肝郁脾虚证模型大鼠血流变及TXB2、PGFla的变化

目的:探查中医肝郁脾虚证模型的血流变及相关调节因子的状态。方法:采用慢性束缚应激+过度疲劳+饮食失节法建立大鼠肝郁脾虚证模型,测定大鼠造模三周、自然恢复一周时的血流变和血浆TXB2、PGF1a。结果:与正常组相比,模型组大鼠造模三周150/s、38/s、10/s、5/s切变率下的全血粘度、还原粘度均显著升高(P<0.001),红细胞聚集指数显著降低(P<0.001),红细胞压积显著升高(P<0.01),红细胞变形指数无显著性差异(P>0.05);血浆TXB2显著升高(P<0.001),6-keto-PGF1a显著降低(P<0.05),TXB2/PGF1a显著升高(P<0.01);模型组大鼠第四周150/s、38/s、10/s、5/s切变率下的全血粘度、还原粘度仍显著升高(P<0.001或P<0.01);红细胞聚集指数显著降低(P<0.001);红细胞压积与变形指数无显著性差异(P>0.05);血浆TXB2和TXB2/PGF1a显著降低(P<0.05),6-keto-PGF1a显著升高(P<0.05)。结论:肝郁脾虚证大鼠存在血液高粘和血栓易形成状态,恢复期血液高粘同时伴有扩血管因素的加强。提示肝郁脾虚证有血流...     

肝郁脾虚证模型大鼠血流变及TXB_2、PGFla的变化（英文）

目的：探查中医肝郁脾虚证模型的血流变及相关调节因子的状态。方法：采用慢性束缚应激＋过度疲劳＋饮食失节法建立大鼠肝郁脾虚证模型,测定大鼠造模三周、自然恢复一周时的血流变和血浆TXB2、PGF1a。结果：与正常组相比,模型组大鼠造模三周150/s、38/s、10/s、5/s切变率下的全血粘度、还原粘度均显著升高（P〈0.001）,红细胞聚集指数显著降低（P〈0.001）,红细胞压积显著升高（P〈0.01）,红细胞变形指数无显著性差异（P〉0.05）;血浆TXB2显著升高（P〈0.001）,6-keto-PGF1a显著降低（P〈0.05）,TXB2/PGF1a显著升高（P〈0.01）;模型组大鼠第四周150/s、38/s、10/s、5/s切变率下的全血粘度、还原粘度仍显著升高（P〈0.001或P〈0.01）;红细胞聚集指数显著降低（P〈0.001）;红细胞压积与变形指数无显著性差异（P〉0.05）;血浆TXB2和TXB2/PGF1a显著降低（P〈0.05）,6-keto-PGF1a显著升高（P〈0.05）。结论：肝郁脾虚证大鼠存在血液高粘和血栓易形成状态,恢复期血液高粘同时伴有扩血管因素的加强。提示肝郁脾虚证有血流变的异常和血浆TXB2-PGI2的平衡失调,主要涉及到血小板和血浆因素的参与。     

急性低氧性缺氧小鼠血液粘度与红细胞流变性变化

目的:观察小鼠急性低氧性缺氧(AHH)后红细胞流变性与血液粘度的变化。方法:32只健康昆明小鼠均分为:对照组、AHH组(复制模型,分为5 min、8 min、11 min三个亚组),在相应时间点,快速颈部脱臼后,从心尖取血,检测各组小鼠血液粘度与红细胞流变性指标。结果:与对照组相比,低氧5 min组各切变率下的全血粘度、全血相对粘度、全血还原粘度均显著降低,红细胞变形指数显著升高;低氧8 min组和低氧11 min组的群体细胞电泳时间显著延长、细胞电泳长度与细胞迁移率显著降低;低氧8 min组的全血相对粘度、全血还原粘度、红细胞聚集指数均显著高于、红细胞变形指数显著低于低氧5 min组。结论:AHH可引起小鼠血液粘度降低、红细胞电泳能力下降。     

大鼠肝癌诱发过程中血粘度及红细胞变形能力的异常改变

为了全面地反映肝癌发生发展整个过程的血液流变性的异常,本实验采用二乙基亚硝胺诱发大鼠肝癌模型,分六个相检测五个切变率下的全血粘度、血浆粘度及红细胞变形能力。结果表明红细胞变形能力随着肿瘤发展逐渐减低,血浆粘度随着诱癌时间延长 渐升高,到肿瘤晚期趋于平缓,而全血粘度先是升高,到诱癌２０周以后反而有下降趋势。     

肝郁脾虚证模型大鼠血流变及TXB2、PGF1a的变化

目的:探查中医肝郁脾虚证模型的血流变及相关调节因子的状态。方法:采用慢性束缚应激 过度疲劳 饮食失节法建立大鼠肝郁脾虚证模型,测定大鼠造模三周、自然恢复一周时的血流变和血浆TXB2、PGF1a。结果:与正常组相比,模型组大鼠造模三周150/s、38/s、10/s、5/s切变率下的全血粘度和还原粘度均显著升高(P＜0．001),红细胞聚集指数显著降低(P＜0．001),红细胞压积显著升高(P＜0．01),红细胞变形指数无显著性差异(P＞0．05);血浆TXB2显著升高(P＜0．001),6-keto-PGF1a显著降低(P＜0．05), TXB2/PGF1a显著升高(P＜0．01);模型组大鼠第四周150/s、38/s、10/s、5/s切变率下的全血粘度和还原粘度仍显著升高(P＜0．001或P＜0．01);红细胞聚集指数显著降低(P＜0．001);红细胞压积与变形指数无显著性差异(P＞0．05);血浆TXB2和TXB2/PGF1a显著降低(P＜0．05),6-keto-PGF1a显著升高(P＜0．05)。结论:肝郁脾虚证大鼠存在血液高粘和血栓易形成状态,恢复期血液高粘同时伴有扩血管因素的加强。提示肝郁脾虚证有血流变的异常和血浆TXA2-PGI2的平衡失调,主要涉及到血小板和血浆因素的参与。     

急性心肌缺血时低切变率下全血粘度变化机理研究

本实验旨在分析狗急性心肌缺血时低切变率下全血粘度异常升高与红细胞电泳率(EM)和血浆纤维蛋白原浓度变化间的关系。实验结果表明,阻断冠脉血流40min时,低切变率下全血粘度已显著升高,EM明显降低,二者呈高度负相关,此时血浆纤维蛋白原浓度仅轻度增加。缺血时间进一步延长时,EM逐渐恢复,而血浆纤维蛋白原浓度显著升高,此时低切变率下全血粘度升高主要与血浆纤维蛋白原变化有关。     

杜仲绿原酸对高脂小鼠血液流变学作用研究

旨以研究杜仲绿原酸对高脂高胆固醇诱导的高血脂模型小鼠血液流变学的影响,以昆明小鼠为实验动物,随机分成5组:阴性对照组,模型对照组和低剂量(25 mg/kg BW)、中剂量(50 mg/kg BW)、高剂量(100 mg/kg BW)杜仲绿原酸组,每组10只.后4组饲以高脂饲粮,同时小鼠灌胃杜仲绿原酸4周,实验结束,分别测定各组小鼠血液流变学参数、血清和肝脏的抗氧化酶活性和脂质过氧化产物MDA含量及其总抗氧化能力和羟自由基清除率.高脂血症小鼠的全血粘度、血浆粘度、红细胞压积、血沉、纤维蛋白原、红细胞刚性指数和聚集指数显著降低(P＜0.05),红细胞变形指数显著提高(P＜0.05),小鼠血清和肝脏SOD、GSH-Px水平、总抗氧化能力和羟自由基清除能力均显著升高(P＜0.05),MDA水平显著降低(P＜0.05).在高脂膳食条件下,杜仲绿原酸能有效提高血液的抗氧化防御功能(包括抗氧化力、抗氧化酶活性)、改变血液流变学参数等,降低血液粘度、红细胞刚性和聚集,增强变形能力,使细胞膜的流动性增高,其中以中剂量效果相对较好.     

清栓酶在治疗慢性粒细胞白血病中的地位：附5例报告

慢性粒细胞白血病慢性期全血粘度,血浆粘度增高伴高粘滞综合症表现.在用马利兰作化疗同时应用清栓酶治疗,结果发现在马利兰未使白细胞下降前,患者全血粘度,血浆粘度明显下降及高粘滞综合症得以缓解,而其它血液流变学指标治疗前后也有明显改变.证明清栓酶能降低慢性粒细胞白血病化疗前血粘度增高,缓解高粘滞综合征临床表现.     

精神分裂症与高粘滞血症

本文通过对我院101例住院精神分裂症患者做了血液流变学10项指标测定,结果表明:患者的全血粘度、血浆粘度、红细胞压积、血小板粘附、红细胞电泳、纤维蛋白原、还原粘度以及体外血栓三项指标中,除还原粘度一项与正常值无显著差异外,其余9项均明显高于正常值。证实精神分裂症存在着高粘滞血症.     

榄香烯对急性血瘀模型大鼠血液流变性的影响

本文观察了榄香烯对急性血瘀模型大鼠血液流变性的影响。实验结果表明：榄香烯６．２５－２５ｍｇ／ｋｇ／ｄ,ｉｐ×７ｄ,可使血瘀模型鼠的高低切变率全血粘度和还原粘度、血浆粘度、血沉、红细胞聚集指数、纤维蛋白原及红细胞电泳时间等显著降低（Ｐ＜０．０５、Ｐ＜０．０１）。提示榄香烯有活血化瘀作用     

Effects of alloxan-induced diabetes on hemorheology in rabbits.

Plasma viscosity (PV), apparent whole blood viscosity (WBV), relative blood viscosity (RV) and erythrocyte deformability (filterability) (EDF) were determined in 13 New Zealand White (NZW) rabbits with alloxan induced-diabetes (AID) and 8 normal NZW rabbits, matched for age, sex and weight. AID rabbits were divided into two groups depending on the duration of hyperglycemia (long-term, greater than 6.0 months (n = 7), and short-term, less than or equal to 3.0 months of hyperglycemia, n = 6). Comparing long-term AID rabbits to normal animals, we found significant increases in WBV (P less than 0.001, 0.005 for high and low rates of shear, respectively), and a marked reduction in EDF (P less than 0.001). There was no significant difference in PV between long-term AID and normal rabbits. Conversely, PV was significantly increased in rabbits with short-term diabetes (P less than 0.01) while there was a concurrent significant increase in WBV measured at high and low rates of shear (P less than 0.001, 0.001, respectively). No difference was detected in EDF between normal and short-term AID rabbits. Furthermore, in long-term AID rabbits there was a strongly positive correlation between RV and reduced erythrocyte deformability (r = 0.94, P = 0.006) while WBV strongly correlated with PV (r = 0.92, P = 0.004) in the short-term AID subgroup. We conclude from these data: (1) elevated blood viscosity in long term AID rabbits is associated with reduced erythrocyte filterability; and (2) elevated WBV in short-term AID rabbits is associated with increased PV.     

Effect of high osmotic media on blood viscosity and red blood cell deformability

Effects of high osmotic media on the shape and deformability of RBC were examined for determining increasing factors of blood viscosity. Dog blood and Urographin (a hypertonic contrast medium) were used; the plasma osmolality was changed by Urografin suspended in blood. The viscosity was measured for normal RBC and glutaraldehyde-treated RBC suspensions with a cell volume concentration. The RBC deformability was evaluated from the difference in viscosity between the two suspensions. It was shown that normal RBC suspension increased the viscosity with increase in osmolality at high shear rate; hardened RBC suspension decreased the viscosity with increase in osmolality. It was concluded that the RBC deformability decreased with increasing osmolality.     

Alteration of blood hemorheologic properties during cerebral ischemia and reperfusion in rats

The cerebral ischemia and reperfusion rat model was employed in this experiment to study the rheological properties (i.e. viscosity, hematocrit, red blood cell deformability and thixotropic properties) of whole blood. The results of this study show that a significant relation exists between the duration of cerebral ischemia and reperfusion and the viscosity, hematocrit and thixotropic parameters of whole blood, but there is no significant influence on the deformability of RBC. Blood viscosity values declined gradually throughout the ischemia period, e.g., after 1h of ischemia, the values of whole blood viscosity under high, middle and low shear rates were 44, 28 and 23% lower than normal, respectively. Whereas after 1h of reperfusion, the values of viscosity increased rapidly to values 160, 57 and 41% higher than normal under the high, middle and low levels of shear rate, while the viscosity values after 12h of reperfusion tended to return to normal values. The values of hematocrit H and thixotropic parameter tau(0) and mu also gradually declined with the increase in the duration of ischemia, but increased significantly after 1h of reperfusion. The values of H, tau(0) and mu after 1h of reperfusion are significantly greater than that in the period of cerebral ischemia, the value of H, tau(0) is also higher than normal. With the increase in reperfusion time, H, tau(0) gradually returned to normal level, at the same time, mu also decreased.     

Blood viscosity after splenectomy.

Blood viscosity and its contributory factors--namely, plasma viscosity, fibrinogen concentration, packed cell volume, red-cell deformability, and platelet count--were measured in 20 asymptomatic patients after splenectomy and compared with those in controls. Whole-blood viscosity was significantly increased after splenectomy and was associated with increased platelet count and, more importantly, decreased red-cell deformability. Blood viscosity was measured in six patients before and after splenectomy and in each an increase in viscosity occurred that did not occur in patients who underwent laparotomy without splenectomy. these findings suggest that the inclusions and protein complexes within the red cell that are normally removed by the spleen decrease red-cell deformability and lead to an increase in blood viscosity. This may account for the observed increase in deaths from ischaemic heart disease many years after splenectomy.     

Concentration-dependent, temperature-dependent non-Newtonian viscosity of lung surfactant dispersions

The bulk shear viscosities of aqueous dispersions of lavaged calf lung surfactant (LS) and its chloroform:methanol extract (CLSE) were measured as a function of concentration, shear rate and temperature. At 10-mg phospholipid per milliliter, dispersions of LS and vortexed CLSE in 0.15 M NaCl (saline) had low viscosities near 1 cp over a range of shear rates from 225 to 1125 s(-1). Lung surfactant viscosity increased with phospholipid concentration and became strongly non-Newtonian with higher values at low shear rates. At 37 degrees C and 40 mg/ml, LS and vortexed CLSE in saline had viscosities of 38 and 34 cp (77 s(-1)) and 12 and 7 cp (770 s(-1)), respectively. Viscosity values for LS and CLSE were dependent on temperature and, at fixed shear, were lower at 23 degrees C than at 37 or 10 degrees C. Hysteresis was also present in viscosity measurements depending on whether shear rate was successively increased or decreased during study. Addition of 5 mM Ca(2+) at 37 degrees C markedly reduced CLSE viscosity at all shear rates and decreased LS viscosity at low shear rates. Dispersion by sonication rather than vortexing increased the viscosity of CLSE at fixed shear, while synthetic phospholipids dispersed by either method had low, relatively Newtonian viscosities. The complex viscous behavior of dispersions of LS and CLSE in saline results from their heterogeneous aggregated microstructure of phospholipids and apoproteins. Viscosity is influenced not only by the aggregate surface area under shear, but also by phospholipid-apoprotein interactions and aggregate structure/deformability. Similar complexities likely affect the viscosities of biologically-derived exogenous surfactant preparations administered to patients in clinical surfactant therapy.     

肠淋巴液引流对失血性休克大鼠红细胞流变性的影响

目的:观察肠淋巴液引流对失血性休克大鼠红细胞流变性指标以及血液黏度的作用。方法:Wistar雄性大鼠均分为假休克组、休克组(复制失血性休克模型)、引流组(复制失血性休克模型,自低血压1 h引流休克肠淋巴液)。在低血压3 h或相应时间,经腹主动脉取血,检测红细胞参数、红细胞电泳、红细胞沉降率(ESR)以及血液黏度,计算红细胞聚集指数、红细胞变形指数。结果:与假休克组比较,休克组红细胞数量、红细胞比积(HCT)、血红蛋白(Hb)、平均红细胞血红蛋白浓度(MCHC)、红细胞电泳率与迁移率、红细胞变形指数、全血黏度、全血低切与高切相对黏度和还原黏度显著降低,休克组平均红细胞体积、红细胞电泳时间、ESR、血沉方程K值与校正K值、红细胞聚集性指数、血浆黏度显著升高;引流组MCHC、红细胞电泳率与迁移率、全血黏度、全血低切与高切还原黏度均显著降低,引流组红细胞体积分布宽度(RDW-SD)显著增加。同时,引流组HCT、RDW-SD、红细胞变形指数、全血黏度、全血低切与高切相对黏度显著高于休克组;ESR、血沉方程K值与校正K值、红细胞聚集性指数、血浆黏度显著低于休克组。结论:休克肠淋巴液引流可改善失血性休克大鼠红细胞流变行为,从而改善血液流变性。     

Haemorrheological response to plasma exchange in Raynaud's syndrome.

Eight patients with Raynaud''s syndrome were treated by weekly plasma exchange for four weeks using a Haemonetics Model 30 Blood Processor. The mean whole-blood viscosity at a shear rate of 0.77/s was significantly lower after treatment, and the mean index of red-cell deformability was significantly improved. In four patients studied serially the mean percentage fall in whole-blood viscosity after a single plasma exchange was 49% at 0.77/s but only 14% at 91/s. All patients noticed symptomatic improvement including healing of ischaemic digital ulcers. In six patients the number of digital arterial segments containing detectable blood flow was measured by directional Doppler; in all six the number increased. It is concluded that plasma exchange is an effective means of haemorrheological treatment and may be beneficial in patients with digital ischaemia.     

Detection of red cell aggregation by low shear rate viscometry in whole blood with elevated plasma viscosity

The viscosity of whole blood measured at low shear rates is determined partly by shear resistance of the red cell aggregates present, stronger aggregation increasing the viscosity in the absence of other changes. Effects of cell deformability can confound interpretation and comparison in terms of aggregation, however, particularly when the plasma viscosity is high. We illustrate the problem with a comparison of hematocrit-adjusted blood from type 1 diabetes patients and controls in which it is found the apparent and relative viscosities at a true shear rate of 0.20 s-1 are lower in the patient samples than age matched controls, in spite of reports that aggregation is increased in such populations. Because the plasma viscosities of the patients were higher on average than controls, we performed a series of experiments to examine the effect of plasma protein concentration and viscosity on normal blood viscosity. Dilution or concentration by ultrafiltration of autologous plasma and viscosity measurements at low shear on constant hematocrit red cell suspensions showed (a) suspension viscosity at 0.25 and 3 s-1 increased monotonically with plasma protein concentration and viscosity but (b) the relative viscosity increased, in concert with the microscopic aggregation grade, up to a viscosity of approximately 1.25 mPa-s but above this the value the relative viscosity no longer increased as the degree of aggregation increased in concentrated plasmas. It is suggested that in order to reduce cell deformation effects in hyperviscous pathological plasmas, patient and control plasmas should be systematically diluted before hematocrit is adjusted and rheological measurements are made. True shear rates should be calculated. Comparison of relative viscosities at low true shear rates appears to allow the effects of red cell aggregation to be distinguished by variable shear rate viscometry in clinical blood samples.     

Pharmacological concentrations of arginine influence human whole blood viscosity independent of nitric oxide synthase activity in vitro

l-Arginine, the natural precursor of NO, is infused in patients to restore endothelial function. Concentrations up to 7.5 mM l-arginine have been measured after parenteral administration. We investigated whether such high concentrations of amino acids influence blood viscosity in vitro. Incubation of whole blood from healthy volunteers with l-arginine, d-arginine, which has no effect on stereospecific NO synthases (NOS), the NOS substrate L-AME, the NOS inhibitor L-NNA, the amino acids l-lysine and l-glutamic acid, and finally NaCl dose-dependently decreased (up to 30% at 10(-2) M) low shear viscosity, which is primarily determined by erythrocyte aggregation. In contrast, the lipophilic NOS inhibitor L-NAME had no effect on low shear viscosity. All molecules failed to influence high shear viscosity, which is primarily determined by red cell deformability, and the erythrocyte shape remained unaltered. We conclude that high concentrations amino acids may decrease blood viscosity at low shear rate independent of NOS activity. This effect may contribute to the improved blood flow after intravascular administration of l-arginine.