庄河地区健康人群血液流变学各项指标参考值的确定

为了解庄河地区正常人群的血液流变学正常值，对我地区900名20～75岁的正常人，分五个年龄组，分别检测全血粘度（高、中、低切）、血浆粘度、血沉、红细胞压积、纤维蛋白原七项指标。结果表明，各年龄组之间，全血粘度（高、中、低切）、血浆粘度、纤维蛋白原，差异无显著性（P〉0．05）；男女之间，血浆粘度、纤维蛋白原差异无显著性（P〉0．05），全血粘度商切、红细胞压积差异有显著性（P〈0．05），全血粘度中切、低切、血沉差异有高度显著性（P〈0．01）。反映出庄河地区不同性别、年龄段的正常人血液流变学特点及七项检测指标的正常参考值界限。     

糖尿病患者血液流变性分析

选取100例糖尿病患者作为观察组,另外选取同期100例健康体检者作为对照组,分析两组的血液流变性。结果两组血液流变性各指标差异显著,具有统计学意义（P〈0.05）。糖尿病患者所具有的血液流变性明显异于正常人,可见血液流变性是诊治糖尿病患者的重要依据。     

深圳市201名小学生血液流变学指标调查研究

目的检测深圳市201名小学生的血液流变学指标,初步建立适宜深圳市低龄人群血液流变学指标的正常参考值,探讨红细胞压积、血脂等因素对血液流变学指标的影响.方法挑选201名健康小学生(男119名,女82名)分别进行血流变各项指标检测统计.结果未成年小学生男女间各项指标及各组血浆粘度无显著差异,红细胞压积对血流变的影响是主要因素.结论报道了深圳市低年龄小学生的血流变参数.该参考值对本(市)区疾病的早期预防、诊断、疗效及预后都有重要的参考应用意义.     

非胰岛素依赖型糖尿病发病机制

<正>非胰岛素依赖型糖尿病(NIDDM)发病机制涉及遗传和环境因素,临床表现为异质性特征,不同亚组发病机制有所不同,现就目前公认的有关机制讨论如下.1 NIDDM胰腺病理和功能特征NIDDM患者B细胞显著减少,A细胞(分泌胰高血糖素)增加,D细胞(分泌生长抑素)减少,90%以上有胰岛淀粉样物质(主要由淀粉样多肽即IA-PP或Amylin组成)沉积,但老年非糖尿病人胰岛也可见少量Amylin,NIDDM者如无Amylin则可能是一种不同的亚组.早期NIDDM基础胰岛素(INS)分泌正常或升高,但与升高的血糖比值相对是低的.正常人静注葡萄糖后2～3分钟内INS分泌升高,为第一时相峰,迅速下降,到10分钟后又缓慢分泌增加,至少持续60分钟,称第二时相峰.NIDDM常缺乏第一时相峰,导致     

糖尿病患者血液流变学指标的改变

目的探讨糖尿病患者血液流变学指标的改变,揭示糖尿病人慢性病变的发病机理.方法对92例糖尿病患者和30例健康对照者血液流变学指标检测结果进行分析.结果糖尿病患者血液呈高粘、高聚、高凝状态,血液流变学指标经统计均有不同程度的增高(P<0.05或P<0.01).结论血液粘度升高,是引起糖尿病患者微血管病变进而导致多种合并症的重要原因.     

糖尿病人的血液流变学观察

糖尿病是当前世界上病死率最高的三大病症(心脑血管病、癌症、糖尿病)之一，而糖尿病人死于心脑血管并发症已增加至70％～80％．这与糖尿病在其整个病程中存在着明显的血液流变学的改变相关。为此，我们观察了沈阳地区老年非依赖型糖尿病病人血液流变学检测结果并与同年龄组的正常人对照。     

非胰岛素依赖型糖尿病患者血清SA水平变化及意义

目的探讨非胰岛素依赖糖尿病(NIDDM)患者血清SA水平变化及意义.方法采用单一试剂(CCM)显色法.结果NIDDM患者血清唾液酸(SA)水平随病程的延长而升高,且有无并发症患者血清SA水平也相差显著,SA水平与其病程及病情相关.结论检测NIDDM患者血清SA水平,对病情的判定及并发症的预测,可能有一定使用价值.     

50例肺心病患者发作期血液流变学变化

应用上海医科大学研制的BME-1型生物医学计算机为主机,连结XN-5型血粘度仪、细胞电泳仪及控温仪,检查50例肺心病人发作期的全血粘度比、血浆粘度比、红细胞电泳时间、红细胞压积的改变与正常对照组比较差异有显著性(p<0.05,p<0.01),血沉则差异无显著性(p>0.05)。同时检测了免疫球蛋白和纤维蛋白原,还对不同性别患者的血液流变学与正常人的对比试验。对于肺心病人红细胞增多反而缺氧的原因进行了一些探讨。     

运动训练对老年2型糖尿病患者血脂、血流变及一氧化氮的影响

目的:探讨运动训练对老年2型糖尿病患者血脂、血流变指标及一氧化氮(NO)的影响。方法:74例老年2型糖尿病患者,随机分为运动训练组(n=36)和对照组(n=38),2组患者均予常规相应性降糖药连续治疗6周,运动组在此基础上作适量运动训练,每周3次,共6周,2组均在治疗6周前后测定血脂、血流变及NO水平。结果:运动训练组治疗6周后NO较前明显提高(P<0.01),血脂、血流变部分参数均值明显下降(P<0.05)。对照组的血脂、血流变部分指标及NO虽有改变,但差异无显著性意义。结论:运动训练能明显降低老年2型糖尿病患者的血脂、血粘度,促进NO水平提高,有利于糖尿病治疗,NO合成能力提高是其可能的治疗机制之一。     

糖尿病患者血液流变学检测200例

目的 探讨血液流变学的变化与糖尿病后遗症心脑血管疾病的关系.方法 通过对200例糖尿病患者全血黏度、血浆黏度、红细胞聚集性、红细胞压积、红细胞沉降率的测定与健康人的测定值相比较.结果 糖尿病患者血液流变学变化显著,其多项指标与健康人相比较差异有统计学意义.结论 通过对糖尿病患者,血流变学各项指标测定,可以预防心脑血管疾病的发生.     

Essential hypertension and insulin resistance in non-insulin-dependent diabetes

A recent study has shown that young, lean, hypertensive subjects are more insulin resistant than corresponding normotensive subjects. Whether this finding can also be demonstrated in the presence of non-insulin-dependent diabetes mellitus (NIDDM) is not known. Therefore, the degree of insulin resistance was studied in 26 middle-aged hypertensive patients with NIDDM (11 men, 15 women) and 14 normotensive patients with NIDDM (eight men, six women) matched for age, metabolic control and the duration of diabetes, utilizing the glucose clamp technique. Non-obese NIDD patients (body mass index less than 27.0 kg m-2) with hypertension (n = 11) had significantly lower glucose disposal rates (GDRs) during the last 60 min of euglycaemic (5.5 mmol l-1) and hyperinsulinaemic (approximately 600 pmol l-1) clamp studies than NIDD patients without hypertension (n = 6) (782 +/- 94 vs. 1418 +/- 97 mumol m-2 min-1, P less than 0.05). In contrast, GDRs were similar in obese NIDD patients with (n = 15) and without (n = 8) hypertension (802 +/- 90 vs. 849 +/- 90 mumol m-2/min-1, respectively, P = NS). Basal hepatic glucose output, suppression of hepatic glucose production during hyperinsulinaemia and insulin secretion capacity did not differ between hypertensive and normotensive subjects.(ABSTRACT TRUNCATED AT 250 WORDS)     

Distribution of diacylglycerols among plasma lipoproteins in control subjects and in patients with non-insulin-dependent diabetes

BACKGROUND: Diacylglycerols (DAGs), which are well-known components of insect lipophorins, have been recently recognized as a major glyceride of human high-density lipoprotein (HDL). Moreover, DAGs are good substrates for hepatic lipase and for the phospholipid transfer protein (PLTP). The present work was undertaken to determine the lipoprotein concentrations of DAGs, in control subjects, in non-insulin-dependent diabetic (NIDD) patients and in patients with severe hypertriglyceridaemia. MATERIALS AND METHODS: Lipoproteins were isolated from 11 control subjects, 17 diabetic patients and three hypertriglyceridaemic patients, using a combination of ultracentrifugation and precipitation. After lipid extraction, DAGs were separated by thin-layer chromatography and quantified by a glyceride assay. RESULTS: DAGs were detectable in all lipoprotein fractions of the three groups of subjects. Total DAGs were correlated with total triglycerides (TGs) and even more strikingly with very low-density lipoprotein triglycerides. Although the majority of DAG was recovered in apo B-containing lipoproteins, the proportion of DAG with respect to TG was most elevated in HDL. CONCLUSION: These findings indicate that DAGs are probably formed from TG during lipolysis and that they can be transported to HDL through the action of PLTP. This raises the question whether DAG might act as an inhibitor of phospholipid transfer by competition for binding to PLTP.     

女性2型糖尿病患者合并无症状菌尿的临床分析

目的 探讨影响女性2型糖尿病合并无症状菌尿(ASB)的主要危险因素以及有关临床特点。方法 采用病例对照研究，2型糖尿病伴无症状菌尿(ASB^ )组128例，2型糖尿病不伴ASB(ASB^-)组300例，正常对照组74例。结果 ①女性2型糖尿病合并ASB的发病率为30％；②与ASB有关的危险因素包括年龄、病程、糖尿病视网膜病变、糖尿病肾病、糖尿病神经病变、既往尿路感染史、大血管疾病、高脂血症、绝经史，其中最主要的3个危险因素是年龄、大量白蛋白尿、既往尿路感染史；③随着糖尿病肾病、视网膜病变病情的加重，糖尿病合并ASB的发病率也相应增加；④糖尿病合并ASB^ 中段尿培养病原微生物以大肠埃希菌为主。结论 ①影响女性2型糖尿病合并ASB的因素众多，主要因素是年龄、大量白蛋白尿、既往尿路感染史；②血糖对女性2型糖尿病合并ASB发病作用降低；③ASB可能是女性2型糖尿病的一个并发症。     

Can reduction in hypertriglyceridaemia slow progression of microalbuminuria in patients with non-insulin-dependent diabetes mellitus?

The objective of this study was to investigate whether reduction in hypertriglyceridaemia is associated with a slower rate of progression of microalbuminuria in patients with non-insulin-dependent diabetes mellitus (NIDDM). Fifteen normotensive NIDDM patients with hypertriglyceridaemia (> 2.5 mmol L⁻¹) and microalbuminuria were randomly selected to receive either placebo (eight patients) or gemfibrozil 600 mg b.i.d. (seven patients). Progression of microalbuminuria was assessed during a 12-month follow-up period with measurements, consisting of blood tests and triplicate 24-h urine collections, at 1, 3, 6, 9 and 12 months. All but one patient in the treatment group showed a favourable response (≥ 20% reduction) of hypertriglyceridaemia to gemfibrozil. One patient in the placebo group showed a spontaneous reduction in triglyceride levels. Progression of microalbuminuria was lower, although not statistically significantly so, in the treatment group (36%) than in the placebo group (65%). In the group with ≥ 20% reduction in triglyceride levels, progression of MA was significantly lower than in the group with stable or increasing triglyceride levels (+1%, range −56% to +49% vs. +97%, range −35% to +202% respectively) ( P  = 0.03). Continued follow-up data of patients switching from placebo to gemfibrozil after the trial further support the role of serum triglyceride reduction in stabilizing albumin excretion. In conclusion, the results indicate that, in microalbuminuric NIDDM patients, effective treatment of dyslipidaemia could be associated with stabilization of urinary albumin excretion.     

Serum amyloid A protein in patients with non-insulin-dependent diabetes mellitus

We determined the serum amyloid A protein (SAA) levels in patients with non-insulin-dependent diabetes mellitus (NIDDM), and investigated the possible association between SAA and the complications of NIDDM.

The concentrations of SAA were measured in the plasma of 105 patients with NIDDM (52 men and 53 women, age mean ± SD, 61 ± 13 years) and 91 healthy subjects (37 men and 54 women, aged 57 ± 11 years). SAA concentrations were assayed by enzyme-linked immunosorbent assay.

SAA concentrations in the patients with NIDDM were significantly higher than those in healthy subjects (2.1 ± 1.3 vs. 1.2 ± 0.5 mg/L). There were no obvious relationships between SAA lebels and duration of diabetes, type of therapy, or control of blood sugar in the patients with NIDDM. However, SAA levels in patients with NIDDM increased significantly, with increase of urinary albumin excretion (p = 0.027). The increase of SAA in the patients with NIDDM did not influence the serum concentrations of lipid or lipoprotein.

The SAA concentration in NIDDM was unrelated to the type of treatment, but seemed to be related to the development of diabetic nephropathy.     

缺血性中风患者红细胞免疫黏附功能和血液流变学测定的临床分析

目的:探讨缺血性中风与红细胞免疫黏附(RCIA)功能和血液流变学的关系.方法:检测148例缺血性中风患者(包括脑梗死、脑血栓、脑栓塞、短暂性脑缺血发作)的RCIA功能和血液流变学指标,并与健康人比较.结果:与健康人比较,缺血性中风患者红细胞受体花环率(RBC-C3bRR)明显降低,红细胞免疫复合物花环率(RBCICR)明显升高;血液流变学呈高凝血症和(或)红细胞聚集症.相关分析显示,脑梗死、脑栓塞的全血高切黏度、全血低切黏度、血浆比黏度和脑血栓的全血高切黏度与RBC-ICR呈正相关.结论:不同类型缺血性中风患者均存在RCIA功能紊乱和血液流变学异常,且是缺血性中风病理的重要因素.     

奥美沙坦酯对原发性高血压患者血流动力学的影响

目的观察奥美沙坦酯对原发性高血压患者血流动力学的影响。方法 32例原发性高血压患者(奥美沙坦组)服用奥美沙坦20~40 mg/d10个月,另选30例原发性高血压患者服用复方降压片作为对照组,观察治疗前、后血流动力学指标的变化。结果奥美沙坦组服用奥美沙坦10个月后血压明显下降(P<0.01),全血低切黏度(ηb)、血浆黏度(ηp)及红细胞聚集指数(AI)全血低切还原黏度红细胞电泳纤维蛋白原(Fib)均显著降低(P<0.01);全血高切黏度、全血高切还原黏度、红细胞比容和红细胞刚性指数(RRI)也有所下降,但无统计学意义(P>0.05)。对照组治疗后仅ηb、ηp及AI较治疗前显著降低。结论原发性高血压患者服用奥美沙坦酯后在血压显著降低的同时,其红细胞聚集性Fib下降和红细胞变形能力增强,红细胞比容、血黏度降低。     

Relationship between obesity and the increased risk of major complications in non-insulin-dependent diabetes mellitus

Obesity and non-insulin-dependent diabetes mellitus (NIDDM) are closely linked. They frequently occur together in patients, and body mass index (BMI) is the strongest risk factor for the development of NIDDM. Both obesity and NIDDM are also major causes of morbidity and mortality from atherogenic macrovascular disease, and they are independent risk factors for coronary heart disease. The risk of developing NIDDM and cardiovascular disease is affected by the regional distribution of body fat. Visceral obesity is associated with a higher degree of risk than peripheral obesity. The metabolic and circulatory changes associated with visceral obesity lead to the development of insulin resistance and increased lipoprotein synthesis. For example, the change in the population profile of lipoproteins in the blood, and alterations in the levels of oxidative stress lead to an increased cardiovascular and macrovascular risk. The changes in lipid metabolism also affect haemorrheological function. They have been linked to decreased fibrinolysis (a serious cardiovascular risk factor) through elevated levels of plasminogen activator inhibitor factor, high blood viscosity, and increased erythrocyte aggregability. Increased BMI also appears to be associated with endothelial dysfunction, which is a major factor in atheroma plaque formation and development of thrombosis. Visceral obesity therefore adds a significant burden to the already increased cardiovascular risk inherent in NIDDM. However, even moderate weight loss may successfully reverse the majority of changes seen with visceral obesity.