巴氏灭活前后人血白蛋白纯度的影响因素相关研究

目的为了提高人血白蛋白的热稳定性,对其影响人血白蛋白热稳定性相关因素进行探索。方法用气相色谱仪、火焰光度计分别测得不同处理制品的辛酸钠浓度以及Na~+的浓度,用电泳仪测得不同处理后制品巴氏灭活前后的纯度,通过统计学的方法分析辛酸钠浓度、Na~+浓度对人血白蛋白纯度的影响结果。结果通过对数据分析得出辛酸钠的含量对人血白蛋白巴氏灭活后的纯度具有显著的影响,而Na~+浓度对人血白蛋白巴氏灭活后的纯度也具有极显著的影响,辛酸钠浓度控制在0.146 mmol/g蛋白、0.160 mmol/g蛋白时,Na~+浓度控制在(133-140)mmol/L、(142-144)mmol/L时,巴氏灭活前后纯度差异较小,制品热稳定性较好。结论不同巴氏灭活条件对人血白蛋白的纯度有影响,其中不同Na~+浓度对人血白蛋白纯度有极显著差异。     

某些患者可能受益

科兰损伤小组得出结论,除了严格地进行随机对照试验,不应当给危重病病人使用人血白蛋白,Offringa在其所加编者的话中也这佯讲。科兰小组发现,对于有低血容量症、烧伤或低白蛋白血症的危重病病人应用白蛋白可能会增加死亡率。 1997年初,作者审查了应用人血白蛋白(4.5％和20％)溶液。结果表明,4.5％人血白蛋白溶液非特异地用于有各种临床情况(包括1例偶然只请求500ml者)的血清中白蛋白含量低下者;20％人血白蛋白溶液主要用于慢性肝病患者。 在这一审查期间,作者就使用人血白蛋白溶液的适应症问题查阅了文献。作者发现在所查的文献中关于其适应症很少一     

对石油醚萃取法检测人血白蛋白制品中辛酸钠含量可靠性的验证

目的对石油醚萃取法检测人血白蛋白制品中辛酸钠含量的可靠性进行学验证。方法采用石油醚作为萃取剂,利用0.01 mol/L氢氧化钠滴定液确定辛酸钠的含量。结果回收率为0.98～1.01,变异系数(CV)(%)为0.60～1.53。结论利用石油醚萃取法检测人血白蛋白制品中辛酸钠含量的方法可靠,与现行中国生物制品规程所要求的气相色谱结果一致。     

离子排斥色谱法测定白蛋白中的辛酸钠含量

人血白蛋白制品在生产过程中,须经60℃、10h的灭活病毒处理.为防止蛋白质发生热变性,需加入适量的辛酸钠作稳定剂.加入的辛酸钠量不够,会降低白蛋白的热稳定性,形成过多的聚合体;而辛酸钠含量太高(>0.18mmol/g蛋白),则有可能导致白蛋白制品引起不良反应,如抑制血小板凝聚、引起低血糖症、抑制肝脏对长链脂肪酸的消除等[1].     

依达拉奉联合奥扎格雷钠治疗急性脑梗死的临床观察

目的观察依达拉奉联合奥扎格雷钠治疗急性脑梗死的临床疗效。方法将200例急性脑梗死患者随机分为二组,治疗组100例,常规治疗基础上应用依达拉奉30 mg(国药集团国瑞药业有限公司生产)加0.9%氯化钠溶液100 ml静脉滴注,2次/d,奥扎格雷钠250 ml(含0.9%氯化钠溶液250 ml,奥扎格雷钠80 mg,石家庄四药有限公司生产)静脉滴注,2次/d。对照组100例,常规治疗基础上应用奥扎格雷钠250 ml(含0.9%氯化钠溶液250ml,奥扎格雷钠80 mg)静脉滴注,2次/d。2周后进行疗效评定。结果治疗组有效率95%,对照组有效率83%。结论依达拉奉联合奥扎格雷钠治疗急性脑梗死疗效肯定,能有效改善急性脑梗死患者的神经功能缺失。     

双氯芬酸钠对骨关节炎大鼠模型软骨细胞炎症和滑膜巨噬细胞极化的影响

目的探究双氯芬酸钠对骨关节炎(OA)大鼠模型软骨细胞炎症和滑膜巨噬细胞极化的影响。方法 45只6周龄雄性Sprague-Dawley大鼠用于本研究,大鼠左膝关节的髌韧带关节内注射单碘乙酸(MIA)溶液诱导OA模型。根据实验目的将实验大鼠分为3组:对照组(关节内注射无菌0.9%氯化钠溶液作为实验对照,n=15),OA模型组(大鼠左膝关节的髌韧带关节内注射MIA诱导OA模型,n=15),双氯芬酸钠组(MIA注射后14 d,用双氯芬酸钠口服治疗8 d,n=15)。通过酶联免疫吸附试验(ELISA)试剂盒检测大鼠血清炎症因子肿瘤坏死因子(TNF-α)、白细胞介素(IL)-1β、IL-12和IL-10浓度。使用相应试剂盒测定大鼠血清丙二醛、还原型谷胱甘肽(GSH)和过氧化物歧化酶(SOD)浓度。通过蛋白印迹分析炎症介质相关蛋白的表达。通过免疫组织化学分析检测CD86和Arg1的蛋白表达。通过免疫细胞化学测定检查大鼠滑膜组织中CD86⁺和CD163⁺巨噬细胞的数量。组织学和免疫组织化学分析大鼠关节组织。通过膝弯曲试验和步态分析得分评估各组大鼠的关节疼痛。...     

姜黄素与地塞米松对百草枯中毒大鼠肺组织损伤治疗作用的对比研究

目的 观察姜黄素和地塞米松对百草枯致肺纤维化大鼠胶原沉积、转化生长因子-β1(TGF-β1)表达的影响.方法 将80只雄性Wistar大鼠随机分为4组,每组20只.百草枯组用百草枯50 mg/kg一次性灌胃染毒,1 h后腹腔注射生理盐水1 ml;姜黄素组染毒1 h后腹腔注射姜黄素200 mg/kg;地塞米松组染毒1 h后腹腔注射地塞米松3 mg/kg;对照组用1 ml生理盐水灌胃,1 h后再腹腔注射生理盐水1 ml.各组每日用药1次,直至处死动物前1 d为止.各组于1、3、7、14 d随机处死5只动物,取肺组织进行苏木素-伊红(HE)染色、Masson染色,观察病理学改变;采用免疫组化染色,检测肺组织中TGF-β1表达水平.结果 地塞米松组和姜黄素组大鼠肺组织胶原沉积较百草枯组明显减少.百草枯组、地塞米松组和姜黄素组7 d和14 d时TGF-β1表达均显著高于对照组,且地塞米松组和姜黄素组明显低于百草枯组(P＜0.05或P<0.01);而地塞米松组和姜黄素组各时间点TGF-β1表达则无明显差异(P均>0.05).结论 姜黄素和地塞米松均可减轻百草枯所致大鼠肺泡炎和肺纤维化,其作用机制可能与抑制TGF-β1有关.姜黄素和地塞米松治疗效果无明显差异,但姜黄素比地塞米松副作用少,更具有临床应用价值.     

人血白蛋白治疗急性脑出血的临床疗效及安全性评价

目的 探讨人血白蛋白治疗急性脑出血的临床疗效及安全性. 方法 急性脑出血患者88例随机分为对照组和治疗组,治疗组在常规治疗基础上加用10%人血白蛋白100 ml静脉滴注,1次/d,连用7d.14 d为一疗程.比较神经功能缺损程度评分变化. 结果 治疗组总有效率及神经功能缺损评分改善情况均优于对照组(P<0.05),治疗过程中无不良反应发生. 结论 人血白蛋白治疗急性脑出血临床疗效确切、安全.     

β-七叶皂甙钠对大鼠脊髓损伤后肢体运动功能的影响

目的:观察β-七叶皂甙钠治疗大鼠急性脊髓损伤后肢体运动功能的变化,探讨β-七叶皂甙钠对大鼠急性脊髓损伤的保护和促进修复作用。方法:实验于2003-12/2004-03在解放军第二军医大学长海医院骨科实验室完成。45只SD大鼠随机分为正常对照组11只,模型对照组12只,10mg/(kg·d)β-七叶皂甙钠治疗组11只,20mg/(kg·d)β-七叶皂甙钠治疗组11只。按Allen改良法制备脊髓损伤动物模型,10mg/(kg·d)和20mg/(kg·d)β-七叶皂甙钠治疗组分别在术后腹腔注射β-七叶皂甙钠注射液10mg/(kg·d)和20mg/(kg·d)。模型对照组和正常对照组在术后注射等量生理盐水,共持续10d。用斜板试验法和BBB评分法观察大鼠脊髓损伤后运动功能的变化。结果:1只10mg/kgβ-七叶皂甙钠治疗组大鼠在术后第2天和1只正常对照组大鼠在术后第1天由于饲养不当死亡,其余43只大鼠均进入结果分析。①各组大鼠斜板试验临界角度:在术后第7,14,21天时10mg/(kg·d)和20mg/(kg·d)β-七叶皂甙钠治疗组明显高于模型对照组[第7天:(37.88±1.76)°,(38.94±2.15)°,(35.48±1.23)°;第14天:(44.39±1.87)°,(45.96±1.81)°,(39.48±1.23)°;第21天:(44.75±2.11)°,(46.66±1.46)°,(41.42±0.98)°,t=2.27～4.67,P<0.05～0.01]。20mg/(kg·d)β-七叶皂甙钠治疗组与10mg/(kg·d)β-七叶皂甙钠治疗组基本一致。②各组大鼠BBB评分结果:在术后第7,14,21天时10mg/(kg·d)和20mg/(kg·d)β-七叶皂甙钠治疗组明显高于模型对照组[第7天:(7.20±0.98),(7.51±0.85),(4.46±0.90)分;第14天:(10.43±0.90),(10.98±0.59),(6.54±0.73)分;第21天:(10.78±0.96),(11.67±0.49),(7.90±0.54)分,t=2.54～8.6,P<0.05～0.01]。20mg/(kg·d)β-七叶皂甙钠治疗组与10mg/(kg·d)β-七叶皂甙钠治疗组基本一致。结论:β-七叶皂甙钠可以增加大鼠实验性急性脊髓损伤后运动功能的恢复速度及最终恢复程度。     

辛伐他汀对脂多糖诱导肺损伤大鼠的肺血管通透性的影响

目的探讨辛伐他汀能否降低脂多糖(LPS)诱导急性肺损伤大鼠的肺血管通透性。方法 30只SD大鼠随机分为对照组、LPS组和辛伐他汀治疗组,治疗组又分1h、3d和7d三组,每组6只;治疗组大鼠在实验前经胃管分别给予辛伐他汀20mg/kg(4ml/kg)治疗1d、3d和7d,每天1次;对照组和LPS组则给予蒸馏水(4ml/kg)管饲7d。在最后一次给药1h后,LPS组和治疗组大鼠从尾静脉注射LPS5mg/kg(2.5ml/kg),对照组则予注射无菌生理盐水(2.5ml/kg)。观察6h后,处死大鼠,取样。计算肺湿/干重比值、肺水含量,比色法测定肺泡灌洗液(BALF)蛋白含量、肺匀浆伊文思蓝(EB)含量和髓过氧化物酶(MPO)活性,ELISA法测定血清IL-6和TNF-α水平,以及行肺组织病理学检测。结果治疗组的肺湿/干重比值、肺水含量显著降低(P<0.001),BALF蛋白、肺匀浆EB亦低于LPS组(1h组P>0.05,3d组P<0.05,7d组P<0.001),具有时间-效应依赖性;治疗组肺匀浆MPO活力和血清IL-6和TNF-α水平均显著下降(P<0.001);肺组织病理学亦显示治疗组的肺损伤程度轻于LPS组。...     

Experimental induction of caprylate-dependent albumin antibodies

To provide evidence for the immune nature of the albumin agglutination phenomenon or caprylate dependent albumin agglutinins (CDAA), rabbits were injected with native serum that had been incubated in a solution of sodium caprylate. Two of three rabbits responded with the production of CDAA, which in vitro behaved identical to human antisera. Human cells were agglutinated only when caprylate stabilized albumin was added to the cell/serum mixture or when caprylate free albumin plus sodium caprylate were used. The CDAA failed to agglutinate rabbit cells, although, both human adult and cord cells were agglutinated. These experiments indicate that the CDAA represent an immune response to native albumin that had been altered by caprylate.     

Effect of saccharated ferric oxide and iron dextran on the metabolism of phosphorus in rats

As a means of investigating the physiologic damage to and histologic deterioration of the kidney caused by saccharated ferric oxide (SFO) and iron dextran (ID), we administered these substances intraperitoneally to rats. The rats were divided into 3 groups. Group 1 rats ( n = 7) were given SFO, 28 mg/kg for 9 days and 20 mg/kg for 19 days. Group 2 rats ( n = 5) were given ID, 28 mg/kg for 9 days and 20 mg/kg for 19 days. Group 3 rats (control, n = 9) were given normal saline solution. After 28 days, serum calcium, total protein, and albumin concentrations were significantly lower in the SFO group than in the ID group. Serum phosphorus concentrations were significantly lower in the SFO group than in the control group. Serum iron concentrations were significantly higher in the ID group than in the SFO group or the control, and the fractional excretion of sodium was significantly lower in the ID group than in the control group. The percent tubular reabsorption of phosphorus was significantly greater in the ID group than in the SFO group or the control group, and the theoretical threshold concentration of phosphorus was also significantly lower in the SFO group than in the ID or the control group. Histologic examination of the kidney after treatment revealed neither iron in the tubules nor any structural damage to the tubules. ID was not found to induce hypophosphatemia, whereas SFO did. We believe that the cause of such hypophosphatemia is impaired tubular reabsorption.     

Amelioration of glomerular injury in doxorubicin hydrochloride nephrosis by dimethylthiourea.

The hydroxyl radical scavengers dimethylthiourea (DMTU), sodium benzoate, and dimethylsulfoxide (DMSO) were administered to rats before doxorubicin hydrochloride (ADR) (5 mg/kg, IV) to probe the role of free radicals in mediating proteinuria in doxorubicin hydrochloride nephrosis (AN). Because ADR stimulates free radical production, the role of renal glutathione was also evaluated; glutathione metabolism is involved in tissue detoxification processes. DMTU administration to rats with AN caused a significant (p less than 0.01) reduction in their proteinuria after 7 days (52.84 +/- 13.21 mg/24 hours) when they were compared with ADR controls (155.81 +/- 20.16 mg/24 hours). In similar fashion, their urine albumin excretion was also significantly reduced when compared with that of ADR controls (11.13 +/- 2.75 mg/24 hours vs 32.08 +/- 4.14 mg/24 hours; p less than 0.01). DMTU-treated rats also had significantly (p less than 0.001) reduced urinary protein and albumin excretion at 14 days when compared with rats that received ADR alone. The urinary excretion of lysozyme and N-acetyl-glucosaminidase, markers of renal tubular injury, were significantly increased after 7 or 14 days in rats with AN, despite DMTU treatment. Creatinine clearance was significantly reduced (p less than 0.05) in rats receiving ADR alone (0.223 +/- 0.011 ml/min/100 gm) when compared with that in normal controls (0.331 +/- 0.027 ml/min/100 gm) or DMTU-treated rats (0.289 +/- 0.035 ml/min/100 gm). Unlike DMTU, neither sodium benzoate nor DMSO reduced proteinuria in rats with AN.(ABSTRACT TRUNCATED AT 250 WORDS)     

Plasma concentration of itraconazole and its antifungal prophylactic efficacy in patients with neutropenia after chemotherapy for acute leukemia

Patients with acute leukemia are at high risk of fungal infection, suggesting that a preventive strategy is required. Fourteen patients receiving intensive chemotherapy for acute leukemia were studied to evaluate antifungal prophylaxis using itraconazole, and the plasma concentration of the drug was measured to determine its relationship to clinical efficacy. The median age of the patients was 50 years (range, 25 to 79 years), and all patients had neutropenia (less than 500 neutrophils/μl) which had lasted a median of 16 days (range, 4 to 30 days). Itraconazole was given orally at a dose of 200 mg (four capsules of 50 mg) once daily for at least 14 days. An H2-receptor antagonist was also given to prevent chemotherapy-induced gastrointestinal toxicity. Trough plasma concentrations of itraconazole and its metabolite, hydroxyitraconazole, were determined by reverse-phase high-performance liquid chromatography. The mean concentrations of itraconazole and hydroxyitraconazole on day 10 were 300 ± 96 ng/ml (range, 131–428 ng/ml) and 776 ± 369 ng/ml (range, 320–1582 ng/ml), respectively. There were marked inter-patient variations in both concentrations. No side effects were observed in the patients, and there was no definite fungal infection episode during this study. Daily oral administration of 200 mg of itraconazole appears to be effective as prophylaxis against fungal infection in neutropenic patients with acute leukemia. However, there were marked individual variations in the itraconazole plasma concentrations, which suggests that the plasma concentration should be monitored in patients with a risk of low absorption of this drug to adjust the dose given to an adequate level. Received: May 31, 1999 / Accepted: August 17, 1999     

粒细胞集落刺激因子与干细胞因子合用对急性心肌梗死模型大鼠心功能的影响

背景:骨髓干细胞动员以其无创伤、无免疫排斥反应,不需要干细胞提取、培养、扩增等工作倍受青睐。目的:观察联合应用粒细胞集落刺激因子和干细胞因子对大鼠急性心肌梗死的治疗作用。设计:随机对照观察。单位:锦州医学院药理教研室实验室。材料:选用32只成年雄性SD大鼠,体质量(200±20)g,购自锦州医学院实验动物中心。重组人粒细胞集落刺激因子(北京双鹭制药),重组人干细胞因子(成都地奥有限公司)。方法:实验于2005-07/11在锦州医学院药理教研室实验室进行。①5mg/kg盐酸异丙基肾上腺素左下腹腔注射复制急性心肌梗死模型,3h后将大鼠随机分为4组,每组8只。综合治疗组:用生理盐水稀释浓度至10mg/L的重组人粒细胞集落刺激因子1mL/kg和重组人干细胞因子1mL/kg皮下注射,连续5d。粒细胞集落刺激因子组:单用生理盐水稀释浓度至10mg/L的rhG-CSF1mL/kg皮下注射,每只大鼠和综合治疗组大鼠注射药品差量用生理盐水(1mL/kg)补足,连续5d。干细胞因子组:单用生理盐水稀释浓度至10mg/L的人干细胞因子1mL/kg皮下注射,每只大鼠和综合治疗组大鼠注射药品差量用生理盐水(1mL/kg)补足,连续5d。对照组:单用生理盐水(2mL/kg)皮下注射。②分别于造模后第14d和28d,摸球法从每组大鼠中抽取4只麻醉,自左心室心尖部插入内充肝素钠的塑料管至左心腔,用Medlab-u18c生物信号采集处理系统描记左心室峰压,左心室舒张末压,左室内压最大上升/下降速度,并同步记录心率。拔出气管插管,立即剪掉心脏,剪掉心房及右心室,微量天平称重,计算左心室质量/体质量,评估心肌重塑情况,将组织块切片,光镜下观测大鼠心肌病理形态及梗死面积。采用细胞图像分析仪病理图文分析每组大鼠心肌梗死面积。主要观察指标:各组大鼠左心功能指标、心肌梗死面积、心率和心室重塑情况及大鼠心肌病理形态。结果:纳入大鼠32只全部进入结果分析,无脱落。①大鼠左心功能指标比较结果:综合治疗组大鼠造模14,28d后左心室收缩压、左心室舒张末压、左心室内压最大上升/下降速度高于其他3组,造模28d时上述各指标均高于14d,差异有统计学意义(P<0.05),粒细胞集落刺激因子组两时间点上述指标均大于干细胞因子组及对照组(P<0.05)。②大鼠两时间点心肌梗死面积、心率和心室重塑情况:综合治疗组大鼠造模14,28d后心肌梗死面积及左心室重量小于其他3组,造模后28d心肌梗死面积小于14d(P<0.05),粒细胞集落刺激因子组两时间点上述指标均小于干细胞因子组与对照组。③大鼠心肌病理形态改变:造模后14及28d,综合治疗组和粒细胞集落刺激因子组均未见明显心肌瘢痕组织,有新生毛细血管生长,粒细胞集落刺激因子组毛细血管密度小于综合治疗组,均有成纤维细胞浸润。干细胞因子组和对照组可见瘢痕组织呈散在的灶性分布,有成堆或散在分布的淋巴细胞,其核小、深染、胞浆少,细胞间胞浆融合,新生肉芽组织增生不明显。结论:粒细胞集落刺激因子和干细胞因子合用对急性心肌梗死大鼠缺血损伤心肌的保护和再生作用优于单用,可改善急性心肌梗死大鼠的心室功能。     

地塞米松注射液对急性呼吸窘迫综合征干预作用的实验研究

目的:探讨地塞米松对油酸诱导大鼠急性呼吸窘迫综合征(ARDS)后肺纤维化的影响。方法:将54只SPF级雄性SD大鼠随机分为3组(n=18)。A组注射生理盐水作为正常对照;B、C组以油酸(0.15 ml/kg)制作模型,制模后6 h测动脉血气,以氧合指数≤200为模型成功,A、B组经静脉注射生理盐水(5 ml/kg),c组经静脉给予地塞米松(2 mg/kg),每天1次,连续1w。各组在给药后第7 d、14 d、28 d麻醉后处死大鼠,测定支气管肺泡灌洗液(BALF)中Ⅲ型前胶原(PcⅢ)浓度,留取右侧肺经包埋后行Masson染色。结果:B组和C组PcⅢ浓度在第7 d、14 d、28 d时均明显高于A组(P0.05),且C组明显低于B组(P0.01),C组肺纤维组织增殖较B组明显减轻。结论:地塞米松可能对ARDS后肺纤维化有抑制作用。     

Micropuncture studies of proximal tubule albumin concentrations in normal and nephrotic rats

The concentration of serum albumin in proximal tubule fluid of normal rats and animals with aminonucleoside nephrosis was studied using renal micropuncture techniques. Albumin was quantitated by an ultramicrodisc electrophoresis method capable of measuring 3 chi 10(-11) g of albumin, in 10 nl volumes. With this sensitivity, only small samples of tubule fluid were required for analysis. Collection times could be kept short, therefore decreasing the opportunity for sample contamination with extraneous serum albumin. The measured mean concentration of albumin in proximal tubule fluid (1 mg/100 ml in females and 0.7 mg/100 ml in males) was somewhat lower than values reported by others, but even these values are apt to have been artifactually high as a result of animal preparation and trace contamination of samples during micropuncture. Rats injected with aminonucleoside of puromycin 4 days earlier, showed a significant increase in tubule-fluid albumin concentration coincident with a fall in serum albumin concentration and a 43-fold increase in urine albumin concentration. Tubular absorption of albumin was small relative to that of water. Although albumin filtration was significantly increased over that in normal animals, the glomerular basement membrane still served as a highly efficient barrier to albumin transfer.     

Effect of Intravenous Albumin Infusion on Brain Salicylate Concentration

Background: Salicylate poisoning appears to result in death, despite supportive care, once a critical brain salicylate concentration is reached. The binding of salicylate to albumin is saturable; free plasma salicylate concentrations rise disproportionately to total drug levels. Because unbound salicylate distributes into the brain, the authors questioned whether an intravenous (IV) infusion of albumin would cause a redistribution of salicylate from the brain back into the plasma, which might allow enough time for hemodialysis to be instituted. Objectives: To determine if IV albumin infusion would lower brain salicylate concentrations through redistribution in a porcine model of acute salicylate poisoning. Methods: In a randomized controlled trial, 17 swine under anesthesia and controlled ventilation received 400 mg/kg of sodium salicylate IV over 15 minutes. At 60 minutes, nine animals received 1.25 g/kg albumin (25% solution) IV over 15 minutes, while eight control animals received an equal volume of normal saline (5 mL/kg). Arterial pH was maintained between 7.45 and 7.55. Serial measurements of serum albumin as well as free and total salicylate concentrations were obtained, and urine was collected for measurement of total salicylate excretion. At 180 minutes, animals were killed and brains harvested for measurement of brain salicylate concentrations. Results: Average peak serum total salicylate concentrations of 105.5 and 109 mg/dL were achieved in control and albumin‐treated animals, respectively. Albumin infusion was accompanied by statistically significant increases in serum total salicylate concentrations (median from 79.5 to 86.9 mg/dL at 75 minutes), while levels decreased slightly in control animals. Serum free salicylate concentrations decreased slightly in albumin‐treated animals, but the difference was not statistically significant. Median brain salicylate concentrations were about 14% lower in the albumin treatment group (17.8 mg/100 g brain) compared with controls (20.5 mg/100 g brain); this approached statistical significance (p = 0.075). Median urinary salicylate excretion was higher in the albumin‐treated group (0.83 vs. 0.48 g; p = 0.072), with similar urinary pH and volumes in both groups. Conclusions: In this animal model of salicylate poisoning, IV infusion of 1.25 g/kg albumin was accompanied by a 14% decline in median brain salicylate concentrations, which approached statistical significance.     

罗格列酮对大鼠重症急性胰腺炎肾损伤的保护作用

目的 探讨高选择性过氧化物酶体增殖物激活受体-γ的激动剂罗格列酮(ROSI)对大鼠重症急性胰腺炎肾损伤的可能作用。方法 雄性Wistar大鼠54只,随机（随机数字法）分为假手术组（SO组）、重症急性胰腺炎组（SAP组）和罗格列酮处理组（ROSI组）,每组大鼠18只。胆胰管逆行注射5％牛磺胆酸钠制备重症急性胰腺炎模型。ROSI组造模前30 min经股静脉注射10％二甲基亚砜(DMSO)溶解的罗格列酮（6mg/kg）;SO组、SAP组则经股静脉注射10％DMSO (0.2 mL/100 g)。术后3,12,24时点分批剖杀大鼠,每个时间点6只。分别检测各组血淀粉酶、血肌酐、血尿素氮、尿微量白蛋白、尿IgG、尿α1-微球蛋白含量,取肾组织行病理学检查。结果 SAP组各时间点血淀粉酶、血肌酐、血尿素氮、尿微量白蛋白、尿IgG、尿α1-微球蛋白等指均较SO组升高(P＜0.05);ROSI组上述指标较SAP组下降,各项指标在12,24h与SAP组差异具有统计学意义(P＜0.05),且随着处理时间的延长,ROSI组与SAP组各项指标的差异更显著。结论 重症急性胰腺炎可导致肾损伤,而罗格列酮可显著减轻重症急性胰腺炎所导致的肾损伤程度。     

复方黄精口服液对心力衰竭大鼠心肌肌球蛋白重链变化的作用

背景阿霉素是蒽环类抗肿瘤药,对多种恶性肿瘤有抑制作用.但由于其毒性大,可引起与剂量依赖性的心脏毒性,严重者可致心力衰竭.复方黄精口服液能抗自由基损伤,有望用于心力衰竭的辅助治疗.目的探讨复方黄精口服液抗心力衰竭疗效及其作用机制.设计随机对照观察.单位福建省医科大学附属第一医院中医科、福建省中医学院及福建省中医学院.材料实验于2000-08/2001-05在福建省高血压研究所完成,选用66只雄性SD大鼠.方法采用阿霉素损伤大鼠心肌致心力衰竭为模型,66只大鼠随机分为6组,每组11只.正常组腹腔注射等体积生理盐水.阿霉素组于实验开始后第2,4天腹腔注射阿霉素1 mg/kg;第6,8天腹腔注射2 mg/kg;第10,12天腹腔注射3 mg/kg;第14,16天腹腔注射4 mg/kg,16 d累计用药量达20 mg/kg.阿霉素+复方黄精口服液2 mL(小剂量组).阿霉素+复方黄精口服液4 mL(中剂量组).阿霉素+复方黄精口服液6 mL(大剂量组).小、中、大剂量组于实验开始后分别每日用复方黄精口服液灌胃.阿霉素的剂量用法同阿霉素单用组.阿霉素+天保宁(天保宁组)天保宁450 mg/kg隔日灌服共8 d.阿霉素的剂量用法同阿霉素单用组.主要观察指标观察各组大鼠心系数,α-肌球蛋白重链,β-肌球蛋白重链的变化.结果纳入实验动物数66只,在整个实验期间阿霉素组有5只大鼠,小剂量组4只大鼠,中剂量组2只大鼠,大剂量组3只大鼠,天保宁组3只大鼠死于明显的充血性心力衰竭,进入结果分析47只.与正常组比较,阿霉素组的α-肌球蛋白重链下降20.88%(P＜0.01),β-肌球蛋白重链上升50.93%(P＜0.01),心系数升高33.83%(P＜0.01).经给药治疗后,心肌β-肌球蛋白重链向α-肌球蛋白重链转化,与阿霉素组比较,各药物治疗组α-肌球蛋白重链上调(P＜0.01),β-肌球蛋白重链下降(P＜0.01),心系数均有不同程度下降(P＜0.01或P＜0.05),以上变化以中剂量组作用最佳.结论复方黄精口服液能减轻阿霉素致心力衰竭的毒性反应,其机制与复方黄精口服液可提高心肌α-肌球蛋白重链的转化有关,且呈剂量依赖性.