Smart Prep技术在肾动脉CTA中的临床应用

目的:探讨Smart Prep技术在肾动脉多层螺旋CT血管造影中的应用。方法:20例行同层动态增强扫描,通过时间-密度曲线获得肾动脉的有效浓度阈值。65例行肾动脉CTA造影,经肘静脉团注370mgI/ml优维显1.5ml/kg后,应用Smart Prep软件实时监控靶血管浓度,当感兴趣区对比剂浓度达有效浓度阈值时触发增强扫描完成数据采集,重组和重建图像显示肾动脉。结果:65例肾动脉CTA造影均获成功,58例(89.2%)增强时相处于最佳扫描时期。增强扫描的延迟时间15~38s不等,个体差异明显,而肾动脉CT值持续位于有效浓度阈值(100HU)以上。结论:Smart Prep技术实时监控肾动脉对比剂浓度变化并及时触发增强扫描,它不受个体差异影响即可确保增强扫描的实施,优于小剂量试验。     

CT对肾结核的诊断意义探讨

目的探讨肾结核的CT表现，分析CT检查在肾结核诊断中的意义。方法对42例肾结核患者进行CT检查及增强扫描并结合其他临床资料作综合分析。结果CT检查肾内有低密度病灶，空洞形成，多发空洞有特征性改变。结论肾结核的CT表现有一定的特征性，CT检查优于其他方法，在肾结核的诊断中有重要意义。     

铜代谢异常相关疾病研究

铜是人类和动物重要的必需微量元素，参与体内蛋白质、氨基酸、核酸等营养物质的代谢，铜代谢异常会造成多种疾病。本文主要综述铜在糖尿病、动脉粥样硬化、冠心病、高脂血症、骨质疏松等的发生发展以及治疗方面的作用。     

12例开放性腋动脉损伤的诊治

目的探讨开放性腋动脉损伤的诊治体会。方法1996年-2002年，共诊治12例开放性腋动脉损伤的患者，从受伤到入院时间为3～14h，入院时均处于不同程度的休克状态，桡动脉搏动减弱或消失。在积极抗休克治疗的同时，急诊进行清创、血管神经探查和修复术。其中行腋动脉修补5例，腋动脉直接吻合6例，自体静脉移植修复1例。结果伤后8h内腋动脉再通8例，8～16h内腋动脉再通4例，无病例发生截肢或死亡。术后伤口均Ⅰ期愈合，桡动脉搏动良好。结论对开放性腋动脉损伤早期诊断和及时手术探查是控制休克、获取良好疗效的关键。     

补肾排毒合剂治疗慢性肾衰竭营养不良60例临床观察

目的:观察补肾排毒合剂治疗慢性肾衰竭营养不良的疗效.方法:90例慢性肾衰竭营养不良患者随机分为治疗组60例和对照组30例,并设健康对照组30例.治疗组和对照组在综合治疗的基础上,治疗组加用补肾排毒合剂,对照组加用爱西特和百令胶囊.比较两组肾功能、营养状态和血浆瘦素、神经肽Y的变化.结果:治疗组治疗后BUN、Scr明显降低,与治疗前及对照组相比均有统计学差异(P<0.05).治疗组营养状态好转,与治疗前及对照组相比均有统计学差异(P<0.05).两组慢性肾衰竭营养不良患者治疗前Leptin、NPY水平均高于健康组(P<0.05),治疗后治疗组Leptin、NPY较治疗前下降,有统计学意义(P<0.05),但与对照组相比无统计学差异(P＞0.05).结论:补肾排毒合剂治疗慢性肾衰竭营养不良疗效明显,可降低BUN、Scr,改善营养不良状态.     

前循环缺血性卒中老年患者颈动脉斑块及其稳定性与血流壁切应力的关系

目的通过探讨前循环缺血性卒中老年患者颈总动脉分叉处血流壁切应力的水平分析其在颈动脉斑块形成过程中的影响。方法本研究选择前循环缺血性卒中老年患者,应用经皮血管彩超测量颈动脉斑块及其稳定性以及对研究对象测量患侧颈动脉血流速度、血管内径和血液粘滞度,通过公式计算血流壁切应力。结果无斑块组和有斑块组之间、高回声和低回声斑块组之间血流壁切应力均有显著性差异(P<0．01)。结论血流壁低切应力促进颈动脉斑块、尤其是不稳定斑块的形成。     

冠状动脉瘘的诊治及新进展

冠状动脉瘘是一种罕见的冠状动脉畸形,绝大多数属于先天性畸形,极少数可由后天因素引起。由于冠状动脉血流向有关心腔、血管异常分流,导致引流部位负荷加重、瘘远端心肌缺血而引起相应临床症状。目前,绝大多数冠状动脉瘘已能由超声心动图明确诊断并可经内科介入技术或外科手术治愈。     

三磷酸腺苷结合盒运转体A1与颈动脉粥样硬化斑块的关系

目的 探讨三磷酸腺苷结合盒运转体A1(ATP binding cassette transporter A1,ABCA1)在人颈动脉粥样硬化斑块中的表达变化及作用机制.方法 收集24例人颈动脉粥样硬化斑块标本和10例肠系膜动脉标本(对照组),采用RT-PCR测定ABCA1 mRNA和视黄酸X受体α(RXRα)mRNA表达水平,并采用Western Blot检测ABCA1及RXRα的蛋白表达水平.24例人颈动脉粥样硬化斑块标本按病理分级,比较病理组织为Ⅲ级和Ⅰ级动脉粥样硬化组织间ABCA1 mRNA、RXRαmRNA表达水平及蛋白表达水平.结果 颈动脉粥样硬化斑块组的ABCA1 mRNA(0.79±0.04)和RXRα mRNA(0.73±0.04)表达与对照组相比上调,差异有统计学意义(P＜0.05);ABCA1 mRNA与RXRα mRNA增加水平相关(P＜0.05);颈动脉粥样硬化斑块的ABCA1蛋白表达(0.22±0.03)下调水平与对照组(0.53±0.03)相比差异有统计学意义(P＜0.05);Ⅲ级和Ⅰ级动脉硬化斑块ABCA1mRNA、RXRα mRNA及蛋白表达水平差异有统计学意义(P＜0.05).结论 ABCA1及RXRα蛋白表达水平下调可能是进展性动脉粥样硬化损害的关键因素.     

Blunted renal dopaminergic system activity in puromycin aminonucleoside-induced nephrotic syndrome.

BACKGROUND: A primary tubular sodium handling abnormality has been implicated in the edema formation of nephrotic syndrome. Dopamine synthesized by renal proximal tubules behaves as an endogenous natriuretic hormone by activating D(1)-like receptors as a paracrine/autocrine substance. METHODS: We examined the time courses of the urinary excretion of sodium, protein and dopamine in puromycin aminonucleoside (PAN)-treated and control rats. The rats were sacrificed during greatest sodium retention (day 7) as well as during negative sodium balance (day 14) for the evaluation of renal aromatic l-amino acid decarboxylase (AADC) activity, the enzyme responsible for the synthesis of renal dopamine. Also, the influence of volume expansion (VE) and the effects of the D(1)-like agonist fenoldopam (10 microg/kg bw/min) on natriuresis and on proximal tubular Na(+),K(+)-ATPase activity were examined on day 7. RESULTS: The daily urinary excretion of dopamine was decreased in PAN-treated rats, from day 5 and beyond. This was accompanied by a marked decrease in the renal AADC activity, on days 7 and 14. During VE, the fenoldopam-induced decrease in proximal tubular Na(+),K(+)-ATPase activity was more pronounced in PAN-treated rats than in controls. However, the urinary sodium excretion during fenoldopam infusion was markedly increased in control rats but was not altered in PAN-treated animals. CONCLUSION: PAN nephrosis is associated with a blunted renal dopaminergic system activity which may contribute to enhance the proximal tubular Na(+),K(+)-ATPase activity. However, the lack of renal dopamine appears not to be related with the overall renal sodium retention in a state of proteinuria.