期刊文献+
共找到5篇文章
< 1 >
每页显示 20 50 100
糖尿病微血管病变发病机制和治疗靶点 被引量:41
1
作者 李红 《浙江大学学报(医学版)》 CAS CSCD 2006年第3期233-237,共5页
糖尿病微血管病变是糖尿病致死致残的主要原因之一,严重影响糖尿病患者的生存质量。其发病机制尚未完全明了,目前认为主要与多元醇通路活跃、氧化应激增加、糖基化终产物形成及蛋白激酶C通路激活有关。以发病机制为靶点的治疗可能会为... 糖尿病微血管病变是糖尿病致死致残的主要原因之一,严重影响糖尿病患者的生存质量。其发病机制尚未完全明了,目前认为主要与多元醇通路活跃、氧化应激增加、糖基化终产物形成及蛋白激酶C通路激活有关。以发病机制为靶点的治疗可能会为预防和延缓糖尿病微血管病变的发生发展带来新的希望。 展开更多
关键词 糖尿病/并发症 糖尿病血管病变/病因学 糖尿病血管病变/病理生理学 糖尿病血管病变/药物疗法
在线阅读 下载PDF
Vascular Calcification:Where is the Cure?
2
作者 Wen-Wen Liu Mei-Lin Liu 《Chinese Medical Sciences Journal》 CAS CSCD 2024年第3期203-216,共14页
With the progress of aging,the incidence of vascular calcification(VC)gradually increases,which is correlated with cardiovascular events and all-cause death,aggravating global clinical burden.Over the past several dec... With the progress of aging,the incidence of vascular calcification(VC)gradually increases,which is correlated with cardiovascular events and all-cause death,aggravating global clinical burden.Over the past several decades,accumulating approaches targeting the underlying pathogenesis of VC have provided some possibilities for the treatment of VC.Unfortunately,none of the current interventions have achieved clinical effectiveness on reversing or curing VC.The purpose of this review is to make a summary of novel perspectives on the interventions of VC and provide reference for clinical decision-making. 展开更多
关键词 vascular calcification CLINICAL PATHOPHYSIOLOGY therapeutic strategies novel findings
在线阅读 下载PDF
代谢综合征及其代谢指标异常对患者血浆vWF与NO含量的影响 被引量:3
3
作者 孙雅逊 胡申江 +3 位作者 张新华 孙坚 朱朝辉 张志杰 《浙江大学学报(医学版)》 CAS CSCD 2006年第3期315-318,共4页
目的:观测代谢综合征(MS)患者血浆中血管性假性血友病因子(vWF)和一氧化氮(NO)含量的改变,探讨其对内皮功能的影响。方法:79例患者按MS代谢指标异常数量的不同分为1~2个代谢指标异常组(n=43)和MS组(n=36),另设正常对照组... 目的:观测代谢综合征(MS)患者血浆中血管性假性血友病因子(vWF)和一氧化氮(NO)含量的改变,探讨其对内皮功能的影响。方法:79例患者按MS代谢指标异常数量的不同分为1~2个代谢指标异常组(n=43)和MS组(n=36),另设正常对照组(n=30),测定其血浆中vWF及NO含量,分析MS代谢指标异常与vWF、NO的关系。结果:MS患者的vWF含量高于1~2个代谢指标异常组(P〈0.05)和正常对照组(P〈0.01),1~2个代谢指标异常组的vWF值高于正常对照组(P〈0.05);MS组的NO含量低于正常对照组(P〈0.05),1~2个代谢指标异常组的NO含量低于正常对照组(P〈0.05),MS组与1~2个代谢指标异常组无明显差异(P〉0.05),但是在两组去除糖尿病患者后,MS组的NO值低于1~2个代谢指标异常组。结论:随着代谢指标异常增多,患者内皮功能受损加重。 展开更多
关键词 代谢综合征X 一氧化氮/血液 von Willebrand因子/代谢 内皮 血管/病理生理学
在线阅读 下载PDF
脊髓背柱在躯体传入冲动抑制中枢性升压反应的上行途径中的作用 被引量:1
4
作者 虞燕琴 夏强 张荣宝 《浙江大学学报(医学版)》 CAS CSCD 2005年第5期436-440,共5页
目的:探讨脊髓背柱(DC)在躯体传入冲动对下丘脑室旁核(PVN)兴奋所致的心血管反应的抑制作用中的地位。方法:电刺激SD大鼠中枢核团PVN及对侧腓深神经(DPN),同时记录大鼠股动脉血压、平均动脉压(MAP)、心电图及心率(HR)。急性损毁大鼠一... 目的:探讨脊髓背柱(DC)在躯体传入冲动对下丘脑室旁核(PVN)兴奋所致的心血管反应的抑制作用中的地位。方法:电刺激SD大鼠中枢核团PVN及对侧腓深神经(DPN),同时记录大鼠股动脉血压、平均动脉压(MAP)、心电图及心率(HR)。急性损毁大鼠一侧背柱或损毁后存活5d,观察DPN传入冲动对兴奋PVN诱发的心血管反应的影响及大鼠的痛反应、肌张力及屈肌反射等。结果:电刺激一侧PVN后,MAP升高,HR变化不一,以下降为主。刺激DPN对刺激PVN诱发的上述反应有抑制作用,MAP上升幅度由单独电刺激PVN时的(3.05±0.29)kPa降为(1.73±0.28)kPa,抑制百分比为43.29%。急性损毁右侧DC后,电刺激右侧或左侧DPN均能抑制刺激对侧PVN引起的升压效应,抑制百分比分别为38.64%和39.97%。左右侧DPN的抑制效应比较无显著差异(P>0.05)。在6只损毁DC后5d的大鼠,电刺激右侧或左侧DPN也均能抑制刺激对侧PVN引起的升压反应,抑制百分比分别为33.87%和36.86%。左右侧DPN的抑制效应比较无显著差异(P>0.05)。损毁DC后大鼠双侧后肢痛反应无明显改变。结论:DPN抑制中枢性升压反应的上行传导途径不通过脊髓背柱。 展开更多
关键词 电刺激 下丘脑室旁核/生理学 脊髓丘脑束/生理学 腓神经 心率 血管系统/病理生理学 血压
在线阅读 下载PDF
Androgen actions on endothelium functions and cardiovascular diseases 被引量:3
5
作者 Jing-Jing CAI Juan WEN +3 位作者 Wei-Hong JIANG Jian LIN Yuan HONG Yuan-Shan ZHU 《Journal of Geriatric Cardiology》 SCIE CAS CSCD 2016年第2期183-196,共14页
The roles of androgens on cardiovascular physiology and pathophysiology are controversial as both beneficial and detrimental effects have been reported. Although the reasons for this discrepancy are unclear, multiple ... The roles of androgens on cardiovascular physiology and pathophysiology are controversial as both beneficial and detrimental effects have been reported. Although the reasons for this discrepancy are unclear, multiple factors such as genetic and epigenetic variation, sex-specificity, hormone interactions, drug preparation and route of administration may contribute. Recently, growing evidence suggests that androgens exhibit beneficial effects on cardiovascular function though the mechanism remains to be elucidated. Endothelial cells (ECs) which line the interior surface of blood vessels are distributed throughout the circulatory system, and play a crucial role in cardiovascular function. Endothelial progenitor cells (EPCs) are considered an indispensable element for the reconstitution and maintenance of an intact endothelial layer. Endothelial dysfunction is regarded as an initiating step in development of atherosclerosis and cardiovascular diseases. The modulation of endothelial functions by androgens through either genornic or nongenomic signal pathways is one possible mechanism by which androgens act on the cardiovascular system. Obtaining insight into the mechanisms by which androgens affect EC and EPC functions will allow us to determine whether androgens possess beneficial effects on the cardiovascular system. This in turn may be critical in the prevention and therapy of cardiovascular diseases. This article seeks to review recent progress in androgen regulation of endothelial function, the sex-specificity of androgen actions, and its clinical applications in the cardiovascular system. 展开更多
关键词 ANDROGEN Cardiovascular diseases Endothelial cells ENDOTHELIUM ESTROGEN
在线阅读 下载PDF
上一页 1 下一页 到第
使用帮助 返回顶部