亲属活体供肾移植后近期及中长期供者和受者的安全性分析

目的 探讨亲属活体供肾移植术后近期及中长期供、受者的安全性.方法 对106名亲属活体供肾者及其受者进行随访.随访日分别为肾移植后2个月至7年,其中32名供者随访时处于术后3个月内,44名处于术后3个月至1年,30名处于术后1年以上(其中术后1～3年者14名,3～5年者11名,5年以上者5名).以GFR作为评估供、受者肾功能的主要指标,比较供、受者手术前后的肾功能以及血压和尿蛋白.GFR的计算采用同位素发射计算机辅助断层显像法(GFR-ECT法)、24 h尿肌酐(Cr)清除率法(GFR-24 h Urine法)及Cockcroft-Gault公式法(GFR-Cr法).结果 取肾前106名供者的GFR-ECT和GFR-Cr分别为(1.51±0.13)和(1.99±0.42)ml/s,GFR-ECT是GFR-Cr的75.8%;术后第5天,供者的GFR-Cr为(1.40±0.33)ml/s,为术前的70.5%;术后3个月内、3个月至1年和1年以上者的GFR-Cr分别为(1.47±0.28)、(1.36±0.24)和(1.37±0.23)ml/s,分别为取肾术前的73.7%、68.0%和68.6%;术后1～3年者、3～5年者及5年以上者的GFR-Cr与超过1年者整体的GFR-Cr比较,差异无统计学意义(P>0.05).4名供者术后尿蛋白为±,均为术后超过1年者;4名供者血压升高.术后3个月、1年及1年以上,受者的GFR-Cr分别为(1.09±0.26)、(1.20±0.31)和(1.07±0.29)ml/s.结论 术后近期供者的GFR会下降,并小幅波动,术后中长期其GFR接近术前70%的水平,并趋于稳定.亲属活体供肾移植术后供、受者具有良好的安全性.     

综合镇痛疗法在肛肠病围手术期的应用

为探讨综合镇痛疗法在肛肠病围手术期的止痛效果,将458例行肛肠病手术患者随机分成综合镇痛组、自控镇痛组和传统镇痛组,对术后各组患者的疼痛程度及尿潴留等副作用发生率进行评估。结果显示,采用综合镇痛疗法的患者术后疼痛程度与自控镇痛组无明显差异（P〉0．05）,但尿潴留、失眠、嗜睡、晕厥、乏力、恶心呕吐等副作用发生率低（P〈0．01）,较传统镇痛组镇痛效果明显（P〈0．01）,尿潴留及失眠等发生率低（P〈0．01）。结果表明,综合镇痛疗法具有可靠的术后镇痛效果,并且能减少术后并发症的发生。     

偏瘫肢体功能锻炼对脑卒中后患者康复评定分析

目的：探讨早期功能锻练对脑卒中后偏瘫患者肢体功能恢复的疗效。方法：选取2006年1月至2008年1月间在我院住院的脑卒中偏瘫患者84例,随机分为康复组和对照组,康复组给予早期肢体功能锻炼,对照组给予常规的医护措施。结果：两组治疗后神经功能缺损程度评分均优于入院时,两者比较差异均具有统计学意义（P〈0．05）;康复组入院2周、4周及出院时神经功能缺损程度评分均优于对照组,两者比较差异具有统计学意义（P〈0．05）;治疗后康复组患者Brunnstrom分级上下肢I级例数明显少于对照组,两者比较差异具有统计学意义（P〈0．05）。结论：早期肢体功能锻炼能明显地改善脑卒中偏瘫患者的肢体功能,并能提高日常生活能力,值得应用。     

BIS用于经鼻蝶垂体瘤切除术指导异氟烷吸入对麻醉恢复的影响

目的研究脑电双频指数（BIS）在显微镜经鼻蝶垂体瘤切除术中指导异氟烷吸入对麻醉恢复的影响。方法行显微镜经鼻蝶垂体瘤切除术患者30例,年龄18-65岁,ASAⅠ-Ⅱ级,随机分为BIS组和对照组,每组15例。所有患者采用标准麻醉诱导,术中以0.8％-3％异氟烷吸入和标准瑞芬太尼持续微量泵输注维持麻醉。BIS组术中调整异氟烷的浓度使BIS维持在40-60,对照组根据患者血流动力学调整异氟烷浓度。术中每5min记录患者BIS、吸入、呼气末异氟烷浓度等,手术结束记录自主睁眼、呼吸时间、拔管时间和达到Aldrete改良评分9-10的时间。结果与对照组相比,BIS组手术期间的BIS升高、术中异氟烷用量减少、呼气末异氟烷浓度降低,从手术结束至自主睁眼、自主呼吸和Aldrete9-10的时间缩短。结论BIS指导异氟烷吸入能减少经鼻蝶垂体瘤切除术中异氟烷用量,加快患者麻醉恢复,有利于尽早进行神经系统检查。     

Reduction of dispersion of repolarization and prolongation of postrepolarization refractoriness explain the antiarrhythmic effects of quinidine in a model of short QT syndrome

Background: Short QT syndrome (SQTS) is a newly described ion channelopathy, characterized by a short QT interval resulting from an accelerated cardiac repolarization, associated with syncope, atrial fibrillation, and sudden cardiac death due to ventricular fibrillation. As therapeutic options in SQTS are still controversial, we examined antiarrhythmic mechanisms in an experimental model of SQTS. Methods and Results: Pinacidil, an I_K‐ATP channel opener, was administered in increasing concentrations (50–100 μM) in 48 Langendorff‐perfused rabbit hearts and led to a significant reduction of action potential duration and QT interval, thereby mimicking SQTS. Eight simultaneously recorded monophasic action potentials demonstrated an increase in dispersion of repolarization, especially between the left and the right ventricle. During programmed ventricular stimulation with up to two extrastimuli, pinacidil significantly increased the inducibility of ventricular fibrillation (1 heart under baseline conditions, 29 hearts during pinacidil administration; P = 0.0001). Additional treatment with the I_Kr blocker sotalol (100 μM) and the class I antiarrhythmic drugs flecainide (2 μM) and quinidine (0.5 μM) randomly assigned to three groups of 16 hearts led to prolongation of repolarization as well as refractory period. Sotalol or flecainide did not reduce the rate of inducibility of ventricular fibrillation significantly (P = 0.63; P = 0.219). However, quinidine reduced the inducibility of ventricular fibrillation by 73% (P = 0.008). The antiarrhythmic potential of quinidine was associated with a significantly greater prolongation of MAP duration, refractoriness, and postrepolarization refractoriness (PRR) as compared with sotalol and flecainide. Moreover, quinidine, in contrast to sotalol and flecainide, reduced dispersion of repolarization. Conclusion: Pinacidil mimics SQTS via increasing potassium outward currents, thereby facilitating inducibility of ventricular fibrillation. Quinidine demonstrates superior antiarrhythmic properties in the treatment of ventricular fibrillation in this model as compared with sotalol and flecainide because of its effects on refractoriness, PRR, and by reducing dispersion of repolarization.     

Velocity recovery function of the compound muscle action potential assessed with doublet and triplet stimulation

Normative values of muscle fiber conduction velocity depend on the conditions in which conduction velocity is measured due to the velocity recovery function (VRF) of muscle fibers. In this study the VRF of the compound muscle action potential (CMAP) was assessed following doublet and triplet stimulation in order to investigate the effect of repetitive muscle activation on muscle fiber conduction velocity. The VRF from doublet and triplet activation showed a peak of 4.6%-15.0% and 6.4%-25.9%, respectively, which is not significantly different. The VRF of the CMAP with doublet stimulation had a plateau between 25-75 ms, similar to that reported for single muscle fibers, and changed as a consequence of previous activation. The VRFs with doublet and triplet stimulation were different for interstimulus intervals in the range of 12-250 ms, where the triplet resulted in a plateau of supernormal conduction velocity. The VRF of the triplet could be explained by linear summation of the effects from doublet stimulations only for small distances between the two conditioning stimuli. These results provide new information on the adaptation of membrane properties of muscle fibers to repetitive activation. Changes in CMAP properties due to repeated activation may influence the accuracy of techniques based on CMAP recordings, such as collision methods.     

Motor and somatosensory evoked potentials in Autosomal Dominant Hereditary Spastic Paraparesis (ADHSP) linked to chromosome 2p, SPG4

The aim of our study was to evaluate Motor Evoked Potentials (MEPs) and cortical excitability, using Transcranial Magnetic Stimulation (TMS) as well as short latency Somatosensory Evoked Potentials (SEPs) in Autosomal Dominant Hereditary Spastic Paraparesis (ADHSP) patients. MEPs were recorded from upper and lower limb muscles in 12 patients (7 m and 5f) affected by ADHSP with spastin mutation (SPG4). We measured: (i) motor threshold (MTh); (ii) total motor conduction time (TMCT); (iii) direct and indirect central motor conduction time (d-CMCT and i-CMCT) calculated by subtracting from the cortical latency those obtained on magnetic spinal stimulation (d-PMCT) and via the F-wave method (i-PMCT); (iv) MEP amplitude (MEP/Mmax ratio%) and (v) duration of the cortical silent period (CSP). Latency, amplitude and persistence of the F-wave obtained with electrical nerve stimulation were also considered; H reflex was also tested from lower extremities. SEPs were recorded from spine and scalp sites following median and posterior tibial nerve stimulation; conventional latency and amplitude measurements were performed. In a comparison with the control group, the MTh recording from lower limbs was significantly higher (67.5 +/- 7.7% versus 52.5 +/- 6.9%), MEPs were absent in one case and showed reduced amplitude in the remainders (22.9 +/- 12.6% versus 66.3 +/- 25.9% of M wave); TMCT resulted to be abnormal (36.5 +/- 3.9 ms versus 27.1 +/- 1.4 ms) and d-CMCT as well as i-CMCT were significantly prolonged (23.1 +/- 3.5 ms versus 13.8 +/- 1.3 ms; and 20.1 +/- 3.4 ms versus 10.6 +/- 1.3 ms, respectively). The CSP, which was normal from the hands, was significantly shortened from the legs and correlated with spasticity scoring (Ashworth scale). Cortical SEPs from lower limbs were abnormal in all cases, whereas SEPs by stimulation of median nerves were normal; F-wave parameters from upper limbs showed no abnormalities, whereas an increased persistence was detected from lower limbs; H reflex amplitudes resulted larger compared with controls. Moreover, shortening of the CSP, being correlated with the Ashworth scale, can be considered an electrophysiological marker of spasticity that seems to arise from impairment of the supraspinal or intracortical inhibitory pathways with an additional contribution of increased segmental motor neuron excitability. These data prove the existence of comparable neurophysiological abnormalities in ADHSP with spastin mutation (SPG4) when long ascending and descending pathways are involved.     

Involvement of NR2A- or NR2B-containing N-methyl-D-aspartate receptors in the potentiation of cortical layer 5 pyramidal neurone inputs depends on the developmental stage

In the cortex, N-methyl-D-aspartate receptors (NMDARs) play a critical role in the control of synaptic plasticity processes. We have previously shown in rat visual cortex that the application of a high-frequency stimulation (HFS) protocol used to induce long-term potentiation in layer 2/3 leads to a parallel potentiation of excitatory and inhibitory inputs received by cortical layer 5 pyramidal neurones without changing the excitation/inhibition balance of the pyramidal neurone, indicating a homeostatic control of this parameter. We show here that the blockade of NMDARs of the neuronal network prevents the potentiation of excitatory and inhibitory inputs, and this result leaves open to question the role of the NMDAR isoform involved in the induction of long-term potentiation, which is actually being strongly debated. In postnatal day (P)18-23 rat cortical slices, the blockade of synaptic NR2B-containing NMDARs prevents the induction of the potentiation induced by the HFS protocol, whereas the blockade of NR2A-containing NMDARs reduced the potentiation itself. In P29-P32 cortical slices, the specific activation of NR2A-containing receptors fully ensures the potentiation of excitatory and inhibitory inputs. These results constitute the first report of a functional shift in subunit composition of NMDARs during the critical period (P12-P36), which explains the relative contribution of both NR2B- and NR2A-containing NMDARs in synaptic plasticity processes. These effects of the HFS protocol are mediated by the activation of synaptic NMDARs but our results also indicate that the homeostatic control of the excitation/inhibition balance is independent of NMDAR activation and is due to specialized recurrent interactions between excitatory and inhibitory networks.     

The Critical Period Hypothesis: Can It Explain Discrepancies in the Oestrogen‐Cognition Literature?

Although there is compelling evidence from small randomised controlled trials and cross-sectional studies indicating that oestrogen helps to protect against cognitive ageing in women, the findings of the large, Women's Health Initiative Memory Study failed to support the earlier findings. The attempt to resolve these discrepancies led to the formulation of the Critical Period Hypothesis which holds that oestrogen has maximal protective benefits on cognition in women when it is initiated closely in time to a natural or surgical menopause but not when treatment is begun decades after the menopause. This article reviews the evidence from basic neuroendocrinology, from animal behavioural studies and from human studies that supports the critical period hypothesis. In view of the promise of this hypothesis and its considerable clinical implications, a direct test of its validity is warranted.     

三种清洁手术围手术期抗菌药物预防性使用的调查与分析

目的了解某三级甲等医院三种清洁手术围手术期抗菌药物预防性使用的合理性。方法对2008年9月份38例清洁手术围手术期抗菌药物使用情况进行回顾性调查分析。结果三种清洁手术围手术期抗菌药物使用率为86.84%。使用频率最高为头孢菌素类药物。66.67%的药物DUI〈1。抗菌药物使用不合理占68.42%。使用不合理现象主要表现为药物种类选择不合理、疗程过长、换药过频、给药方法不当等。结论某三级甲等医院三种清洁手术围手术期预防性抗菌药物使用普遍存在不合理现象,需建立有效的监管机制以促进药物应用的合理化。