血管内皮细胞位于血流和血管壁之间，除受化学因素的调节外还受力学因素的影响。切应力可通过刺激相应的力学感受系统来调节内皮细胞某些基因的表达，其中包括诱导内皮细胞表达IL-8。为了阐明MA PK信号途径中的ERK1/2 信号通路是否参与调控低切应力上调人脐静脉内皮细胞IL-8基因表达，采用Westernblot分析了低切应力（4.20 dyne/cm2）处理不同时间内皮细胞ERK1/2的磷酸化水平及TPK抑制剂Genistein,M EK抑制剂PD98059对其磷酸化的影响; 采用定量RT-PCR 检测内皮细胞经低切应力刺激或给予阻断剂后再行切应力刺激等处理后IL-8基因的表达。结果显示：（1）低切应力处理可引起内皮细胞ERK1/2蛋白磷酸化水平上调，其磷酸化水平与切应力作用时间有关，具有快速、双向性的特点（在刺激10min时达到高峰，2h左右降至未刺激水平），阻断剂Genistein和PD98059处理后，ERK1/2磷酸化水平与低切应力刺激10min比较明显降低；（2）阻断剂Genistein，PD98059可显著抑制低切应力所致的内皮细胞IL-8mRNA上调。结果表明低切应力可通过ERK1/2信号途径上调人脐静脉内皮细胞IL-8基因的表达。

The theological properties of whole human blood exhibit thixotropic behavior at low shear rates up to about ten reciprocal seconds (1). The accepted cause of this shear rate-dependent and time-dependent behavior is the progressive breakdown of rouleaux into individual red cells. Huang developed a theological e uation which incorporates the kinetics of rouleau breakdown in his models (2). This five-parameter e uation was used successfully to represent the hysteresis loop and the tor ue-decay curve of whole human blood. Numerical values of these five thixotropic parameters, which characterize the rheological behavior of the blood from apparently healthy human subjects, were established (3). In this communication, we examine the effect of hematocrit on each of the above mentioned parameters. The results show that the following parameters will increase their values with an increase in hematocrit: the yield stress, Newtonian contribution of viscosity, non-Newtonian contri-bution of viscosity, apparent viscosity and the e uilibrium value of the structural parameter which indicates the relative amount of rouleaux in blood. Mathematical e uations were developed to give the relationship between parameters and hematocrit. Two other thixotropic parameters, viz. the kinetic rate constant of rouleaux breakdown into individual red cells and the order of the breakdown reaction, were found to be independent of the hematocrit. It is consistent with reaction kinetic theory that the rate constant and the order of reaction are independent of the concentration of reactants.

白细胞介素-8（Interleuk in-8，IL-8）是趋化因子CXC亚家族的一员，对中性粒细胞有趋化作用，可以诱导平滑肌细胞的增殖和迁移，是一个促血管生成因子，在动脉粥样硬化慢性炎症过程中起着重要作用。本文通过建立兔高脂血症动脉粥样硬化斑块模型，动态监测了在动脉粥样硬化发展过程中IL-8的蛋白和基因表达，以了解IL-8在动脉粥样硬化中的作用。采用免疫组化的方法定位IL-8在高脂血症兔动脉粥样硬化斑块模型主动脉升弓部血管壁的蛋白表达，8、12周模型组内膜显著增厚并有明显阳性染色，半定量分析A S模型组阳性染色的面积分别是对照组的4.48、8.76倍，平均积分光密度（IOD）值分别是对照组的4.16、4.36倍。采用双抗夹心EL ISA法测定兔血管组织匀浆液中的IL-8蛋白表达量，8、12周A S模型组IL-8蛋白含量与总蛋白比值和对照组比较均有显著性差异，分别是对照组的1.84、2.06倍。用原位杂交的方法定位IL-8mRNA的表达，8周模型组血管内膜有强的阳性染色，IL-8mRNA的表达增加。本研究通过建立动脉粥样硬化模型，动态监测了整个动脉粥样硬化过程中IL-8的蛋白和基因表达。IL-8的蛋白和基因上调主要是在高脂血症兔动脉粥样硬化模型的脂纹期。

In order to demonstrate that IL-8 mRNA expression in endothelial cells is not only regulated by chemical factors, but also by mechanical factors, in this article, after pretreating cultured human umbilical vein endothelial cells (HUVECs) with shear stress for different time, we employed both RT-PCR to assay IL-8mRNA expression and immunocytochemical staining to detect NF-kB activation in HUVECs. We found that: (i) IL-8mRNA expressed little in HUVECs untreated or pretreated with low laminar shear stress for 0.5 hour; IL-8mRNA expression was increased when HUVECs were pretreated with low laminar shear stress for 1 hour, and increased further when pretreated for 2 hours; (ii) the immunoreactivity of NF-kB p65 in the nuclei of HUVECs untreated or pretreated with low laminar shear stress for 0.5 hour was negative, while it became weak positive in the nuclei of HUVECs pretreated with shear stress for 1 hour and positive in the nuclei of HUVECs pretreated for 2 hours. The results imply that low laminar shear stress was capable of inducing IL-8 gene expression and activating NF-kB, which were both time-dependent. The induction of IL-8 gene expression by laminar shear stress is probably due to the activation of NF-kB. We suggest that IL-8mRNA expression in endothelial cells induced by low shear stress may play a key role in the pathogenesis and development of both inflammation and arterioatherosclerosis.

The adhesion of leukocytes to vascular surface is an important biomedical problem and has drawn extensive attention. In this study, we propose a compound drop model to simulate a leukocyte with a nucleus adhering to the surface of blood vessel under steady shear flow. A two-dimensional computational fluid dynamics (CFD) is conducted to determine the local distri-bution of pressure on the surface of the adherent model cell. By introducing the parameter of deformation index (DI), we investigate the deformation of the leukocyte and its nucleus under controlled conditions. Our numerical results show that: (i) the leukocyte is capable of deformation under external exposed flow field. The deformation index increases with initial contact angle and Reynolds number of external exposed flow. (ii) The nucleus deforms with the cell, and the de-formation index of the leukocyte is greater than that of the nucleus. The leukocyte is more de-formable while the nucleus is more capable of resisting external shear flow. (iii) The leukocyte and the nucleus are not able to deform infinitely with the increase of Reynolds number because the deformation index reaches a maximum. (iv) Pressure distribution confirms that there exists a region downstream of the cell, which produces high pressure to retard continuous deformation and provide a positive lift force on the cell. Meanwhile, we have measured the deformation of human leukocytes exposed to shear flow by using a flow chamber system. We found that the numerical results are well consistent with those of experiment. We conclude that the nucleus with high viscosity plays a particular role in leukocyte deformation.