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目的探讨睡眠呼吸暂停综合征（ＳＡＳ）发生肺心病和心脑血管病的机制，并对ＳＡＳ的全血粘度，血浆粘度和红细胞变形性进行测定。方法随机分ＳＡＳ组２２例，健康对照组１８例，用瑞士ｌｏｗ－ｓｈｅａｒ ３０型轴圆筒式粘度计测定全血粘度，利用重力驱动法测定红细胞变形性、结果ＳＡＳ组全血粘度（ｍＰａ·Ｓ）：高切 ４．６８±０．４．低功 １９． ６３±３．０，对照组分别为： ４． ２９±０．４３．１３．５±２．７。血浆粘度（ｍＰａ·ｓ）；ＳＡＳ组为１．９２±０．１５，对照组为１．３５±０．１１，ＳＡＳ全血粘度和血浆粘度较正常对照组明显提高（Ｐ＜０．０５）；ＳＡＳ红细胞滤过速度（％）３０、６１±１２．３３明显高于正常对照组２１、４５±１１．１０（Ｐ＜０．０５），表明红细胞变形性明显下降。结论ＳＡＳ病人血粘度增高，可能是形成血栓的原因之一，而细胞变形性下降影响微循环灌注，使血管阻力增高很可能是影响ＳＡＳ病人易发生肺心病，脑血管病和冠心病高血压的因素。
Objective To investigate the mechanism of pulmonary heart disease and cardiovascular disease in sleep apnea syndrome (SAS). The whole blood viscosity, plasma viscosity and erythrocyte deformability of SAS were measured. Methods A total of 22 patients were randomly divided into SAS group and healthy control group. The whole blood viscosity was measured by a Swiss low-shear 30-axis cylindrical viscometer. The erythrocyte deformability was measured by gravitation-driven method. Results The whole blood viscosity (mPa · S): High cut 4.68 ± 0.4. Low power 19. 63 ± 3.0, the control group were: 4. 29 ± 0.43.13.5 ± 2.7. Plasma viscosity (mPa · s); SAS group was 1.92 ± 0.15, the control group was 1.35 ± 0.11, SAS whole blood viscosity and plasma viscosity was significantly higher than the normal control group (P <0.05) ; SAS erythrocyte filtration rate (%) 30,61 ± 12.33 was significantly higher than the normal control group 21,45 ± 11.10 (P <0.05), indicating that erythrocyte deformability decreased significantly. Conclusions The increased blood viscosity of patients with SAS may be one of the causes of thrombus formation. Decreased cellular degeneration may affect microcirculation perfusion, which may result in the increase of vascular resistance which may affect the susceptibility to pulmonary heart disease, cerebrovascular disease and coronary heart disease in SAS patients factor.