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1.
经犬主胰管逆行加压注射犬自体胆汁(0.5ml/kg)制成AHP动物模型;AHP第2小时,门静脉全血高切粘度、全血低切粘度、红细胞压积与红细胞聚集性增加,血清自发光强度增加;AHP第6小时,血液流变学紊乱的上述参数逐渐加重,血清自发光强度与脂质过氧化物均增加。同时,全血高切粘度、全血低切粘度、红细胞压积与红细胞聚集指数与血清自发光强度在AHP时相互关系明显。结果表明:高血粘与自由基反应在AHP发展过程中起一定的作用,二者相互影响。  相似文献   

2.
高速投射物伤伤后血液流变性的变化特点及意义   总被引:2,自引:0,他引:2  
探讨压力波对血液流变性的影响。方法:将实验犬24只随机分为二组:一组以5.56mm军用弹致伤犬的双后肢;另一组伤前暂时结扎犬双后肢股动静脉,以阻断致伤时压力波传播,伤后立即去除结扎。二组伤前、伤后0.5、2、6和10h分别采静脉血,用锥板粘度法测全血粘度并计算红细胞压积、红细胞变形指数和红细胞聚集指数。结果:伤后二组动物全血低切粘度(3.84S-1)、红细胞压积、红细胞聚集指数较伤前明显升高;伤后6h内红细胞变形指数较伤前明显下降。结扎组变化程度明显小手致伤组。结论:高速投射物伤时,血液流变性发生了明显变化,可能与致伤时压力波沿血管传播有关。  相似文献   

3.
大鼠高脂血症与血液粘度关系研究   总被引:3,自引:0,他引:3  
目的:研究血脂与全血粘度、血浆粘度及其相关因素的关系。方法:以高脂血症大鼠模型,大鼠饲以高脂饲料,连续7周测血脂。结果:血浆TG增加2倍,TC增加13.2倍,LDL增加51.8倍,而HDL无明显改变。随血浆脂质的升高,大鼠血浆粘度也显增加,而红细胞刚性指数、红细胞变形指数及红细胞聚集指数显下降;全血高、中、低切粘度,全血还原粘度,红细胞计数、红细胞压积及红细胞电泳时间均无明显改变。与此同时,血浆纤维蛋白溶酶活性降低而血小板聚集功能增高。结论:上述结果表明,高脂血症主要导致血浆粘度增加,纤维蛋白溶酶活性和血小板聚集功能异常改变。  相似文献   

4.
韩烨  雷蕾  陈吉 《中国微循环》2002,6(5):316-316
目的探讨心力衰竭患者血液粘度与QT离散度 (QTd)关系。方法十二道同步自动分析心电图机测定58例心力衰竭患者QTd ,按QTd大小分组 ,QTd≥50ms组 ,QTd<50ms组。检查两组的全血粘度 ,并进行比较。结果QTd≥50ms组较QTd<50ms组的全血粘度 (低切 )、红细胞聚集指数明显增高 ,具有显著性意义 (P<0.05~0.01)。结论心力衰竭患者QTd增加与全血粘度有关。降低血粘度可能有助降低QTd ,对防止QTd增加导致心律失常有意义  相似文献   

5.
小儿紫绀型先天性心脏病血浆MDA和血液流变学变化   总被引:1,自引:0,他引:1  
测定35例青紫型先天性心脏病患儿红细胞、血浆丙二醛(MDA)含量、红细胞膜微粘度及血液流变学指标。结果患儿红细胞、血浆MDA、膜微粘度、全血粘度、经细胞比积、红细胞聚集指数、刚性指数均显著高于正常组;MDA含量,膜微粘度、红细胞刚性指数、聚集指数及全血粘度之间均存在正相关关系。提示患儿红细胞脂质过氧化反应增强,导致膜流动性降低、红细胞变形性差,聚集性增加,可能是血液粘度增加较为主要的原因。  相似文献   

6.
应用荧光偏振法测定31例青紫型先天性心脏病患儿红细胞膜微粘度及血液流变学指标。发现息儿红细胞膜微粘度、全血粘度、红细胞比积、红细胞聚集指数及刚性指数均显著高于正常组(P<0.01);膜微粘度与全血粘度、红细胞刚性指数呈明显正相关(P<0.01)。研究表明,青紫型先天性心脏病红细胞膜微粘度增加、流动性降低,可能是引起红细胞变形性差、血液粘度增高的主要原因之一。  相似文献   

7.
本文调查了48例Binswanger病血液流变学10项指标,并与44例正常老年人及47例脑梗塞患者作对照。结果表明;(1)Binswanger病组全血粘度、血浆高切粘度、血沉、红细胞聚集指数、红细胞刚性指数、血沉方程K值、全血还原粘度显著高于正常对照组(P<0.001);全血粘度、血浆高切粘度、红细胞聚集指数、红细胞刚性指数、全血还原粘度与脑梗塞组相似。(2)Binswanger病组红细胞变形指数明显低于正常对照组(P<0.001),但显著高于脑梗塞组(P<0.01)。结论:Binswanger病患者血液流变学处于一种高粘状态。  相似文献   

8.
急性肺炎患者血液流变性分析   总被引:2,自引:0,他引:2  
目的 :探讨急性肺炎患者血液流变性变化。方法 :检测 32例急性肺炎患者全血粘度、血浆粘度、纤维蛋白原、红细胞变形指数和红细胞聚集指数 ,并与 38例健康对照组比较。结果 :急性肺炎患者全血粘度 ,血浆粘度 ,纤维蛋白原含量和红细胞聚集指数明显高于对照组 (P <0 .0 1 ) ,而红细胞变形指数明显低于对照组 (P <0 .0 1 )。结论 :本组结果提示急性肺炎患者血液处于高粘状态。  相似文献   

9.
本文研究了油酸致大鼠急性肾衰时血液流变性的改变。观察了樟柳碱,东莨菪碱及山莨菪碱对这些改变的影响。结果表明,急性肾衰时,低切至高切变率时的全血粘度均明显增高,红细胞比积,血浆粘度及红细胞聚集指数也明显高于对照组。樟柳碱及东莨菪碱能降低血浆粘度、红细胞聚集指数及全血粘度;山莨菪碱能降低血浆粘度及红细胞聚集指数。结果说明,急性肾衰时血液的流变性有明显障碍,三种莨菪药均能改善急性肾衰时血液的流变性。  相似文献   

10.
目的 :探讨红细胞聚集改变与纤维蛋白原的关系及其对心绞痛发病的影响。方法 :测定 80例不稳定性心绞痛患者和 40例健康人的红细胞聚集指数 (光密度法 )、红细胞变形指数 (激光衍射法 )、血浆及全血粘度 (旋转式粘度计 )和纤维蛋白原 (双缩脲法 )。结果 :不稳定性心绞痛患者红细胞聚集指数和全血粘度 ( 4 0s- 1 )及纤维蛋白原浓度均高于对照组 (P均 <0 .0 1~ 0 .0 5 ) ,且红细胞聚集指数与纤维蛋白原呈直线正相关 ,与全血粘度 ( 4 0s- 1 )无相关性。结论 :纤维蛋白原含量增加是红细胞聚集增强的主要原因之一 ;红细胞聚集能力增强导致血液高粘滞 ,与心绞痛发作有关 ;选择 10s- 1 以下切变率测定低切全血粘度 ,利于观察全血粘度与红细胞聚集的关系  相似文献   

11.
Hypoxia is caused by insufficient oxygen availability for the organism leading to reduced oxygen delivery to tissues and cells. It has been regarded as a severe threat to human health and it is indeed implicated in pathophysiological mechanisms involved in the development and progression of many diseases. Nevertheless, the potential of controlled hypoxia interventions (i.e. hypoxia conditioning) for improving cardio-vascular health is gaining increased attention. However, blood rheology is often a forgotten factor for vascular health while aging and hypoxia exposure are both suspected to alter hemorheological properties. These changes in blood rheology may influence the benefits-risks balance of hypoxia exposure in older individuals. The benefits of hypoxia exposure for vascular health are mainly reported for healthy populations and the combined impact of aging and hypoxia on blood rheology could therefore be deleterious in older individuals.This review discusses evidence of hypoxia-related and aging-related changes in blood viscosity and its determinants. It draws upon an extensive literature search on the effects of hypoxia/altitude and aging on blood rheology. Aging increases blood viscosity mainly through a rise in plasma viscosity, red blood cell (RBC) aggregation and a decrease in RBC deformability. Hypoxia also causes an increase in RBC aggregation and plasma viscosity. In addition, hypoxia exposure may increase hematocrit and modulate RBC deformability, depending on the hypoxic dose, i.e, beneficial effect of intermittent hypoxia with moderate dose vs deleterious effect of chronic continuous or intermittent hypoxia or if the hypoxic dose is too high. Special attention is directed toward the risks vs. benefits of hemorheological changes during hypoxia exposure in older individuals, and its clinical relevance for vascular disorders.  相似文献   

12.
动态测定了常压间断低氧大鼠全血和肺组织谷胱甘肽过氧化物酶(GSH-PX)活性及还原型谷胱甘肽(GSH)含量。结果发现随低氧时间延长,肺动脉压逐渐升高的过程中有全血及肺组织GSH-PX活性及GSH含量的显著降低。维生素E和山莨菪碱有部分保护作用。提示间断低氧过程中活性氧自由基生成增多,消耗了较多的抗氧化酶(剂)。氧自由基生成增多可能在其肺动脉高压的发生中起一定作用。  相似文献   

13.
目的:观察二十六味余甘子丸和藏红花粗提物对缺氧大鼠肺动脉压及血液流变学的作用。方法:10%常压缺氧3~5周,同时用上述两种药物灌胃,右心导管测肺动脉压,毛细血管离心法测红细胞压积,旋转粘度计测血液粘度,荧光偏振法测红细胞膜流动性,微孔滤法测红细胞变形性。结果:所用两种药物均可以降低缺氧引起的肺动脉高压和减轻右心室肥厚。但对红细胞压积、全血粘度、红细胞膜流动性和红细胞变形性无明显影响。结论:这两种药物的降缺氧大鼠肺动脉高压作用,是主要通过改善肺循环而实现的。  相似文献   

14.
目的:本文观察了低氧引起的癌症患者血液流变学参数的变化。结果表明:全血粘度、血浆粘度、红细胞压积、全血还原比粘度、血沉值低氧组略低于对照组;红细胞电泳时间、纤维蛋白元值低氧组略高于对照组,但均无明显差异;血沉方程K值低氧组明显高于对照组(P<0.05)。这些结果提示,佩戴低氧呼吸装置所产生的短时间急性缺氧,不会对人体血液流变学产生明显影响。  相似文献   

15.
Chronic hypoxia caused by migration of native sea-level dwellers to high altitude or chronic lung disease leads to the development of increased pulmonary vascular resistance and pulmonary hypertension. This altitude-induced hypertension offers no obvious benefit and may indeed be maladaptive. A major mechanism thought to contribute to the development of pulmonary hypertension is hypoxia-induced loss of small blood vessels, sometimes termed rarefaction or pruning. More recent evidence caused us to question this widely accepted concept including the potent angiogenic effect of chronic hypoxia in all other vascular beds and the demonstration that new vessels can form in the pulmonary circulation when stimulated by chronic infection and lung resection. We tested the hypothesis that chronic environmental hypoxia causes angiogenesis in the adult pulmonary circulation by using stereological techniques combined with confocal microscopy to examine the resultant changes in pulmonary vascular structure in rats. We found that chronic hypoxia resulted in increased total pulmonary vessel length, volume, endothelial surface area and number of endothelial cells in vivo . This is the first reported demonstration of hypoxia-induced angiogenesis in the mature pulmonary circulation, a structural adaptation that may have important beneficial consequences for gas exchange. These findings imply that we must revise the widely accepted paradigm that hypoxia-induced loss of small vessels is a key structural change contributing to the development of pulmonary hypertension in high altitude adaptation and chronic lung disease.  相似文献   

16.
Hemodynamic functions and blood viscosity changes in hypothermia (core approximately 25 degrees C) were studied in 14 pentobarbital-anesthetized dogs subjected to surface cooling. The viscosity of blood (eta B) increased progressively to 173% of that at 37 degrees C when body temperature was lowered to 25 degrees C. The increase in blood viscosity was caused by: a) the direct effect of low temperature on plasma viscosity, b) hemoconcentration as a result of plasma loss, and c) the low-flow (low-shear) state induced by hypothermia. A larger portion of the increased viscosity was caused by the low-flow state in hypothermia. The systemic flow resistance (SFR) increased to 271% of control, and this was attributable about equally to the increases in blood viscosity and systemic vascular hindrance (SFR/eta B). Similarly, the viscosity of blood contributed significantly to raising the pulmonary flow resistance. The relative constancy of mixed venous O2 saturation suggests that the cardiac output at low body temperature is generally adequate to meet the metabolic needs.  相似文献   

17.
通过对45例活动性肺结核病患者的血液流变检查,发现其流变性特点是血浆粘度明显增高,在血粘异常综合征中,属单纯由血浆纤维蛋白原增高引起的血浆粘度增高型,提示该病中医辨证中"阴虚血瘀"的物质基础和本质。  相似文献   

18.
目的 探讨肺心病急性加重期患者血液流变学及凝血功能的变化.方法 选取2014年6月至2016年1月在我院治疗的51例肺心病急性加重期患者为急性加重组,在我院接受治疗的51例恢复期患者为恢复组和社会招募51例健康受试者为正常组,考察肺心病急性加重期患者血液流变学中红细胞计数、红细胞压积、全血高切黏度、全血低切黏度、血浆黏度、血沉,凝血功能中凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)、纤维蛋白原(FIB)、凝血酶时间(TT)的变化.结果 肺心病急性加重期部分患者的红细胞计数偏离正常值范围,整体肺心病急性加重期患者的红细胞计数与恢复期和正常组受试者差异无统计学意义.肺心病急性加重期患者红细胞压积、全血高切黏度、全血低切黏度、血浆黏度、血沉均较恢复期和正常组受试者的值高,并且差异具有统计学意义(P<0.05).肺心病急性加重期患者的PT、APTT、FIB、TT高出正常值范围,并且与恢复期和正常组相比差异具有统计学意义(P<0.05).结论 肺心病急性加重期的患者血液黏度升高、凝血功能紊乱.因此血液黏度和凝血功能检查,可以作为肺心病急性加重期患者病情判定与评估的一种手段.  相似文献   

19.
1. In anaesthetized open-chest cats and dogs, blood flow and gas tensions were measured in a circuit inserted into a pulmonary vein while ventilating the lobe which it drained with low O(2) and high CO(2) mixtures.2. Both hypoxic and hypercapnic mixtures caused a reduction in blood flow from the lobe.3. Stimulus-response curves relating blood flow to pulmonary venous P(O2) and P(CO2) were obtained. Those for hypoxia were usually asymptotic in shape; the curves became steep below 100 torr and flow sometimes fell to zero. The mean reduction in blood flow for every 20 torr fall in P(O2) was 15.7% in cats and 11.8% in dogs. Those for hypercapnia were steep at first but levelled out at high P(CO2) values; the maximum reduction in flow was 40-60% as vasoconstriction was only observed over a limited P(CO2) range.4. Hypoventilation of the lobe led to a reduction in blood flow. This was mainly attributable to hypoxia though other factors such as hypercapnia may sometimes have contributed.5. Total occlusion of the bronchus of an O(2)-filled lobe caused blood flow to fall in two phases. The first phase could be attributed to a rise in P(CO2) and the second to a fall in P(O2).6. The results confirm the hypothesis that hypoxia is an important factor regulating local blood flow in relation to local ventilation.  相似文献   

20.
白花前胡对大鼠血流动力学和流变学作用研究   总被引:2,自引:0,他引:2  
本文观察并研究了白花前胡提取物PPD对肺动脉高压大鼠的血流动力学和血液流变学作用及相应参数的物理意义和数学关系。结果表明:PPD能明显改善肺动脉压力和血管尺寸等指标;显著降低全血粘度和还原粘度;增加肺循环血流量。  相似文献   

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