纳洛酮联合多巴胺对中重度缺氧缺血性脑病新生儿神经行为发育的影响

目的 观察纳洛酮联合多巴胺对中重度缺氧缺血性脑病新生儿神经行为发育的影响.方法 将58例新生儿随机分为治疗组24例和对照组34例.对照组接受常规对症治疗,治疗组在常规治疗基础上,早期给予多巴胺联合纳洛酮治疗,对比2组新生儿神经行为发育情况.结果 治疗组神经行为发育评分高于对照组,差异均有统计学意义（P＜0.05）.结论 早期采用纳洛酮联合多巴胺治疗中重度缺氧缺血性脑病,对于患儿的神经行为起到较好的改善作用,值得应用.     

早期应用多巴胺联合纳洛酮对中重度缺氧缺血性脑病新生儿神经行为发育的影响

目的:探讨早期应用多巴胺联合纳洛酮对中重度缺氧缺血性脑病新生儿神经行为发育的影响.方法:收集我院2013年8月~2014年8月46例中重度缺氧缺血性脑病患儿,对其早期应用多巴胺联合纳洛酮进行治疗,设定为观察组进行临床研究;选取同时期的46例中重度缺氧缺血性脑病患儿,单纯使用纳洛酮进行治疗,设定为对照组进行临床比较,经15个月的随访,观察两组发育商(DQ)及神经行为发育情况.结果:观察组治疗后的第6、9、12、15个月DQ值与对照组比较明显提高(P<0.05);观察组在大运动、适应性、个人社交、语言、精细运动方面的评分与对照组比较均明显提高(P<0.05).结论:早期应用多巴胺联合纳洛酮对中重度缺氧缺血性脑病新生儿可有效改善神经行为发育,值得临床推广.     

复方丹参和脑活素治疗新生儿缺氧缺血性脑病疗效观察

新生儿缺氧缺血性脑病 (HIE)是造成新生儿早期发病和死亡的重要原因。 1994年以来 ,应用复方丹参注射液和脑活素治疗新生儿缺氧缺血性脑病 2 5例 ,取得满意疗效。报告如下 :1　资料与方法1.1　一般资料　 1994年～ 1999年收治 45例新生儿缺氧缺血性脑病患儿 ,均符合 1989年 8月济南会议制定的新生儿缺氧缺血性脑病的诊断标准 [1 ]。随机分为两组 :治疗组 2 5例 ,男 2 0例 ,女 5例 ;足月儿 2 3例 ,早产儿 2例 ;出生体重2 50 0 g～ 40 0 0 g 2 3例 ,>40 0 0 g 2例 ;入院日龄 <2 4h 2 2例 ,2 4h～ 2 8h 3例 ;重度 HIE5例 ,中度 14例 ,轻度 6…     

新生儿缺氧缺血性脑病伴胃肠功能障碍的临床分析

目的分析小剂量多巴胺在新生儿缺氧缺血性脑病伴胃肠功能障碍中的治疗价值。方法将80例新生儿缺氧缺血性脑病伴胃肠功能障碍患儿随机分为两组,每组40例,给予常规治疗者为A组,在常规治疗的基础上加用小剂量多巴胺治疗者为B组,对比两组在接受治疗后脑部及腹部症状消失时间,治疗前后腹胀及肠鸣音改善情况和临床治疗总有效率。结果 B组脑病及腹部症状消失时间分别为(4.16±1.19)d及(2.68±0.64)d,均明显低于A组的(5.12±1.21)d及(3.26±0.68)d(P<0.05)。同时两组治疗前腹胀及嗳气评分比较未见统计学差异(P>0.05),而B组治疗后腹胀及肠鸣音改善优于A组(P<0.05)。此外,B组临床治疗总有效率明显优于A组(P<0.05)。结论新生儿缺氧缺血性脑病伴胃肠功能障碍治疗中加用小剂量多巴胺可有效的提高临床治疗效果。     

小剂量甘露醇早期治疗新生儿缺氧缺血性脑病疗效观察

目的观察小剂量甘露醇早期治疗新生儿缺氧缺血性脑病的疗效。方法治疗组40例,在新生儿缺氧缺血性脑病第1天开始吸氧、保持呼吸道通畅,维持正常血糖、血压等综合治疗,并给予20%的甘露醇,0.25～0.5g/kg,静脉滴注8h/次,连用3d,与对照组48例综合治疗及用地塞米松0.5mg/kg,呋噻米1mg/kg静脉滴注相比较。结果治疗组有效率达95%,对照组有效率85%,两组疗效对比,治疗组有效率明显高于对照组。结论小剂量甘露醇早期治疗新生儿缺氧缺血性脑病疗效显著,是安全的,甘露醇越早应用,效果越显著,并大大改善新生儿缺氧缺血性脑病的愈后不良率。     

纳洛酮治疗早期新生儿缺氧缺血性脑病临床观察

目的 :探讨新生儿缺氧缺血性脑病时早期应用纳洛酮治疗的效果。方法 :新生儿缺氧缺血性脑病患儿92例 ,随机分为治疗组56例 ,对照组36例 ,两组均采用统一的常规综合治疗 ,治疗组加用纳洛酮注射液。结果 :治疗组意识状态、原始反射、呼吸恢复情况的总有效率分别为83 9 %、82 1 %、85 7 % ;对照组总有效率分别为66 7 %、55 6 %、63 9 % ,经统计学处理 ,二组差异有显著性(P<0 05)。结论 :新生儿缺氧缺血性脑病患儿在常规综合治疗基础上早期应用纳洛酮治疗 ,患儿意识状态、原始反射、呼吸恢复均明显优于对照组。     

纳洛酮防治新生儿缺氧缺血性脑病疗效观察

目的 :探讨早期应用纳洛酮防治新生儿缺氧缺血性脑病的疗效。方法 :将2000年1月～2002年9月收治的窒息复苏后新生儿及窒息复苏后新生儿缺氧缺血性脑病患儿65例为治疗组 ,将1997年1月～1999年12月收治的同种患儿96例作为对照组 ,两组患儿均采用吸氧纠正酸中毒、止惊、抗感染、脱水降颅压、抗氧化剂、脑活素、胞二磷胆碱、能量合剂辅以高压氧治疗 ,治疗组在此基础上加用纳洛酮治疗 ,剂量0 2mg加入10 %葡萄糖30ml,以10ml/h的滴速静滴 ,每日1次 ,连用5日。结果 :治疗组显效30例 ,有效24例 ,无效11例。对照组显效31例 ,有效33例 ,无效30例 ,两组比较差异显著 (u=2.205 ,P<0 05)。结论 :纳洛酮对于新生儿缺氧缺血性脑病有疗效显著 ,无毒副作用之优点 ,可作为新生儿缺氧缺血性脑病防治的常规药物     

纳洛酮治疗新生儿缺氧缺血性脑病临床观察

目的　观察早期伍用纳洛酮干预治疗新生儿缺氧缺血性脑病 (HIE)的疗效。方法　 4 4例新生儿缺氧缺血性脑病患儿随机分为两组 ,治疗组在常规治疗基础上伍用纳洛酮 0 1mg/kg ,静推一次后再改为0 0 5mg·kg-1·d-1 10 %GS 4 0～ 6 0ml静脉点滴 (持续 4～ 6h) ,治疗 1周。分别观察患儿临床症状、体征变化 ,并行NBNA评分。结果　经伍用纳洛酮早期干预治疗后临床症状评分明显减低 ,NBNA评分高于对照组 ,差异有显著意义 (P <0 0 5 )。结论　纳洛酮早期干预治疗HIE能起到更好的脑保护作用 ,降低患儿致残率 ,提高生存质量。     

纳络酮与脑活素治疗中重度新生儿缺氧缺血性脑病的疗效观察

新生儿缺氧缺血性脑病 (ＨＩＥ)是新生儿早期发病和死亡的重要原因。目前尚无特殊的治疗方案 ,正确处理新生儿缺氧缺血性脑病对降低围产期死亡率 ,预防和减少远期后遗症有重要意义。我科对 4 0例确诊中、重度新生儿缺氧缺血性脑病的患儿 ,在应用脑活素与传统综合治疗的基础上 ,加用纳络酮治疗 ,疗效显著 ,现报告如下。1　临床资料1 1　病例选择　对 79例中、重度ＨＩＥ患儿随机分组进行对照观察 ,诊断标准及临床分度根据 1989年 9月济南全国儿科会议确定的原则[1] ,并经头颅ＣＴ检查证实。治疗组4 0例 ,男 18例 ,女 2 2例 ;其中 ,中度 2 4例…     

新生儿缺氧缺血性脑病的早期干预和康复治疗临床观察

目的：探讨新生儿缺氧缺血性脑病的早期干预和康复治疗临床疗效。方法98例新生儿缺氧缺血性脑病患儿作为本次的研究对象,以治疗方式的不同将其分为观察组和对照组,每组49例。对照组行常规治疗,观察组行早期干预和康复治疗,比较两组患儿的治疗效果。结果两组患儿采用不同治疗方式治疗后6、12、18、24个月的发育商比较,差异均具有统计学意义(P<0.05)。结论采用早期干预和康复治疗方式对新生儿缺氧缺血性脑病患儿进行治疗可有效的提高治疗效果,改善患儿发育商,有较高的应用价值,值得临床推广应用。     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg.kg) or i.p. (50 mg.kg) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) l.h. kg in the male rat and 10.6 (95% CI: 7.5, 15.0) l.h. kg in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p 0.001) in plasma obtained from the male (8.8 2.0%) compared with the female rat (11.7 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

Quantitative in vivo and in vitro sex differences in artemisinin metabolism in rat

1. The pharmacokinetics of the antimalarial compound artemisinin were compared in the male and female Sprague-Dawley rat after single dose i.v. (20 mg x kg(-1)) or i.p. (50 mg x kg(-1)) administration of an emulsion formulation. 2. Plasma clearance of artemisinin was 12.0 (95% confidence interval: 10.4, 13.0) 1 x h(-1) x kg(-1) in the male rat and 10.6 (95% CI: 7.5, 15.0) 1 x h(-1) x kg(-1) in the female rat suggesting high hepatic extraction in combination with erythrocyte uptake or clearance. Artemisinin half-life was approximately 0.5 h after both routes of administration in both sexes. Values for plasma clearance and half-lives did not statistically differ between the sexes. 3. After i.p. administration artemisinin AUCs were 2-fold higher in the female compared with male rat (p < 0.001). Artemisinin disappearance was 3.9-fold greater in microsomes from male compared with female livers and it was inhibited in male microsomes by goat or rabbit serum containing antibodies against CYP2C11 and CYP3A2 but not CYP2B1 or CYP2E1. 4. The unbound fraction of artemisinin in plasma was lower (p < 0.001) in plasma obtained from the male (8.8 +/- 2.0%) compared with the female rat (11.7 +/- 2.2%). 5. The possibility of a marked sex difference, dependent on the route of administration, has to be taken into account in the design and interpretation of toxicological studies of artemisinin in this species.     

Interindividual variability in metabolic activation in humans in vivo

In assessing interindividual variability in metabolic activation, the toxic metabolite is often too unstable for conventional analysis. Possible alternatives include a stable product of the reactive metabolite e.g. cysteinyl derivatives of N-acetyl-4-benzoquinoneimine, the toxic metabolite of paracetamol, adducts with DNA or protein, and indirect measurement of the activity of the enzyme(s) producing the active metabolite. An example of the last approach is the use of furafylline, a highly specific inhibitor of human CYP1A2, to determine the extent of the metabolic activation of the cooked food mutagens PhIP and MeIQx. The extent of inhibition, determined from levels of unchanged amine in urine, is an indirect measure of the activity of the activation pathway. Further refinement of this approach, allied to improved measures of the biological process of interest should prove of value in evaluating interindividual variability and its role in the risk assessment process.     

Theophylline kinetics in peripheral tissues in vivo in humans

Several biochemical and cellular effects have been described for methylxanthines under in vitro conditions. However, it is unknown, whether threshold concentrations required to exert these effects are attained in target tissues in vivo. We therefore employed the microdialysis technique for measuring theophylline concentrations in peripheral tissues under in vivo conditions.Following in vitro and in vivo calibration, microdialysis probes were inserted into the medial vastus muscle and into the periumbilical subcutaneous adipose layer of healthy volunteers. Following single oral dose administration of 300 mg or i.v. infusion of 240 mg theophylline, in vivo time courses of theophylline concentrations were monitored in tissues and plasma. Major pharmacokinetic parameters (c_max, t_max, AUC) were calculated for plasma and tissue time courses. The mean AUC_tissue /AUC_plasma-ratio was 0.56 (p.o.) and 0.55 (i.v.) for muscle and 0.55 (p.o.) and 0.72 (i.v.) for subcutaneous adipose tissue.We conclude that microdialysis provides important information on the distribution and the tissue pharmacokinetics of theophylline.Abbreviations FPIA Fluorescence polarisation immuno assay - AUC Area under the curve - t_max Time to peak concentration - c_max Peak concentration     

休克时血中氧自由基的变化

本实验测定10名休克患者血浆和红细胞的丙二醛(MDA)、血浆总抗的氧化活性(AOA)的含量。结果表明:休克病人红细胞膜和血浆 MDA 含量(4.298±0.722;5.348±0.834)与对照组(3.235±0.682;4.356±1.081)比较明显增高(P<0.05);血浆 AOA(39.65±7.858)与对照组(48.21±10.81)比较明显降低(P<0.01)。提示:休克时,患者机体内自由基反应增强是引起组织细胞损伤的原因之一。     

Trichinellosis in immigrants in Switzerland

We describe a case of trichinellosis diagnosed at the Division of Infectious Diseases, Hospital of Lugano, in January 2009. This case was associated with a cluster of cases and was traced to the consumption of contaminated meat after a wild boar hunt in Bosnia.     

Changes in angiopoietin expression in glomeruli involved in glomerulosclerosis in rats with daunorubicin-induced nephrosis

AIM: To study the potential pathological role of endogenous angiopoietins in daunorubicin-induced progressive glomerulosclerosis in rats. METHODS: Seventy male Wistar rats were allocated randomly into a daunorubicin group (DRB; n=40) or a control group (n=30). The rats in the DRB group were injected with DRB (15 mg/kg), in their tails. Subsequently, at intervals of 1, 2, 4, 6, 8, and 12 weeks, 5 male Wistar rats in each group were chosen randomly for 24 h urinary protein quantitative measurements (24 h UPQM), and determination of plasma tumor necrosis factor alpha (TNF-alpha), angiopoietin-1 (Ang1), and angiopoietin-2 (Ang2) levels. Kidney sections were examined by electron microscopy, Periodic Acid Schiff (PAS) staining, immunohistochemical staining and in situ hybridization histochemistry. RESULTS: As glomerulosclerosis progressed in the DRB group, expression of Ang1 mRNA and protein in glomeruli decreased and expression of TNF-alpha protein, Ang2 mRNA and protein in glomeruli increased. Expression of Ang1 mRNA and protein in glomeruli were negatively correlated with 24 h UPQM, Fn protein expression, and mean area of extracellular matrix (MAECM). In comparison, expression of Ang2 mRNA and protein in glomeruli were positively correlated with 24 h UPQM, Fn protein expression and MAECM; furthermore, there was a positive correlation between plasma Ang2 and 24 h UPQM. Plasma TNF-alpha and expression of TNF-alpha in glomeruli were positively correlated with expression of Ang2 mRNA and protein in glomeruli. There was a negative correlation between Ang1 protein expression and Ang2 protein expression in glomeruli. CONCLUSION: During DRB-induced glomerulosclerosis, podocyte injury led to a shift in the balance of Ang1 and Ang2 in glomeruli. Increased TNF-alpha in plasma and glomeruli may upregulate Ang2 expression in glomeruli. Elevated Ang2 in both plasma and glomeruli may mediate protein permeability through the glomerular filtration barrier. Moreover, local expression of Ang2 may facilitate the progress of glomerulosclerosis by upregulating a component expression of extracellular matrix.     

Hyperkalaemia in patients in hospital

A survey of all laboratory blood specimens with a plasma potassium concentration greater than or equal to 5.5 mmol/L was conducted over a three month period. Of 331 specimens with hyperkalaemia, 71 were excluded because the specimens was haemolysed, old or contaminated. The laboratory served a population of 348,561 and during this time measured the plasma potassium on 25,016 occasions. Sixty-six outpatients and 20 neonates were not evaluated. The survey was undertaken on 86 of 102 inpatients (46 males), 48 of whom were over 66 years of age. Fifty-seven patients were admitted under a medical service and 29 under a surgical service. Fifty-nine had a single episode of hyperkalaemia. Thirty-two underwent a surgical procedure. The commonest contributing factor was impaired renal function which was present in 71 (83%) patients. Although a definitive causative role for drugs could be identified in only five patients, in 52 (60%) patients drugs were a contributing factor (potassium supplements 24, ACE inhibitors 16, nonsteroidal antiinflammatory drugs 12). Thirty-five of the 86 (41%) patients died during their hospital admission. Nineteen of the 35 deaths occurred within three days of the hyperkalaemia being recorded. A normal plasma potassium was eventually documented in 50 of the 86 patients. Of the remaining 36 patients, 25 (69%) subsequently died. In general the treatment of patients with hyperkalaemia focused on identifying and treating the underlying cause. Hyperkalaemia must always be considered seriously and regard given to the overall clinical status of the patient, with particular attention to drug therapy, renal and cardiac function, acid base status and the possibility of sepsis.