高龄患者下肢深静脉血栓超声诊断的Logistic回归分析

目的：应用Logistic回归筛选高龄患者下肢深静脉血栓灰阶及彩色多普勒超声诊断特征。方法：对我院150例主动要求下肢深静脉血栓灰阶及彩色多普勒超声检查的高龄患者,应用超声检查观察血管管径、管腔内回声及血流动力学等特征,进行Logistic回归分析,筛选超声诊断特征,对Logistic回归模型预测诊断绘制受试者工作曲线图（ROC）,评估模型效果。结果：150例超声检查高龄患者,发生下肢深静脉栓塞129例,占86.00%。Logistic回归筛选,血管管径、管腔内回声、管壁内壁、血流信号改变4个变量进入回归模型,Logistic回归模型预测超声检出的ROC曲线下面积为0.903,灵敏度为90.3%,特异度为93.8%。结论：以高龄患者下肢深静脉血栓超声特征建立的Logistic回归模型对该病具有较好的预测诊断价值。     

兔急性肠系膜上静脉血栓形成模型建立及其病理学观察

目的 建立稳定的兔急性肠系膜上静脉血栓形成模型,观察其病理学变化.方法 采用扎闭静脉、损伤血管壁、激活凝血因子等方法建立模型,分期观察病理学改变.结果 成模后可见血管腔内明显血栓形成;肠道粘膜上皮细胞水肿至坏死脱落伴大量炎性细胞浸润;血管内皮细胞从凹陷到局部坏死脱落,直至大面积坏死脱落,内皮下基质暴露.结论 本实验可成功建立兔肠系膜上静脉血栓形成模型,病理学改变符合临床,模型稳定可靠.     

Morphological evaluation of the state of the structural elements of arterial and arteriolar walls in experimental kidney ischemia

Resetting of arterial and arteriolar wall structural components have been studied in the white rat kidney glomeruli after experimental ischemia (30 min, 1-3 h) without blood flow recovery and with the following recirculation for 3-30 days. The experiments have established that acute renal ischemia caused by the vascular leg ligation for 30-60 min without the following blood flow recovery results in slight microstructural alterations of arterial and arteriolar wall elements. With increased ischemia duration (2-3 h) pathological changes become more prominent and separation of vascular endothelial cells and defibering of the internal elastic membrane take place. In transitory (30-60 min) ischemia of the remaining kidney (one kidney is removed) three days later desquamation of endothelial cells occurs in some arteries. Thinning of arterial walls and overstrain of internal elastic membrane are observed. However, later on (in 30 days) short-term ischemia (30 min) is followed by complete recovery of structural components of arterial and arteriolar walls. In more durable ischemia (2-3 h) of the remaining kidney the recovered blood flow causes marked destructive life-threatening changes in vascular walls.     

Theoretical study on flow-dependent concentration polarization of low density lipoproteins at the luminal surface of a straight artery

It is suspected that physical and fluid mechanical factors play important roles in the localization of atherosclerotic lesions and intimal hyperplasia in man by affecting the transport of cholesterol in flowing blood to arterial walls. Hence, we have studied theoretically the effects of various physical and fluid mechanical factors such as wall shear rate, diffusivity of low density lipoproteins (LDL), and filtration velocity of water at the vessel wall on surface concentration of LDL at an arterial wall by means of a computer simulation of convective and diffusive transport of LDL in flowing blood to the wall of a straight artery under conditions of a steady flow. It was found that under normal physiologic conditions prevailing in the human arterial system, due to the presence of a filtration flow of water at the vessel wall, flow-dependent concentration polarization (accumulation or depletion) of LDL occurs at a blood/endothelium boundary. The surface concentration of LDL at an arterial wall takes higher values than that in the bulk flow in that vessel, and it is affected by three major factors, that is, wall shear rate, gamma w, filtration velocity of water at the vessel wall, Vw, and the distance from the entrance of the artery, L. It increases with increasing Vw and L, and decreasing gamma w hence the flow rate. Thus, under certain circumstances, the surface concentration of LDL could rise locally to a value which is several times higher than that in the bulk flow, or drop locally to a value even lower than a critical concentration for the maintenance of normal functions and survival of cells forming the vessel wall. These results suggest the possibility that all the vascular phenomena such as the localization of atherosclerotic lesions and intimal hyperplasia, formation of cerebral aneurysms, and adaptive changes of lumen diameter and wall structure of arteries and veins to certain changes in hemodynamic conditions in the circulation are governed by this flow-dependent concentration polarization of LDL which carry cholesterol.     

The intestinal blood circulation in the River lamprey, Lampetra fluviatilis

Serial sections, injections with india ink and latex, and observations on fresh material, have been used to determine the pattern of blood circulation within the intestine of larval and adult lampreys. Attention has also been paid to resolving the variable terms previously applied to many of the blood vessels, and to the possible functional significance of the differences found between the two life cycle stages. In the larva, the main arterial supply to the intestine consists of a typhlosolar artery, while the venous return is comprised of a posterior and a left and right anterior intestinal vein that usually unite before entering the liver. Although a typhlosolar artery is also present in the adult, the main venous return of the ammocoete is replaced at metamorphosis by a newly formed typhlosolar vein. Moreover, in the ammocoete a considerable amount of blood is discharged into the haemopoietic sponge-work of the typhlosole and the arterial supply to the intestine is poorly developed. By contrast, the typhlosolar sponge-work is lost in the adult and a more efficient arterial supply is developed within the lamina propria of the various intestinal regions. Furthermore, vascular couples are developed in the adult which facilitate the flow of blood in opposite directions in the intestinal wall. Since, during both life cycle stages, the arterial blood passes into tissue spaces, there is no true capillary network in the intestine and no evidence was found for the presence of a lymphatic system. It is suggested that the changes which take place in the intestinal blood supply and the internal structure of the gut during metamorphosis result in improvements both to the vascular system and to the assimilation efficiency.     

Influence of non-Newtonian properties of blood on the wall shear stress in human atherosclerotic right coronary arteries

The objective of this work is to investigate the effect of non-Newtonian properties of blood on the wall shear stress (WSS) in atherosclerotic coronary arteries using both Newtonian and non-Newtonian models. Numerical simulations were performed to examine how the spatial and temporal WSS distributions are influenced by the stenosis size, blood viscosity, and flow rate. The computational results demonstrated that blood viscosity properties had considerable effect on the magnitude of the WSS, especially where disturbed flow was observed. The WSS distribution is highly non-uniform both temporally and spatially, especially in the stenotic region. The maximum WSS occurred at the proximal side of the stenosis, near the outer wall in the curved artery with no stenosis. The lumen area near the inner wall distal to the stenosis region experienced a lower WSS during the entire cardiac cycle. Among the factors of stenosis size, blood viscosity, and flow rate, the size of the stenosis has the most significant effect on the spatial and temporal WSS distributions qualitatively and quantitatively.     

Sequential venous anastomosis design to enhance patency of arterio-venous grafts for hemodialysis

Arterio-venous grafts (AVGs), the second best option as long-term vascular access for hemodialysis, face major issues of stenosis mainly due to development of intimal hyperplasia at the venous anastomosis which is linked to unfavorable hemodynamic conditions. We have investigated computationally the utility of a coupled sequential venous anastomotic design to replace conventional end-to-side (ETS) venous anastomosis, in order to improve the hemodynamic environment and consequently enhance the patency of AVGs. Two complete vascular access models with the conventional and the proposed venous anastomosis configurations were constructed. Three-dimensional, pulsatile blood flow through the models was simulated, and wall shear stress (WSS)-based hemodynamic parameters were calculated and compared between the two models. Simulation results demonstrated that the proposed anastomotic design provides: (i) a more uniform and smooth flow at the ETS anastomosis, without flow impingement and stagnation point on the artery bed and vortex formation in the heel region of the ETS anastomosis; (ii) more uniform distribution of WSS and substantially lower WSS gradients on the venous wall; and (iii) a spare route for the blood flow to the vein, to avoid re-operation in case of stenosis. The distinctive hemodynamic advantages observed in the proposed anastomotic design can enhance the patency of AVGs.     

Reconstructing the breast mound employing a secondary island omental skin flap

We have shown in an initial animal study that omentum will adequately vascularize a skin flap and allow transfer of this tissue composite for use in surgical reconstruction of the breast. Based on this experimental procedure, a technique employing a two-stage operation has been developed and used in 21 female patients in reconstruction of the breast after radical mastectomy. In the first stage, the omentum, attached to one gastroepiploic artery and vein, is exteriorized to the subcutaneous tissue of the lower abdominal wall. In the second stage, the distal omentum, now vascularizing the overlying skin and soft tissue, is moved as a secondary island flap to the anterior chest wall to complete the breast reconstruction. In all but 1 of our 21 patients who have been followed for 1 to 8 years, reconstruction of large defects, including the chest wall, breast mound, and infraclavicular axillary fold depression, was performed without use of a prosthesis. In one patient, there was complete necrosis of the flap due to vascular impairment; there were three instances of delayed healing and a significant but partial loss of the flap in one patient. All complications were encountered in the first 10 patients of the series during the time the technique was being refined.     

Hypoxia-induced pulmonary vascular remodeling: contribution of the adventitial fibroblasts

Vascular repair in response to injury or stress (often referred to as remodeling) is a common complication of many cardiovascular abnormalities including pulmonary hypertension, systemic hypertension, atherosclerosis, vein graft remodeling and restenosis following balloon dilatation of the coronary artery. It is not surprising that repair and remodeling occurs frequently in the vasculature in that exposure of blood, vessels to either excessive hemodynamic stress (e.g. hypertension), noxious blood borne agents (e.g. atherogenic lipids), locally released cytokines, or unusual environmental conditions (e.g. hypoxia), requires readily available mechanisms to counteract these adverse stimuli and to preserve structure and function of the vessel wall. The responses, which were presumably evolutionarily developed to repair an injured tissue, often escape self-limiting control and can result, in the case of blood vessels, in lumen narrowing and obstruction to blood flow. Each cell type (i. e. endothelial cells, smooth muscle cells, and fibroblasts) in the vascular wall plays a specific role in the response to injury. However, while the roles of the endothelial cells and smooth muscle cells (SMC) in vascular remodeling have been extensively studied, relatively little attention has been given to the adventitial fibroblasts. Perhaps this is because the fibroblast is a relatively ill-defined cell which, at least compared to the SMC, exhibits few specific cellular markers. Importantly though, it has been well demonstrated that fibroblasts possess the capacity to express several functions such as migration, rapid proliferation, synthesis of connective tissue components, contraction and cytokine production in response to activation or stimulation. The myriad of responses exhibited by the fibroblasts, especially in response to stimulation, suggest that these cells could play a pivotal role in the repair of injury. This fact has been well documented in the setting of wound healing where a hypoxic environment has been demonstrated to be critical in the cellular responses. As such it is not surprising that fibroblasts may play an important role in the vascular response to hypoxia and/or injury. This paper is intended to provide a brief review of the changes that occur in the adventitial fibroblasts in response to vascular stress (especially hypoxia) and the role the activated fibroblasts might play in hypoxia-mediated pulmonary vascular disease.     

Effects of diffusion coefficients and struts apposition using numerical simulations for drug eluting coronary stents

In the context of drug eluting stent, we present two-dimensional numerical models of mass transport of the drug in the wall and in the lumen to study the effect of the drug diffusion coefficients in the three principal media (blood, vascular wall, and polymer coating treated as a three-compartment problem) and the impact of different strut apposition configurations (fully embedded, half embedded, and not embedded). The different conditions were analyzed in terms of their consequence on the drug concentration distribution in the arterial wall. We apply the concept of the therapeutic window to the targeted vascular wall region and derive simple metrics to assess the efficiency of the various stent configurations. Although most of the drug is dispersed in the lumen, variations in the blood flow rate within the physiological range of coronary blood flow and the diffusivity of the drug molecule in the blood were shown to have a negligible effect on the amount of drug in the wall. Our results reveal that the amount of drug cumulated in the wall depends essentially on the relative values of the diffusion coefficients in the polymer coating and in the wall. Concerning the strut apposition, it is shown that the fully embedded strut configuration would provide a better concentration distribution.     

Primary versus secondary structural changes of the blood vessels in hypertension

Various researchers have hypothesized that the thickening of the vascular wall plays an important role in the maintenance of hypertension. Such an alteration can increase the vascular resistance by exerting two effects. A thickened vascular wall could occlude the lumen of the blood vessel and (or) cause the artery to hyperreact to contractile stimuli. Until recently, it has been a general conclusion that such alterations were a secondary adaptation produced by the elevation of blood pressure. Consistent with this view, certain classes of larger arteries do exhibit a thickened vascular wall late during hypertension development and such changes can be prevented from occurring by antihypertensive treatment. However, recent studies involving the mesenteric and renal arteries of Wistar-Kyoto spontaneously hypertensive rats have shown that wall thickening of the vasculature occurs prior to hypertension development and is present even under conditions where the blood pressure has been normalized throughout the animal's life. These latter observations suggest that some structural alterations in the blood vessels observed in hypertension are pressure independent and could be of etiological importance in the initiation of hypertension.     

Chronic hyperhomocysteinemia causes vascular remodelling by instigating vein phenotype in artery

In the present study we tested the hypothesis whether hyperhomocysteinemia, an elevated homocysteine level, induces venous phenotype in artery. To test our hypothesis, we employed wild type (WT) and cystathionine β-synthase heterozygous (+/-) (CBS+/-) mice treatment with or without folic acid (FA). Aortic blood flow and velocity were significantly lower in CBS+/-mice compared to WT. Aortic lumen diameter was significantly decreased in CBS+/-mice, whereas FA treatment normalized it. Medial thickness and collagen were significantly increased in CBS+/-aorta, whereas elastin/collagen ratio was significantly decreased. Superoxide and gelatinase activity was significantly high in CBS+/-aorta vs WT. Western blot showed significant increase in MMP-2, -9,-12, TIMP-2 and decrease in TIMP-4 in aorta. RT-PCR revealed significant increase of vena cava marker EphB4, MMP-13 and TIMP-3 in aorta. We summarize that chronic HHcy causes vascular remodelling that transduces changes in vascular wall in a way that artery expresses vein phenotype.     

On the detection of messages carried in arterial pulse waves

The hypothesis is made that a disturbance in blood flow at one place can be detected in the arterial pulse waves at a distant site. This hypothesis was motivated by the traditional Chinese medicine which uses arterial pulse waves as a principal means of diagnosis. We formulated a test by asking whether a disturbance to the blood flow in a leg can be detected by changes in the pulse waves in the radial arteries. In particular, we ask whether the radial artery can differentiate a disturbance in the right leg from that in the left leg. We put force transducers on the radial arteries, depressed them by a specific amount, and recorded the force waves in response to a 2-min occlusion of the blood flow in the right or left tibial artery. The results show that the radial artery force waves do change in response to the flow disturbance. For a given individual, the force varies with the location of the force transducer on the radial artery, the specific amount of initial depression, and the right or left leg occlusion. Generally, an occlusion in the right leg reduces the force level in both radial arteries, the more so in the right radial artery than in the left. Although the discrimination is not very strong, the phenomenon is novel, and warrants further investigation.     

The effect of asymmetry in abdominal aortic aneurysms under physiologically realistic pulsatile flow conditions

In the abdominal segment of the human aorta under a patient's average resting conditions, pulsatile blood flow exhibits complex laminar patterns with secondary flows induced by adjacent branches and irregular vessel geometries. The flow dynamics becomes more complex when there is a pathological condition that causes changes in the normal structural composition of the vessel wall, for example, in the presence of an aneurysm. This work examines the hemodynamics of pulsatile blood flow in hypothetical three-dimensional models of abdominal aortic aneurysms (AAAs). Numerical predictions of blood flow patterns and hemodynamic stresses in AAAs are performed in single-aneurysm, asymmetric, rigid wall models using the finite element method. We characterize pulsatile flow dynamics in AAAs for average resting conditions by means of identifying regions of disturbed flow and quantifying the disturbance by evaluating flow-induced stresses at the aneurysm wall, specifically wall pressure and wall shear stress. Physiologically realistic abdominal aortic blood flow is simulated under pulsatile conditions for the range of time-average Reynolds numbers 50 < or = Rem < or = 300, corresponding to a range of peak Reynolds numbers 262.5 < or = Repeak < or = 1575. The vortex dynamics induced by pulsatile flow in AAAs is depicted by a sequence of four different flow phases in one period of the cardiac pulse. Peak wall shear stress and peak wall pressure are reported as a function of the time-average Reynolds number and aneurysm asymmetry. The effect of asymmetry in hypothetically shaped AAAs is to increase the maximum wall shear stress at peak flow and to induce the appearance of secondary flows in late diastole.     

Numerical analysis of the cooling effect of blood over inflamed atherosclerotic plaque

Atherosclerotic plaques with high likelihood of rupture often show local temperature increase with respect to the surrounding arterial wall temperature. In this work, atherosclerotic plaque temperature was numerically determined during the different levels of blood flow reduction produced by the introduction of catheters at the vessel lumen. The temperature was calculated by solving the energy equation and the Navier-Stokes equations in 2D idealized arterial models. Arterial wall temperature depends on three basic factors: metabolic activity of the inflammatory cells embedded in the plaque, heat convection due to luminal blood flow, and heat conduction through the arterial wall and plaque. The calculations performed serve to simulate transient blood flow reduction produced by the presence of thermography catheters used to measure arterial wall temperature. The calculations estimate the spatial and temporal alterations in the cooling effect of blood flow and plaque temperature during the measurement process. The mathematical model developed provides a tool for analyzing the contribution of factors known to affect heat transfer at the plaque surface. Blood flow reduction leads to a nonuniform temperature increase ranging from 0.1 to 0.25 degrees Celsius in the plaque/lumen interface of the arterial geometries considered in this study. The temperature variation as well as the Nusselt number calculated along the plaque surface strongly depended on the arterial geometry and distribution of inflammatory cells. The calculations indicate that the minimum required time to obtain a steady temperature profile after arterial occlusion is 6 s. It was seen that in arteries with geometries involving bends, the temperature profiles appear asymmetrical and lean toward the downstream edge of the plaque.     

Venous stagnation induced by 7 dyas in HDT, in the cerebral, ophtalmic, renal and splancnhic territories

The scientific objectives was to quantify the vascular changes in the brain, eye fundus, renal parenchyma, and splanchnic network. Heart, Portal, Jugular, femoral veins were investigate by Echography. The cerebral mesenteric, renal and ophthalmic arteries were investigated by Doppler. Eye fundus vein an papilla were investigated by optical video eye fundus. The Left ventricle volume decreased as usual in HDT. The cerebral and ophthalmic vascular resistances did'nt change whereas the eye fundus papilla and vein, and the Jugular vein increased. These arterial and venous data confirm the existence of cephalic venous blood stasis without sign of intracranial hypertension. On the other hand the kidney volume increased which is in agreement with blood flow stagnation at this level. At last the Mesenteric vascular resistance decreased and the Portal vein section increased in HDT which is in favor of an increase in flow and flow volume through the splanchnic area.     

Endothelial Cell Self-fusion during Vascular Pruning

During embryonic development, vascular networks remodel to meet the increasing demand of growing tissues for oxygen and nutrients. This is achieved by the pruning of redundant blood vessel segments, which then allows more efficient blood flow patterns. Because of the lack of an in vivo system suitable for high-resolution live imaging, the dynamics of the pruning process have not been described in detail. Here, we present the subintestinal vein (SIV) plexus of the zebrafish embryo as a novel model to study pruning at the cellular level. We show that blood vessel regression is a coordinated process of cell rearrangements involving lumen collapse and cell–cell contact resolution. Interestingly, the cellular rearrangements during pruning resemble endothelial cell behavior during vessel fusion in a reversed order. In pruning segments, endothelial cells first migrate toward opposing sides where they join the parental vascular branches, thus remodeling the multicellular segment into a unicellular connection. Often, the lumen is maintained throughout this process, and transient unicellular tubes form through cell self-fusion. In a second step, the unicellular connection is resolved unilaterally, and the pruning cell rejoins the opposing branch. Thus, we show for the first time that various cellular activities are coordinated to achieve blood vessel pruning and define two different morphogenetic pathways, which are selected by the flow environment.     

Ultrasound studies in varicocele

Renal function, the anatomic and functional status of the vena cava inferior, renal arteries and veins, and spermatic veins were evaluated in healthy individuals and patients with varicocele before and 12 months after laparoscopic ligation of the left spermatic vein. The renal vessels were assessed by color Doppler ultrasonography and renal function was examined by complex radionuclide study with 99mTc-pentatech. There were no significant changes in the diameter of renal arteries and vena cava inferior and the right arterial blood flow velocities in healthy individuals and patients. No difference were found in the diameter of renal veins and in the blood flow velocity in renal arteries and veins. The enlarged renal veins and decreased mean blood flow velocity in the left renal vein in healthy persons and patients with varicocele and lower blood flow in the left renal artery than in the right one indicate left-sided renal hypertension that is attributable to left renal vein overload due to a great variety of collaterals and to compression at the site of "a forcepts". At the same time 12-month postoperative ultrasonic, Doppler and complex radionuclide studies revealed no significant changes in the diameter and blood flow velocity in the left renal vein.     

Multiphysics simulation of blood flow and LDL transport in a porohyperelastic arterial wall model

Atherosclerosis localizes at a bend andor bifurcation of an artery, and low density lipoproteins (LDL) accumulate in the intima. Hemodynamic factors are known to affect this localization and LDL accumulation, but the details of the process remain unknown. It is thought that the LDL concentration will be affected by the filtration flow, and that the velocity of this flow will be affected by deformation of the arterial wall. Thus, a coupled model of a blood flow and a deformable arterial wall with filtration flow would be invaluable for simulation of the flow field and concentration field in sequence. However, this type of highly coupled interaction analysis has not yet been attempted. Therefore, we performed a coupled analysis of an artery with multiple bends in sequence. First, based on the theory of porous media, we modeled a deformable arterial wall using a porohyperelastic model (PHEM) that was able to express both the filtration flow and the viscoelastic behavior of the living tissue, and simulated a blood flow field in the arterial lumen, a filtration flow field and a displacement field in the arterial wall using a fluid-structure interaction (FSI) program code by the finite element method (FEM). Next, based on the obtained results, we further simulated LDL transport using a mass transfer analysis code by the FEM. We analyzed the PHEM in comparison with a rigid model. For the blood flow, stagnation was observed downward of the bends. The direction of the filtration flow was only from the lumen to the wall for the rigid model, while filtration flows from both the wall to the lumen and the lumen to the wall were observed for the PHEM. The LDL concentration was high at the lumenwall interface for both the PHEM and rigid model, and reached its maximum value at the stagnation area. For the PHEM, the maximum LDL concentration in the wall in the radial direction was observed at the position of 3% wall thickness from the lumenwall interface, while for the rigid model, it was observed just at the lumenwall interface. In addition, the peak LDL accumulation area of the PHEM moved about according to the pulsatile flow. These results demonstrate that the blood flow, arterial wall deformation, and filtration flow all affect the LDL concentration, and that LDL accumulation is due to stagnation and the presence of filtration flow. Thus, FSI analysis is indispensable.     

Collagen of umbilical cord vein and its alterations in pre-eclampsia

The state of the vascular system of the mother and of placenta is known to exert a great influence on intrauterinal development of the fetus. Pre-eclampsia is the most common pathological syndrome connected with pregnancy. Since collagen is one of the main constituents of the vessel wall a comparison was made with collagen content and its molecular polymorphism in umbilical cord veins of newborns from healthy and pre-eclamptic mothers. It was found that umbilical cord veins of newborns from mothers with pre-eclampsia contained 18% less collagen than those of the newborns from normal pregnancies. This decrease was accompanied by a slight decrease of collagen solubility, but all its types (I, II, IV, V and VI) were present. However, the umbilical vein wall of newborns from mothers with pre-eclampsia contained relatively less of type I and more of type III collagen than the normal umbilical cord. These differences may be connected with a disturbance of blood flow in fetus of a woman with pre-eclampsia.