小鼠肾小球系膜细胞的增龄性改变及油酸对其影响

目的探讨C57BL／6J小鼠肾小球系膜细胞增龄性改变以及油酸对系膜细胞的影响。方法实验动物采用28月龄、3月龄小鼠，测定小鼠血清肿瘤坏死因子α（TNFα）水平，检测系膜细胞的增殖状况，测定肾小球系膜细胞培养上清中胶原Ⅰ、胶原Ⅳ和基质金属蛋白酶2（MMP-2）的含量，观察油酸对系膜细胞的影响。结果28月龄小鼠与3月龄小鼠比较，血清TNFα水平明显增高，分别为（71．6±17．3）μg／L和（59．7±9．7）μg／L，差异有统计学意义（P〈0．05）；肾小球系膜细胞增殖能力明显增强；细胞培养上清中胶原Ⅰ[（52．1±4．6）ng／1万个细胞对（20．3±3．5）ng／1万个细胞]、胶原Ⅳ[（26．3±3．5）ng／1万个细胞对（7．6±1．3）ng／1万个细胞]的水平明显增高；随着鼠龄的增加，细胞培养上清中MMP-2的活性明显下降。油酸可以刺激小鼠肾小球系膜细胞的增殖和胶原Ⅳ的分泌，尤以28月龄小鼠为著。结论与3月龄小鼠比较，28月龄小鼠的肾小球系膜细胞出现明显硬化病变倾向，油酸可刺激28月龄小鼠肾小球系膜细胞的增殖及胶原的分泌。     

肥胖蛋白、肥胖与血脂、血糖、内科疾病的关系

本文用特异性放免法测定60例病人血浆肥胖蛋白（OP）的含量，其均值低于对照组（158．08±8．58pg／ml比194．34±17．74pg／ml，P＜0．05）；肥胖症（BMI≥25）组低于非肥胖（BMI＜25）组（117．88±9．70pg／ml比201．13±6．36pg／ml，P＜0．001），OP与高密度脂蛋白胆固醇（HDL—C）呈正相关（P＜0．001），与BMI、总胆固醇（TC）、甘油三酯（TG）、低密度脂蛋白胆固醇（LDL—C）、动脉粥样硬化指数（ASI）、血糖（BG）均呈负相关（P均＜0．001），BMI与HDL-C呈负相关（P＜0．01），与TC、TG、LDL-C、ASI、BG均呈正相关（P均＜0．001），OP水平较低者，其肥胖症、高血压、冠心病、脑血管病、糖尿病和高脂血症发病率高（P＜0．01～0．001）。提示肥胖患者OP缺乏，OP具有调节体内脂肪贮存量及代谢的激素样作用，肥胖促使心脑血管及代谢性疾病的发生与发展。     

正常高值血压与尿微量白蛋白的关系

目的探讨尿微量白蛋白含量与血压水平的相关性。方法根据《2004年中国高血压防治指南》选择正常高值血压者（≥120／80mmHg）109例及正常血压者（〈120／80m／nHg）49例，测量血压，计算体重指数（BMI），测定空腹血糖（VBS）、血清总胆固醇（CHO）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL—C）、低密度脂蛋白胆固醇（LDL—C）、尿微量白蛋白（EusA法）等，并做比较。结果正常高值血压组与正常血压组相比，尿微量白蛋白含量升高[（3．08±1．58）mg／L比（3．86±1．7）mg／L，P〈0．01]，CHO、TG、HDL—C和LDL—C两组差异无统计学意义（P〉0．05）。Spearman相关分析显示，尿微量白蛋白与血压、血糖呈正相关，相关系数收缩压r=0．177，P〈0．05；舒张压r=0．252，P=0．001；空腹血糖r=0．279，P〈0．01。校正年龄、性别、血脂、体重指数偏相关分析表明，尿微量白蛋白含量与血压、血糖水平仍呈正相关，相关系数收缩压r=0．156，P=0．055；舒张压r=0．233，P〈0．05；空腹血糖r=0．251，P〈0．05。结论①正常高值血压组尿微量自蛋白水平较高，血糖、体重指数有异常变化，但血脂无异常变化。②尿微量白蛋白发生与舒张压、血糖关系更密切。     

丙丁酚可干预小鼠动脉粥样硬化病变并调节B类I型清道夫受体的表达

目的研究丙丁酚对高脂高胆固醇饲养的载脂蛋白E基因敲除小鼠和C57BL6／J小鼠血脂及动脉粥样硬化病变的影响，以及肝脏B类Ⅰ型清道夫受体和PPARγ表达的变化。方法分别随机将20只载脂蛋白E^-/^-小鼠和20只C57BL6／J小鼠分为载脂蛋白E^-／^-高脂组和载脂蛋白E^-/^-高脂＋0．5％丙丁酚组。     

肥胖及2型糖尿病患者血清apelin水平及其相关因素分析

目的测定肥胖及新诊断2型糖尿病患者血清apelin水平，探讨apelin与体脂、糖、脂代谢、胰岛素抵抗等的相关性。方法62例2型糖尿病患者和72例正常糖调节（NGR）者按体重指数（BMI）≥25kg／m^2或〈25kg／m^2又各自分为超重／肥胖与正常体重亚组，采用放射免疫分析法检测空腹血清apelin水平，同时检测空腹血糖（FPG）、HbA1C、血脂各项指标及空腹胰岛素（FINS）水平，计算BMI和腰臀比，并以稳态模型计算胰岛素抵抗指数（HOMA-IR）。结果校正年龄及性别后，2型糖尿病组血清apelin水平高于NGR组[（317．9±99．6vs279．0±66．8）ng／L，P〈0．01]，2型糖尿病组和NGR组中的超重／肥胖者均高于非肥胖者[（354．0±114．4vs274．1±53．0）ng／L，（299．2±74．5vs252．8±48．9）ng／L，均P〈0．05]，且2型糖尿病超重／肥胖组明显高于NGR肥胖组（P〈0．01）；偏相关分析显示，空腹血清apelin与BMI、ln（HOMA-IR）、FPG、总胆固醇（TC）呈正相关（r=0．353，r=0．355，r=0．224，r=0．241，均P〈0．01），与腰围、收缩压呈正相关（r=0．263，r=0．183，P〈0．05）。多元逐步回归分析发现，BMI、ln（HOMA—IR）和TC是血清apelin的独立相关因素。结论血清apelin水平在肥胖和初发的2型糖尿病人群中升高，且与BMI、HOMA-IR及脂代谢相关，推测apelin可能参与构成胰岛素抵抗综合征的病理生理基础。     

AMPK基因在C57BL／6J小鼠糖脂代谢中的作用

目的研究腺苷酸活化蛋白激酶（AMPK）基因在C57BL／6J小鼠糖脂代谢中的作用。方法分别取5周龄AMPK基因敲除（AMPK-KO）小鼠和C57BL／6J对照小鼠各24只,分为正常饲料（ND）喂养和高脂高糖饲料（HFD）喂养两组。喂养12周,每两周测定小鼠禁食4h血糖（FBG）,实验结束前行口服糖耐量实验（OGTT）,解剖取样,检测血生化指标、脂酶活性及相关蛋白的表达。结果AMPK-KO小鼠血糖、TC、LDL-C、HbA1c、6-磷酸葡萄糖脱氢酶（G6PD）活性、糖原合成酶激酶（GSK）活性、肝脏PPAR7蛋白表达量明显高于对照小鼠（P〈0．05）;其胰岛素含量、肝糖原含量、肌糖原含量、肝脂酶（HL）活性、脂蛋白酯酶（LPL）活性、总脂酶活性、葡萄糖激酶（GK）活性、肝组织P-AMPK蛋白、葡萄糖转运蛋白4（GluT-4）蛋白的表达量低于对照组（P〈0．05）。结论AMPK基因通过调节C57BL／6J小鼠糖脂代谢,在T2DM的发病中起重要作用。     

不稳定性心绞痛患者红细胞变形性改变的机理及其意义

观察13例不稳定性心绞痛（USAP）患者红细胞变形能力（ED）、红细胞膜收缩蛋白（SP）、钠泵（Na＋－K＋－ATPase）活性以及血脂的变化，并分析其相关性。结果显示，与对照组比较USAP患者红细胞变形指数（DI）、SP含量及Na＋－K＋－ATPase活性均明显降低（P＜0．001、0．01、0．01），而血脂（Ch、TG）明显升高（P＜0．01、0．05）。Ch浓度与Na＋－K＋－ATPase活性呈负相关（r＝－0．5941，P＜0．01），Na＋－K＋－ATPase活性与SP含量呈正相关（r＝0．6215，P＜0．01），DI与Na＋－K＋－ATPase活性和SP含量有正相关关系（τ＝100dyn／cm2时，r＝0．5732、0．5976，P＜0．05；τ＝200dyn／cm2时，r＝0．6781、0．6497，P＜0．01）。提示USAP患者ED减退与血脂增高以及SP含量和Na＋－K＋－ATPase活性降低有关，并且变形性减退的红细胞对动脉粥样硬化形成可能有直接作用。     

雌激素替代治疗对绝经后妇女冠心病者血脂代谢及抗氧化作用的研究

对32例绝经后妇女（PMW）冠心病患者（CHD组）进行雌激素替代治疗（ERT），以观察对其血脂代谢及机体抗氧化水平的影响。另选取绝经后健康妇女30例为对照组。CHD组口服尼尔雌醇（CEE3）每月2次，每次2mg，连用6个月，分别于用药前、用药后3个月及6个月检测总胆固醇（TC）、甘油三酯（TG）、高密度脂蛋白胆固醇（HDL－C）、低密度脂蛋白胆固醇（LDL－C）、脂蛋白（a）［LP（a）］、氧化修饰低密度脂蛋白（Ox－LDL）、丙二醛（MDA）及超氧化物歧化酶（SOD）。结果表明ERT前CHD组与对照组比较LP（a）、Ox－LDL及MDA水平明显升高（P＜0．05），而SOD总活力显著降低；CHD组于ERT后TC无明显变化，TG呈升高趋势（P＞0.05），而LDL-C、TC／HDL－C和LDL－C／HDL－C显著下降（P＜0．01），LP（a）也明显降低（P＜0．05），而HDL－C显著上升（P＜0．01）；血浆Ox－LDL、血清MDA显著下降（P＜0．01），血清SOD总活力明显上升（P＜0．05），提示ERT不仅能显著改善PMW之CHD患者血脂紊乱，而且能有效地提高机体抗氧化水平。     

老年高血压、冠心病与血清高密度脂蛋白胆固醇的相关性研究

目的：探讨血清高密度脂蛋白胆固醇（HDL－C）与老年性高血压病（EH）、冠心病（CHD）的相关性。方法：选择住院60岁以上的疗养员879例，分EH组、CHD组和老年性冠心病并高血压病（CHD－EH）组，另139例老年健康人为对照组。检测各组的血压、血清总胆固醇（TC）和血清HDL－C的含量。结果：EH组和CHD－EH组的血清HDL－C含量显低于对照组（P＜0．05）；CHD组的血清HDL－C含量非常显低于对照组（P＜0．01）。对照组TC／HDL－C＝2．72；EH组、CHD－EH组、CHD组的血清TC／HDL－C分别为3．45，4．37，4．57，较对照组均明显升高（P＜0．01）。结论：EH组、CHD组和CHD－EH组的血清HDL－C明显低于对照组。     

雄性激素对小鼠骨髓巨噬细胞杜氏利什曼原虫感染水平的影响

目的：研究雄性激素对杜氏利什曼原虫感染的C57BL／6J小鼠骨髓巨噬细胞（BMMs）水平的影响。方法：用雄性激素处理小鼠3wk后，收集BMMs，培养5d后，按BMMs前鞭毛体＝110的比例，接种杜氏利什曼原虫，用吉姬氏染色法观察不同时相的感染水平。结果：与植物油处理的对照组相比，雄性激素处理的小鼠BMMs对前鞭毛体较为易感，并随着感染时间的延长其感染水平增高（感染后3h，P＜0．05；24h，48h和72h，P＜0．01）。结论：雄性激素可增加杜氏利什曼原虫对BMMs 的感染水平, 这可能与雄性激素诱导的免疫抑制作用有关。     

Helicobacter pylori eradication lowers serum homocysteine level in patients without gastric atrophy

AIM: To determine whether Helicobacter pylori ( H pylori)infection caused hyperhomocysteinemia by altering serum vitamin B12, serum folate and erythrocyte folate levels and whether eradication of this organism decreased serum homocysteine level.METHODS: The study involved 73 dyspeptic H pylori-positive patients, none of them had gastric mucosal atrophy based on rapid urease test and histology. Out of 73 patients, 41 (56.2%) showed a successful eradication of Hpylori4 wk after the end of treatment. In these 41 patients, fasting serum vitamin B12, folate and homocysteine levels, and erythrocyte folate levels before and 4 wk after Hpylorieradication therapy were compared.RESULTS: The group with a successful eradication of Hpylori had significantly higher serum vitamin B12 and erythrocyte folate levels in the post-treatment period compared to those in pre-treatment period (210±97 pg/mL vs237±94pg/mL, P<0.O01 and 442±212 ng/mL vs 539±304 ng/mL,P = 0.024, respectively), but showed no significant change in serum folate levels (5.6±2.6 ng/mL vs 6.0±2.4 ng/mL,P= 0.341). Also, the serum homocysteine levels in this group were significantly lower after therapy (13.1±5.2 μmol/L vs 11.9±6.2 μmol/L, P = 0.002). Regression analysis showed that serum homocysteine level was positively correlated with age (P = 0.01) and negatively with serum folate level before therapy (P = 0.003).CONCLUSION: Eradication of H pylori decreases serum homocysteine even in patients who do not exhibit gastric mucosal atrophy. It appears that the level of homocysteine in serum is related to a complex interaction among serum vitamin B12, serum folate and erythrocyte folate levels.     

Increased serum levels of granulocyte-macrophage colony-stimulating factor in hypercholesterolemic patients

Background: Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a cytokine that may be implicated in multicellular events of the atherosclerotic inflammatory process. Methods: To investigate the impact of hypercholesterolemia on serum levels of GM-CSF, we determined circulating GM-CSF, soluble intercellular adhesion molecule-1 (sICAM-1), and soluble vascular cell adhesion molecule-1 (sVCAM-1) in 25 hypercholesterolemic patients with no clinical evidence of cardiovascular disease and in 15 normocholesterolemic control subjects who were matched for age and sex to the hypercholesterolemic group. Results: Hypercholesterolemic patients had higher levels of GM-CSF than did controls (5.8±2.1 vs. 2.1±0.9 pg/ml, P<0.05). They also displayed increased serum levels of sICAM-1 (236.1±19.7 vs. 183.5±13.1, P<0.01) and of sVCAM-1 (673.8±27.3 vs. 591.3±23.4, P<0.01). A significant correlation was observed between GM-CSF levels and LDL-C values (r=0.58, P<0.01) as well as between GM-CSF and sICAM-1 levels (r=0.78, P<0.001). Conclusions: These results suggest that hypercholesterolemia is associated with elevated serum GM-CSF levels. The increased levels of circulating GM-CSF in hypercholesterolemic patients may be related to the monocyte/endothelial cell adhesive interaction and subsequent inflammatory process that accompany the hypercholesterolemia and characterize the early stages of atherogenesis.     

Relevance of erythrocyte deformability to the concentration of soluble cell adhesion molecules and glomerular filtration rate in patients with untreated essential hypertension

Relationship between erythrocyte deformability and: a) soluble cell adhesion molecules concentration, b) glomerular filtration rate (eGFR) has been investigated in three study groups: a group of 20 patients with diagnosed arterial hypertension, a group of 20 individuals with exclusively hypercholesterolemia and a group of 22 healthy persons. The individuals with hypertension or hypercholesterolemia were free of any other cardiovascular disease risk factor and were not on any therapy prior to entering the study. Clinical and laboratory data included systolic and diastolic blood pressure (obtained by ABPM), lipids profile, eGFR, red blood cell (RBC) deformability (assessed by shear stress laser diffractometry) and levels of circulating soluble vascular adhesion molecules-1 (sVCAM-1) as well as soluble intracellular adhesion molecules-1 (sICAM-1). In the group of hypertensives, RBC deformability and concentration of circulating soluble adhesion molecules showed statistically significant negative correlations: RBC deformability decreases with increasing level of: a) sVCAM-1, R = -0.61, p < 0.002, b) sIVCAM-1, R = -0.53, p < 0.009. In parallel, statistically significant increase of eGFR was observed with rising erythrocyte deformability, R = 0.60, p < 0.005. In the groups of healthy individuals and patients with hypercholesterolemia there was no sign of any correlations between the considered parameters. The observed correlations suggest that in patients diagnosed exclusively with hypertension, firstly, erythrocyte deformability may serve as a marker of endothelial dysfunction and, secondly, red blood cells may be mediators of adverse changes in kidneys.     

The relation between the erythrocyte nitric oxide and hemorheological parameters

We stimulated human erythrocytes obtained from patients with hypercholesterolemia (HC; n = 42), renal transplantation (RT; n = 18) and hypertension (HT; n = 10) with acetylcholine (ACh 10 microM) and measured the amperometric NO production, comparing with the NO levels achieved on erythrocytes of healthy persons (n = 27). We also measured the hemoglobin, hematocrit, erythrocyte aggregation, erythrocyte deformability, plasma viscosity and fibrinogen concentration from human blood samples. The erythrocytes NO levels were of 2.5 +/- 0.7 nM (P = 0.038, HC), 2.4 +/- 1.1 nM (RT) and 2.2 +/- 0.8 nM (HT) against the 2.0 +/- 0.8 nM for the control groups. For each group and at each shear stress value, the erythrocytes deformability decreases with the increase of the NO concentration after ACh stimulation. We observed a significant increase of the control values on the erythrocyte aggregation results on each patient group. Besides the lower erythrocyte deformability obtained on HC, RT and HT blood samples, the erythrocytes produced higher NO levels after ACh stimulation than the healthy ones. The power of erythrocyte hemorheological behaviour could be compensated by the NO production at the presence of acetylcholine. We can hypothesises that cholinergic drugs could be used as co-adjuvants of specific therapeutics compounds on these studied diseases.     

载脂蛋白M与冠状动脉病变的关系

目的探讨冠心病患者血清载脂蛋白M水平与冠状动脉病变的关系。方法根据冠状动脉造影结果,将120例受试者分为冠心病组(73例)和对照组(47例),应用酶联免疫吸附法检测受试者血清载脂蛋白M水平。比较冠心病组与对照组血清载脂蛋白M水平;比较不同冠状动脉病变数量和狭窄程度血清载脂蛋白M水平。结果冠心病组患者血清载脂蛋白M水平(10.12±1.79 mg/L)明显低于对照组(11.69±2.02 mg/L,P<0.01);冠心病患者多支病变组载脂蛋白M水平(9.19±1.22 mg/L)明显低于单支病变(11.22±1.69 mg/L)和双支病变(10.36±1.94 mg/L)组(P均<0.01);轻度狭窄组(11.39±1.58 mg/L)、中度狭窄组(10.14±1.46 mg/L)及重度狭窄组(9.04±1.30 mg/L)载脂蛋白M水平逐渐降低(P<0.05);冠状动脉病变数量(r=-0.485)和狭窄程度(r=-0.508)与血清载脂蛋白M水平呈负相关(P均<0.01)。结论载脂蛋白M可能是抑制动脉粥样硬化的保护因子。     

胰岛素样生长因子1在原发性高血压中的作用

目的　为了研究原发性高血压可能机制。方法　对 2 8例原发性高血压患者和 16例正常人测定了血清胰岛素样生长因子 1( IGF- 1)和一氧化氮 ( NO)水平 ,并与临床分级进行了相关分析。结果　原发性高血压患者 IGF- 1水平显著低于正常人 (分别为 2 6.2 2± 2 0 .2 3 μg/ l和 48.0 2± 3 3 .42 μg/ l,P<0 .0 5 ) ;且 IGF- 1水平与临床分级呈负相关 ( r=- 0 .43 7,P<0 .0 5 )。 NO水平显著低于正常人 (分别为 5 8.0 6± 13 .5 7m m/ l和 74.3 5± 2 4.86mm / l,P<0 .0 5 ) ;IGF- 1水平与 NO水平呈正相关 ( r=0 .45 5 ,P<0 .0 1)。结论　 IGF- 1可能参与了原发性高血压的病理生理过程 ,其可能途径之一就是通过降低 NO来进行     

Blood Viscosity: A Pathogenetic Factor in the Development of Essential Hypertension?

Inhibition of the ouabain-sensitive Na-K-ATPase by digoxin significantly decreases erythrocyte deformability (5). Since first a decrease in this transport system has been discussed as a pathogenetic factor in the development of essential hypertension and second an increase in blood viscosity, due to an increased hematocrit has been observed in elderly hypertensives, hemorheology and sodium transport systems were examined in adolescent hypertensives and compared with age-matched normotensive controls. 73 normotensives (N; mean blood pressure 127/80 mmHg) and 53 hypertensives (H; mean blood pressure 147/94 mmHg) aged 23-27 yrs were randomly selected from an epidemiological survey, covering 1342 adolescents.

While apparent whole blood viscosity at different shear rates, hematocrit, plasma fibrinogen were not significantly different, erythrocyte deformability, measured with a positive pressure filter system (pore ø 5 μ) and expressed as Q = ΔP/ery.susp.Hct 10%/ΔP/plasma was significantly attenuated with Q = 1.77 ± 0.05 in H, compared to 1.64 ± 0.04 in N (p < 0.05) The decrease in erythrocyte deformability was not accompanied by an inhibition of the Na-K-pump nor of total K⁺-uptake in erythrocytes, both measured with the ⁸⁶Rb uptake. There was only a slight increase in Na⁺-excretion in urine of 184.4 + 12.2 mval in H, compared to 162.0 ± 10.4 mval in N (n.s.). K⁺-excretion and serum electrolytes did not show any difference. Whether the decrease in erythrocyte deformability may contribute to an increase in peripheral vascular resistance in essential hypertension has to be further clarified.     

再生障碍性贫血对血粘度影响的初步研究

本文观测了42例慢性再障病人的血红蛋白(Hb)、红细胞滤过指数(EFI)和血粘度诸项指标,并与60例健康人对照。结果显示再障病人的全血比粘度、还原比粘度均显著低于正常人(P<0.01),其 EFI 显著高于对照组(P<0.05)。再障组的 Hb 和其全血比粘度、血浆比粘度均呈正相关(P<0.0001,P<0.001),Hb 和 EFI 则呈负相关(P<0.0001),其 EFI 与全血比粘度、血浆比粘度均呈负相关(P<0.05,P<0.05,)。本研究证实再障病人存在血粘度减低并有红细胞变形能力受损。     

脂滴自噬在丙型肝炎病毒核心蛋白下调沉默信息调节因子1诱导小鼠肝脂肪变性中的作用

目的研究脂滴自噬在HCV核心蛋白下调沉默信息调节因子1(SIRT1)诱导小鼠肝脂肪变性中的作用。方法小鼠随机分为两组,每组10只。实验组小鼠尾静脉注射HCV core重组表达载体。对照组小鼠尾静脉注射磷酸盐缓冲溶液。1个月后处死小鼠。检测肝功能、脂联素、血清和肝内甘油三酰(TG)、肝脏组织病理学检查肝脂肪变性程度。蛋白质免疫法检测肝脏SIRT1蛋白、脂联素受体(AdipoR)蛋白以及脂滴自噬相关蛋白微管相关蛋白1轻链3-Ⅱ(LC3-Ⅱ)、脂肪分化相关蛋白(ADRP)、尾部作用蛋白(TIP-47)和P62蛋白的表达。计量资料采用t检验。结果与对照组相比,HCV组小鼠出现肝脂肪变性;肝脏TG含量明显增加[(80.9±20.1)比(45.8±10.5)μg/mg,t=4.964,P0.01];血清脂联素[(1.05±0.25)比(1.41±0.45)ng/mL,t=2.211,P0.05]水平下降;SIRT1蛋白水平(0.4±0.1比0.9±0.2,t=7.071,P0.01)和AdipoR2蛋白水平(0.4±0.1比0.8±0.2,t=5.656,P0.01)下降;LC3-Ⅱ蛋白(0.8±0.2比0.4±0.1,t=5.656,P0.01)、TIP-47蛋白(0.9±0.3比0.4±0.1,t=5.000,P0.01)和ADRP蛋白(0.8±0.3比0.4±0.1,t=4.000,P0.01)表达增加;而p62蛋白(0.7±0.2比0.8±0.3,t=0.877,P0.05)表达水平差异无统计学意义。结论 HCV核心蛋白下调SIRT1表达,下调脂联素及受体表达,引起不完全脂滴自噬导致肝脂肪变性。     

Haemorheologic studies in patients with reduced coronary vasodilator capacity but normal coronary angiogram (syndrome X)

The cause of syndrome X, i.e. typical angina, positive exercisetest, normal coronary angiogram, normal resting cardiac function,but reduced coronary vasodilator capacity is still unknown.The purpose of the study was to investigate blood fluidity asa possible cause of syndrome X. Haematocrit, plasma viscosity,erythrocyte aggregation, and erythrocyte deformability wereexamined in 14 patients with syndrome X (group 1), 24 patientswith typical angina, positive exercise test, but normal coronaryvasodilator capacity (group 2), and 37 patients with atypicalchest pain and normal coronary arteries (control group). Coronaryvasodilator capacity was determined by the argon method. Comparedwith normals, patients with syndrome X showed an elevated plasmaviscosity (1.31 ±0.05 mPas vs l.26±0.04 mPas,2P>001), an elevated erythrocyte photometric aggregationindex (141 ±27% vs 100 ±23%, 2?>001) and areduced erythrocyte filterability (0.51 ±0.12 vs 0.66± 0.09, 2P > 0.01). Significant differences in thehaemorheologic parameters between group 1, group 2 and the controlgroup, however, were not detected. Multiple regression analysisdid not reveal a significant relationship between coronary vasodilatorcapacity and the haemorheologic parameters tested. The datasuggest that the reduction in coronary vasodilator capacityin patients with syndrome X cannot be attributed to haemorheologicalterations.