法-林效应产生的机理

本文应用二相流模型、流速阶梯状分布模型、法氏效应和红细胞单列流动模型所揭示的规律阐明了法-林效应及其逆转的机理.使法-林效应及其逆转在理论上得以完善.并以此理论解释了对微循环血液灌注的影响.     

流过有孔壁面的剪切流及其对粒子筛滤的应用

微血管分叉处支管流出的红细胞比积H_D一般低于主管上游的供血红细胞比积H_F。其主要机理有二:一是血浆撇取效应;二是细胞筛滤效应。前者指主管近壁处有一层无细胞的血浆层,使流入支管的血液稀释;后者则指红细胞进入支管所受阻力     

关于微血管分叉处进入支管流体分界面形状的数值研究

在微血管分叉的支管中,红细胞压积常低于主管上游的值,造成这一现象的原因之一是“血浆撇取”效应,即由于主管中近壁面处有一无细胞的血浆层,从而使流入支管中的红细胞较少。要计算这一效应的大小,关键是确定主管上游横截面分界     

微血管分叉处血浆撇取的三维分析

微血管管壁附近有一层没有红细胞的血浆层,因而使由侧支微血管流出的红细胞比积HD低于主管中的供血红细胞比积HF,这叫血浆撇取效应。本文作者最近分析过简单剪切流流过大平面上小孔时的血浆撇取,在本文中推广到圆管的T形分叉,考虑了主管上游泊肃叶速度剖面的影响。本文首次引入了表征这一现象的无量纲参数     

血管直径对于微血管分叉处红细胞分布的影响

在微血管分叉处流入支管的红细胞与其流量不成比例的主要原因通常是“血浆撇取”。本文采用四种不同的主管直径Dp与支管直径Dd(100×100,50×50,100×50,50×25μm),研究不同管径及不同管径比对于支管红细胞比积的影响。作者采用不同的方法来测量支管的红细胞比积,发现电视荧光法对流入支管的流量太大或太小时都不准确,这可能是由于红细胞流动太快时不容易把红细胞数全(一般以流入支管的流量占25-75%时用此法为宜,否则宜用直接采集血样计数法)。实验结果表     

上游红细胞比积均匀分布时微血管T形分叉处的血浆撇取

本文是对严宗毅等人关于血浆撇取效应之生物力学模型(见本刊1991年第14卷第6期文摘第199号)的进一步发展,适用于主管与支管半径之比R_P≥2且无量纲参数Q≤0.2的情形。这里Q=1/8Q~*Rp~3,Q~*是支管与主管流量之比(微循环中Q约为0.1量级)。本文假设主管上游的红细胞均匀分布,但在近壁血浆层中没有红     

动脉分支和血流分配的定量分析

目的 详细分析动脉分支角和血管半径的关系。方法 运用生物学中的基本原理和方法进行分析。结果 动脉分支的分支角和血管半径有关，子管半径（r)和母管半径（r0)之比（r/r0)越小，分支角（θ)越大，cosθ=r/r0。动脉分支处的子管中的平均血流速度（v)与子管半径成正比，与母管中平均血流速度（v0)的关系是v=v0cosθ。用子管半径越小，子管中的红细胞压积越低的结果，解释了血液的血浆撇取效应。结论 血管不仅是血液输运器官，也是血流分配器官和红细胞分配器官。     

法-林效应与微循环灌注

法-林效应早在1931年已被发现，直到近三十多年来血液流变学研究在国内外成为热门，才受到人们关注。上世纪末以来，法-林效应作为微循环知识被编人我国统编（规划）教材《生理学》中，但未阐明其机理。本文试图依据微循环流变性的基本理论揭示法-林效应的机理，进而利用法-林效应对微循环正常血液灌注和微循环障碍作出正确的血液流变学解释。     

心血管力学生物学研究的新进展

力学生物学研究力学环境对生物体健康、疾病或损伤的影响,研究生物体的力学信号感受和响应机制,阐明机体的力学过程与生物学过程如生长、重建、适应性变化和修复等之间的相互关系,从而发展有疗效的或有诊断意义的新技术。本刊报道了国内心血管力学生物学研究的一些新进展。心血管力学生物学探讨血管的“应力-生长”关系,阐明力学因素如何产生生物学效应而导致血管重建;基于心血管系统建模与定量分析,建立精确规范的心血管功能新的无创检测和分析技术。这些研究不仅对于揭示正常血液循环的生物力学机理,认识血管生长、衰老的自然规律,而且对于阐明血管疾病的发病机理以及提供诊断、治疗的一些基本原理包括心血管新型药物和新技术的研发都将有重要的理论和实际意义。     

红细胞非惯性升力对血液流动的影响

目的 为准确模拟血流,研究红细胞变形性对血液流动的影响。方法 基于血液流变特性和红细胞力学特性分析,对现有血液两相流流动模型进行改进,改进模型中考虑了易变形红细胞受剪切流场或血管壁面作用而产生的非惯性升力的影响。利用改进模型对多个不同直径血管内的血液流动进行模拟。结果 由红细胞所受非惯性升力导致的径向运动对血管内红细胞体积分数、运动速度分布有明显影响;当血管直径为0.1~3.0 mm时,用改进模型得到的血液相对黏度的模拟值与测量值接近。结论 非惯性升力是血流呈现Fahraeus-Lindqvist效应的主要原因之一。考虑非惯性升力的改进模型可以准确模拟血液流动,为循环系统诊疗机制和细胞分选等过程的模拟提供更为准确的方法。     

红细胞非惯性升力对血液流动的影响

目的为准确模拟血流,研究红细胞变形性对血液流动的影响。方法基于血液流变特性和红细胞力学特性分析,对现有血液两相流流动模型进行改进,改进模型中考虑了易变形红细胞受剪切流场或血管壁面作用而产生的非惯性升力的影响。利用改进模型对多个不同直径血管内的血液流动进行模拟。结果由红细胞所受非惯性升力导致的径向运动对血管内红细胞体积分数、运动速度分布有明显影响;当血管直径为0.1~3.0 mm时,用改进模型得到的血液相对黏度的模拟值与测量值接近。结论非惯性升力是血流呈现Fahraeus-Lindqvist效应的主要原因之一。考虑非惯性升力的改进模型可以准确模拟血液流动,为循环系统诊疗机制和细胞分选等过程的模拟提供更为准确的方法。     

红细胞非惯性升力对血液流动的影响

目的 为准确模拟血流,研究红细胞变形性对血液流动的影响。方法 基于血液流变特性和红细胞力学特性分析,对现有血液两相流流动模型进行改进,改进模型中考虑了易变形红细胞受剪切流场或血管壁面作用而产生的非惯性升力的影响。利用改进模型对多个不同直径血管内的血液流动进行模拟。结果 由红细胞所受非惯性升力导致的径向运动对血管内红细胞体积分数、运动速度分布有明显影响;当血管直径为0.1~3.0 mm时,用改进模型得到的血液相对黏度的模拟值与测量值接近。结论 非惯性升力是血流呈现Fahraeus-Lindqvist效应的主要原因之一。考虑非惯性升力的改进模型可以准确模拟血液流动,为循环系统诊疗机制和细胞分选等过程的模拟提供更为准确的方法。     

Changes in haemorheology in the racing greyhound as related to oxygen delivery

Summary Arterial blood samples were obtained from six greyhounds during rest, immediately before, and after a 704-m (7/16th mile) race. Measurements were made of various haematological (red cell count, haemoglobin, packed cell volume, white cell count, plasma proteins) and haemorheological variables. Blood and plasma viscosity were determined at high wall shear stresses (67–200 dynes · cm^–2, 670–2000 N · cm^–2) in a 20-m glass capillary device which was designed to take the diameter dependence of blood viscosity (Fahraeus-Lindgvist effect) into account. Compared to values at rest, substantial haemoconcentration occurred before the race, mainly due to splenic discharge of red cells. Additional haemoconcentration was found after the race. The increase of effective blood viscosity caused by elevation of packed cell volume was greater than the increase in O₂ binding capacity resulting from the elevated haemoglobin concentration, suggesting that the haemoconcentration observed in the exercising greyhound does not enhance O₂ delivery to skeletal muscle. The main physiological effect of red cell discharge from the contracting spleen appeared to be a consequence of the volume rather than the composition of the circulating blood.     

Spatial properties of X and Y cells in the lateral geniculate nucleus of the cat and conduction velocities of their inputs

Summary Visual neurons in the lateral geniculate nucleus (LGN) of the cat may be separated into distinct X and Y classes based on a test of the linearity of spatial summation. Y cells produce nonlinear responses especially when the visual stimulus is a fine spatial grating. X cells exhibit mainly linear summation properties. X cells respond mainly at the fundamental modulation frequency of a contrast reversal grating while Y cells respond at the fundamental and at the second harmonic of the modulation frequency. The spatial resolution of X cells' fundamental responses and Y cells' second harmonic responses is about the same, and both are two to eight times higher than the spatial resolution of the Y cells' fundamental response. The conduction velocity of the Y optic tract afferents is greater than that of the velocity of the X afferents. However, the LGN latencies of the responses of the two classes of cells to optic chiasm stimulation overlap considerably.     

915MHz低强度微波辐射对红细胞膜特性的影响

本文利用新型宽带横电磁波传输室（ＢＴＥＭＣＥＬＬ）作为基本装置，在９１５ＭＨｚ频率上，对离体红细胞进行照射，研究电磁场对细胞膜在面受体的特异性，膜的通透性的影响，对其机理进行了初步的探讨。     

淋巴细胞转移干扰素抗病毒活性的机理研究

本文研究了人淋巴细胞与羊膜FL细胞之间干扰素介导的抗病毒活性转移的机理。受者FL细胞表达的抗病毒转移活性具有下述特征:1.用放线菌素D抑制FL细胞的RNA合成,能抑制抗病毒活性的表达;2.共同培养中存在的抗2-5_P_3A_3抗体不干扰细胞间抗病毒活性的转移;3.FL细胞膜上干扰素受体用植物血凝素封闭后,不影响抗病毒活性转移的表达。因此,我们认为,淋巴细胞膜上干扰素活化的第二信使分子可能是在细胞之间传递干扰素信息的重要效应物质。     

Regulation of human erythrocyte metabolism by insulin: cellular distribution of 6-phosphofructo-1-kinase and its implication for red blood cell function

Human erythrocytes are highly specialized cells whose function is oxygen transport. These cells' sole metabolic source of energy is the fermentation of glucose via glycolysis. They contain an active insulin receptor and respond to insulin by increasing phosphorylation of tyrosine residues in several proteins. However, no metabolic effects have yet been associated with activation of this receptor in human erythrocytes. Here, we show that insulin increases the rate of glycolysis in human erythrocytes. Lactate production increased 56 and 173% in the presence of 10 and 100 nM insulin, respectively. A higher insulin concentration (1000 nM) partially reversed the stimulation of glycolysis. These effects occur through activation of the key glycolytic enzyme 6-phosphofructo-1-kinase, which exhibits the same pattern of modulation by insulin as seen for glycolytic flux. This modulation also occurs physiologically since ex vivo experiments revealed 50% stimulation of 6-phosphofructo-1-kinase (PFK) activity following a high carbohydrate meal. Insulin increases phosphorylation of PFK and redistributes the enzyme in red blood cells, causing it to detach from the erythrocyte membrane: upon insulin stimulation, the amount of enzyme associated with the plasma decreases by 86%. Detachment is a common mechanism of enzyme activation. As a consequence, insulin prevents up to 68% of red cells hemolysis. These results show that insulin regulates erythrocyte glycolysis and viability and suggest that this regulation is associated to other erythrocyte functions such as oxygen transport. Finally, we suggest that this regulatory mechanism might be compromised in patients with diabetes mellitus.     

Anaphylactic antibodies in mice genetically selected for antibody production

The genetic selection of mice for the character `agglutinin production to sheep red cells' also operates for the synthesis of reagins and γ₁ antibodies against egg albumin.     

Effects of lithium on water intake and renal concentrating ability in rats with vasopressin-deficient diabetes insipidus (Brattleboro strain)

Male and female Long Evan rats and Brattleboro rats with ADH-deficient diabetes insipidus were treated with lithium administered in the diet for 12 weeks. The plasma lithium level was about 1 mmol/l in all groups. Lithium caused polydipsia and polyuria and lowering of renal concentrating ability in normal rats. In rats with ADH deficiency lithium tended to increase water intake, but did not influence spontaneous urine osmolality or maximal urine osmolality during water deprivation. The results indicate that the renal concentrating defect caused by lithium in rats can be explained by ADH-blockade as the only mechanism. However, there is circumstantial evidence that lithium in addition may stimulate thirst mechanisms by an ADH-independent action.