙星、芦氟沙星、托氟沙星、那氟沙星、司氟沙星、吉米沙星等。  相似文献   

7.
从药物动力学观点看喹诺酮类药物的不良反应   总被引:9,自引:0,他引:9  
评述氟喹诺酮类药物最新的药物动力学、相互作用和特殊的耐受性。左氧氟沙星的口服吸收最高(99%~ 10 0 % ) ,口服 5 0 0mg后比司帕沙星 (4 0 0mg)或环丙沙星 (5 0 0mg ,每日 2次 )达到更高的初始浓度 ,2 4h后下降缓慢。口服 2 5 0mg后的Cmax范围从环丙沙星、加替沙星和莫西沙星的 1.2、1.71和 2 .17mg/L ,到左氧氟沙星的2 48mg/L(P <0 .0 1)。环丙沙星的AUC最低为 4.6h·mg/L ,加替沙星、左氧氟沙星和莫西沙星分别为 15、17.9和19 7h·mg/L(P <0 .0 1)。所有氟喹诺酮类药物与含有多价阳离子的物质具有相互作用 ,并且当与含铁化合物共同使用时 ,生物利用度降低 5 0 % (环丙沙星和莫西沙星所受的影响比左氧氟沙星或gemifloxacin更大 )。在氟喹诺酮类药物中 ,与茶碱相互作用最明显的是依诺沙星、培氟沙星和环丙沙星 ,而左氧氟沙星无此相互作用的报道。司帕沙星与心脏的QT间期延长有关 ,并有高光毒性。正在观察莫西沙星的QT间期作用。左氧氟沙星无QT间期延长 ,且光毒性非常低 ,使其成为最安全的氟喹诺酮类药物  相似文献   

8.
本文综述了近年来国内药学期刊报道的有关氟喹诺酮类药物所致癫痫发作的文献。其中主要有环丙沙星、左氧氟沙星、氟罗沙星、洛美沙星、司帕沙星、加替沙星、莫西沙星等,提示临床医师应重视此类药物所致的不良反应的危害性,保证用药安全。  相似文献   

9.
喹诺酮类药物的不良反应   总被引:18,自引:0,他引:18  
从1985年至今,在氟喹诺酮类药物的进展中,严重的药物不良反应受到关注,包括有光毒性的依诺沙星,培氟沙星,氟罗沙星;替马沙星与严重的溶血性尿毒症的并发症有关;洛美沙星引起光毒性并对中枢神经系统有影响,司帕沙星与光毒性和QT间期延长有关;托氟沙星引起严重的血小板减少症和肾炎;曲伐沙星有肝毒性,格帕沙星由于对心血管的影响而被撤出市场,克林沙星与光毒性和血糖过少有关。奎诺酮类药物的结构直接与其活性和不良反应相关,连接在喹诺酮母核上的特殊的取代基的关系已被阐明,日本在药物上市后5年的市场监督研究表明,氟喹诺酮相关性特殊的不良反应发生率,左氧氟沙星为1.3%,帕珠沙星为3.3%,托氟沙星为3.6%,加替沙星为4.5%,巴洛沙星为5.4%,胃肠反应是所有氟喹诺酮类药物中最常见的不良反应,在研究的喹诺酮类药物中,左氧氟沙星对中枢神经系统和皮肤的不良反应最低。  相似文献   

10.
喹诺酮类抗菌药物的严重不良反应   总被引:1,自引:0,他引:1  
喹诺酮类是人工化学合成抗菌药物,目前临床常用的喹诺酮类药物有诺氟沙星、氧氟沙星、环丙沙星、左氧氟沙星、培氟沙星、加替沙星、莫西沙星、洛美沙星、氟罗沙星和依诺沙星等。与其他抗生素相比,其价格低廉,口服吸收良好,  相似文献   

11.
AIM: To study the relationship between chondrotoxicity and toxicokinetics of ciprofloxacin (CPFX). METHODS: Rats, 4-week old, were treated with CPFX 0, 400, 800, and 1200 mg/kg ig once daily on seven consecutive days. The knee joint cartilage was examined histopathologically. The concentration of CPFX in venous blood and knee joint cartilage samples were determined by a microbioassay using Escherichia coli 44102. The effects of CPFX on proliferation of chondrocytes and secretion of soluble proteoglycans were determined with 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) and 1,9-dimethylmethylene blue (DMB) assay, respectively. RESULTS: Cartilage was severely lesioned after treatment with CPFX 800 or 1200 mg/kg for 7 d, such as matrix swelling and loss of chondrocytes. The thickness of cartilage was significantly decreased compared with the control group. The maximum serum concentration (Cmax), the area under the plasma concentration-time curve (AUC0-∞2), and concentration in cartila  相似文献   

12.
荆靓艳  王慧玲  薛欣  谢广宏 《中国医药》2012,7(11):1450-1452
目的 比较6种氟喹诺酮类药物对临床分离凝固酶阴性葡萄球菌耐药突变体的选择能力.方法 选择呼吸道标本,对苯唑西林、环丙沙星敏感的凝固酶阴性葡萄球菌34株,采用标准琼脂二倍稀释法、标准琼脂平板稀释法,测定6种氟喹诺酮类药物对凝固酶阴性葡萄球菌的最低抑菌浓度(MIC)、防耐药变异浓度(MPC).结果 MPC值比较,莫西沙星最低(MPC90为1 mg/L),左氧氟沙星和环丙沙星最高(MPC90均为32 mg/L).莫西沙星、卡屈沙星和加替沙星的MPC90/MIC90较低,均为2.结论 莫西沙星、卡屈沙星和加替沙星对凝固酶阴性葡萄球菌的MPC值较低,突变选择窗范围相对较窄.  相似文献   

13.
目的比较6种氟喹诺酮类药物对临床分离金黄色葡萄球菌耐药突变体的选择能力。方法用呼吸道标本,选择对苯唑西林、环丙沙星敏感的金黄色葡萄球菌36株,采用标准琼脂二倍稀释法、标准琼脂平板稀释法,测定6种氟喹诺酮类药物对金黄色葡萄球菌的MIC、MPC。结果 MPC值比较,莫西沙星最低;而环丙沙星最高。选择指数(MPC90/MIC90)较低有如下4种:莫西沙星、卡屈沙星、加替沙星和帕珠沙星,均为2。6种药物MPC90值与其体内药动学参数比较,莫西沙星和卡屈沙星小于其Cmax。结论莫西沙星、卡屈沙星和加替沙星对金葡菌的MPC值较低,突变选择窗范围相对较窄。  相似文献   

14.
The purpose of this study was to evaluate the distribution of three fluoroquinolones (pazufloxacin, ciprofloxacin and ofloxacin) and a beta-lactam, ceftazidime in the tissue interstitial and intracellular spaces after a single intravenous administration to rats based on muscle microdialysis. The unbound concentration in the tissue interstitial fluid (C(isf,u)) after administration was estimated from the concentration in the dialysate by muscle microdialysis, the in vitro permeability rate constant, and the previously reported effective dialysis coefficient. The C(isf,u)s of pazufloxacin, ciprofloxacin, ofloxacin and ceftazidime in the muscle were close to their unbound concentrations in the venous plasma. These results were consistent with ones previously obtained at steady state. Based on these results, the total concentration in the tissue interstitial fluid (C(isf)) was calculated from the ratio of plasma protein binding, the plasma concentration, and previously reported interstitial-to-plasma albumin ratio in muscle of rats. The calculated C(isf) was compared with the muscle concentration (C(m)) obtained using the homogenized tissue. The C(isf) of ceftazidime was higher than the C(m). The C(isf) of pazufloxacin was found to be almost equal to its C(m). The C(isf)s of ciprofloxacin and ofloxacin were lower than their C(m)s with the exception of the values at 5 min after administration. These results indicate that ceftazidime is mainly distributed in the interstitial space of the muscle, that pazufloxacin is distributed equally in both the interstitial space and the tissue cells, and that ciprofloxacin and ofloxacin are mainly distributed in the tissue cells rather than the interstitial space.  相似文献   

15.
Two hundred and seven clinical isolates of Pseudomonas aeruginosa were collected at Tenri Hospital between April 2003 and March 2004. We determined the minimum inhibitory concentration (MIC) of 16 antimicrobial agents, including prulifloxacin, pazufloxacin and biapenem which were recently published in Japan, against these isolates according to the guidelines of the Clinical and Laboratory Standards Institute. For the fluoroquinolones, the rank order of activity was prulifloxacin (MIC50, 0.5 microg/ml)>ciprofloxacin (1 microg/ml)> pazufloxacin (2 microg/ml)=levofloxacin (2 microg/ml)>gatifloxacin (4 microg/ml). For the carbapenems, the rank order of activity was meropenem (MIC50, 1 microg/ml)=biapenem (1 microg/ml)>imipenem (2 microg/m)>panipenem (8 microg/ml). For the cephalosporins and monobactam, the overall rank order of activity was cefozopran (MIC50, 4 microg/ml)= ceftazidime (4 microg/ml)>cefepime (8 microg/ml)=piperacillin/tazobactam (8 microg/ml)>aztreonam (16 microg/ml)= cefoperazone/sulbactam (16 microg/ml)=cefpirome (16 microg/ml). The rates of susceptibility to antimicrobial agents as per the criteria of the Japanese Society of Antimicrobial Chemotherapy were especially high for cefozopran (63%), biapenem and meropenem (61%), and pazufloxacin (53%) and ciprofloxacin (53%). These findings suggest that prulifloxacin, pazufloxacin and biapenem, which are newly introduced, are clinically effective in the treatment of infection caused with P. aeruginosa.  相似文献   

16.
Aim: The use of biological agents (BAs) for treating diseases such as rheumatoid arthritis (RA), spondyloarthropathy, and systemic lupus erythematosus to reduce inflammation has been fruitful. Especially as part of the increasing number of studies on the intra-articular application of BAs, the effects of BAs on cartilage have been widely investigated. In the present study, the effects of rituximab, abatacept, and adalimumab, all approved antirheumatic agents, on human primary chondrocytes were investigated comparatively and on the molecular level through viability, proliferation, and toxicity analyses. Materials and methods: Osteochondral tissues from the distal femur and proximal tibia were resected during total knee arthroplasty from patients (n?=?3) with confirmed gonarthrosis in whom all medical or conservative treatments had failed. Standard human primary chondrocyte cell culturing was carried out. Immunophenotyping was performed on the cells that adhered to the flask, and their chondrotoxicity was observed using a flow cytometry device. Images of the cells showing chondrotoxicity were analyzed using invert and environmental scanning microscopes, and microimages were obtained. The MTT-enzyme linked immunosorbent assay was performed to observe the toxic effects of BAs on the proliferation of chondrocytes at 24 and 48?h. The results were analyzed using the number of cells and proliferation; statistical comparisons among the groups were carried out using one-way ANOVA. The alpha significance level was set at <0.01. Results: These pharmaceutical agents were chondrotoxic, especially on viability and proliferation (p?=?0.0000). Conclusion: BAs are generally used during active inflammation, and following the management of inflammation, their dosage should be determined taking into consideration their cellular-level toxic effects on chondrocytes.  相似文献   

17.
尹培荣  吴承龙  叶川  宋华 《贵州医药》2005,29(6):483-485
目的探讨肝素与碱性成纤维细胞生长因子(bFGF)对兔软骨细胞的增殖影响及其协同作用。方法体外培养3周龄的新西兰大白兔的原代关节软骨细胞。将第二代软骨细胞加入不同浓度的肝素、碱性成纤维细胞生长因子(bFGF)及肝素 bFGF联合应用,于48及72小时分别进行MTT检测软骨细胞的成活数。结果bFGF浓度在10ng/ml时即可显著促进软骨细胞增殖,当浓度增至50ng/ml,其促进作用达到最大值;单纯使用肝素并不促进软骨细胞增殖,当联用bFGF,bFGF浓度为50ng/ml、肝素浓度为1250ng/ml时协同作用最明显。结论bFGF可明显促进软骨细胞增殖,单用肝素对细胞增殖无明显影响,与bFGF联用时呈现协同效应,具有增强bFGF促软骨细胞增殖作用。  相似文献   

18.
Povidone-iodine (polyvinyl-pyrrolidone-iodine complex, PVP-iodine, CAS 25655-41-8) is a commonly used antiseptic because of its broad spectrum of antimicrobial effect and its comparatively low allergic risk. It is also used for open joint lavage. Animal and organ culture studies provide controversial results about the risk of cartilage damage due to povidone-iodine. There is a paucity of in vitro study data concerning the effect of povidone-iodine on chondrocyte cultures are still missing. The aim of this study was therefore to investigate the effect of different concentrations and exposition times of povidone-iodine on cell growth and differentiation of human chondrocytes. Using of a vitality test (MTT) and a proliferation assay (BrdU) in the fibroblast-like cell line BALB3T3, suitable concentrations and incubation times were identified to investigate the influence of povidone-iodine on proteoglycan synthesis and DNA synthesis of primary human chondrocytes. Concentrations of up to 1% povidone-iodine had no significant effect on proteoglycan and DNA synthesis of chondrocytes after incubation for 30 min. An incubation time of 24 h did not inhibit DNA- and proteoglycan synthesis, until a concentration of 0.2% povidone-iodine was used. DNA synthesis rate was impaired after 10 min incubation with 0.2% and fully inhibited with 1% povidone iodine. BALB3T3 reacted more sensitively than chondrocytes. Vitality and proliferation rate were fully inhibited at a concentration of 0.5% after the same exposition time. However, cells recovered 24 h after 30 min incubation with 0.5% povidone-iodine. After incubation with 5% povidone iodine cells did not recover. From the results it can be concluded that low concentrations of povidone-iodine (< 1%) and short incubation times (< 30 min) have no damaging influence on chondrocytes. Previous studies have reported the antimicrobial effectiveness of low concentrations of povidone-iodine on the reduction of tissue damage by microorganisms. Data from previus studies and the current findings from this investigation support the clinical use of povidone-iodine at low concentrations and short incubation times for antiseptic treatment of cartilage tissues.  相似文献   

19.
Quinolone-induced chondrotoxicity is possibly associated with the magnesium-chelating properties of quinolones. This toxic effect seems to be restricted to a rather short time period during postnatal development as shown in rats and dogs. We studied developmental changes of the integrin pattern on canine chondrocytes (e.g. the alpha(v)beta(3)- or alpha(5)beta(1)-integrin), because integrin function depends on divalent cations, as well as the matrix composition (e.g., collagen type II, fibronectin), in 11-, 18-, and 55-week-old Beagles (n=8) by immunohistochemistry. We also analyzed the magnesium and calcium content by atomic absorption spectroscopy in cartilage and bone and studied the effects of a magnesium-deficient diet on joint cartilage in four immature Beagles (18 weeks old at necropsy). The dogs were fed the magnesium-deficient diet for 40 to 46 days. All dogs exhibited gait alterations ('limping') after 4 weeks on the magnesium-deficient diet. Male, magnesium-deficient dogs exhibited pronounced weakness in their front legs; in one of these dogs the front legs were hyperextended to a 90 degrees angle. We observed no significant differences in the integrin pattern in samples from dogs at different developmental stages or in magnesium-deficient dogs in comparison to age-matched controls. Localization of fibronectin in the joint cartilage was found to vary with the age of the dogs as well as with the site of collection. In the middle zone of immature joint cartilage, corresponding to the predilective site of quinolone-induced cartilage lesions, we observed a slight increase in staining with the fibronectin antibody in some samples from magnesium-deficient dogs. Electron microscopy revealed alterations in chondrocytes from the magnesium-deficient dogs (e.g., swollen mitochondria and enlarged endoplasmic reticulum) which are also seen after treatment with quinolones. In summary, we found no significant differences of the integrin pattern on chondrocytes from joint cartilage of dogs at various developmental stages. However, magnesium deficiency in immature dogs induced similar clinical symptoms as quinolone treatment as well as distinct alterations in chondrocytic fibronectin staining and their ultrastructure. This corroborates our findings in rats where magnesium chelation is an important event in quinolone-induced chondrotoxicity.  相似文献   

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