检索结果-南通市图书馆

世界核心医学期刊文摘（神经病学分册） 2005年第12期1卷 27-27页

作者： Krishnan A.V. Phoon R.K.S. pussell b.a. M.C. Kiernan 袁海峰 Dr.Prince of Wales Medical Research Institute Barker Street Sydney NSW 2031 Australia

Although multiple toxins have been implicated in the development of uraemic neuropathy, no causative agent has been identified. In the present study, the excitability properties of lower limb motor nerves in patients with end-stage kidney disease treated with haemodialysis were measured before, during and after a standard 5 h haemodialysis session, in an attempt to explore the pathophysiology of uraemic neuropathy. Compound muscle action potentials were recorded from tib.a.is anterior and extensor digitorum brevis, following stimulation of the common peroneal nerve in 14 patients. Measures of excitability were assessed in relation to changes in serum levels of potential neurotoxins, including potassium, calcium, urea, uric acid, parathyroid hormone and β-2-microglobulin. before dialysis, measures of nerve excitability were significantly abnormal in the patient group for axons innervating tib.a.is anterior and extensor digitorum brevis, consistent with axonal depolarization: refractoriness was increased and superexcitability and depolarizing threshold electrotonus were reduced. Pre-dialysis excitability abnormalities were strongly correlated with serum K+. Correlation was also noted between the severity of symptoms and excitability abnormalities. Haemodialysis normalized the majority of nerve excitability parameters. In conclusion, lower limb motor axons in uraemic patients are depolarized before dialysis. The correlation between serum K+and excitability measures indicates that hyperkalaemia is primarily responsible for uraemic depolarization, and a likely contributing factor to the development of neuropathy.

关键词：终末期肾病神经兴奋性尿毒症性神经病甲状旁腺激素去极化下肢运动神经胫骨前肌趾短伸肌超兴奋性兴奋性指标

来源：

维普期刊数据库

同方期刊数据库评论

在线全文

学校读者我要写书评

暂无评论

缺血导致终末期肾病轴突兴奋性的异常改变

引用

世界核心医学期刊文摘(神经病学分册) 2006年第11期 13-14页

作者： Krishnan A.V Phoon R.K.S pussell b.a.M.C.Kiernan 高中宝 Prince of Wales Medical Research Institute Barker Street Sydney NSW 2031 Australia Prof.

Peripheral neuropathy is present in 65%of patients with end stage kidney disease (ESKD). No cause is yet established: nerve excitability studies have shown that axons are chronically depolarized, primarily owing to hyperkalaemia, but in vitro studies have suggested a role for axonal Na+/K +pump dysfunction. To investigate Na+/K+pump activity in vivo, lower limb ischaemia was induced in five ESKD patients and six healthy controls by a sphygmomanometer cuff, inflated to 200 mm Hg and maintained for 13 min. The peroneal nerve was stimulated at the fibular neck and excitability parameters were recorded from tib.a.is anterior (TA) and extensor digitorum brevis (EDb) before, during and after the ischaemic period. baseline excitability studies in ESKD patients demonstrated reductions in threshold electrotonus and superexcitability and increased refractoriness, consistent with memb.a.e depolarization. During ischaemia, threshold increased in ESKD patients [by +23.6 ±5.0%(TA); +32.1 ±7.3%(EDb)] in contrast to the persistent threshold reduction observed in normal controls [-2.4 ±5.2%(TA); -13.0 ±8.2%(EDb); P by increased refractoriness and reduced superexcitability in both ESKD and control groups, consistent with ischaemic depolarization. Conversely, there was reduction in strength-duration time constant towards the end of ischaemia. Following release of ischaemia, the marked increase in threshold observed in normal controls was not evident in ESKD patients, but the rapid return of threshold to baseline argues against significant Na+/K+pump dysfunction. The abnormal pattern of response to ischaemia in the ESKD patients was not fully explained by the hyperkalaemic memb.a.e depolarization and suggests that another dialysable factor affects nerve excitability in ESKD patients, most likely H+ions, but that this factor only becomes evident during ischaemia. blockade of persistent Na+conductances by H+would also explain the reduction in stren

关键词：终末期肾病患者 ESKD 兴奋性应激性轴突轴索神经纤维

来源：

同方期刊数据库评论

在线全文

同方期刊数据库

学校读者我要写书评

暂无评论

欢迎您,

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

请选择保存的检索档案：

请选择收藏分类：

通借通还

欢迎您,

建议与咨询 留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

时间限定

文献类型

馆藏选择

核心期刊

语言

文献类型

帮助

文字说明：

检索规则说明：

检索范例：

分类表

所选分类

限定检索结果

文献类型

馆藏范围

日期分布

学科分类号

主题

机构

作者

语言

在线全文

在线全文

请选择保存的检索档案： 新增检索档案 确定 取消

请选择收藏分类： 新增自定义分类 确定 取消

通借通还

建议与咨询留下您的常用邮箱和电话号码，以便我们向您反馈解决方案和替代方法

请选择保存的检索档案：

请选择收藏分类：