硝普钠对动物血管力学参数的影响

有研究表明硝普钠具有增加动脉顺应性的趋势和降低外周阻力的作用,但是硝普钠对血管中血流惯性的影响却不统一。本文以Coldwyn等建立的动脉系改良风箱力学模型为主要研究方法对动物动脉血管顺应性(包括中央和外周顺应性),血流惯性和外周阻力等进行了研究,并建立了动脉系总阻抗的公式。然后评价硝普钠对总阻抗的影响以及总阻抗做为一种血管力学参数的灵敏性。实验结果表明:硝普钠具有统计学意义地增加外周血管的顺应性(P<0.05);有增加中央动脉顺应性和血流惯性的趋性;并能降低外周阻力和动脉系总阻抗(P<0.05)。结果还表明动脉系总阻抗是一种灵敏度高的血管力学参数。因此,硝普钠能影响血管参数,对外周血管顺应性和血管总阻抗的作用尤其明显。     

心血管系统电网络模型的脉动信号仿真分析

脉搏波蕴含了人体丰富的生理病理信息,研究脉搏波与心血管系统生理参数的关系不但有利于心血管疾病的临床诊断与治疗,而且有助于新型医疗设备的开发。本文在经典双弹腔模型的基础上,采用电网络模型法建立了人体心血管仿真系统,对动脉内血压与血流的变化规律进行仿真,分析了外周阻力与血管顺应性对血流分布的影响,并将仿真结果与临床监测结果进行对比分析,以预测人体的生理病理状态。结果表明,血压与血流的仿真波形于第二个心动周期后逐渐趋于稳定;随着外周阻力的增大,动脉的收缩压增大,舒张压保持不变,而脉压逐渐增大;随着血管顺应性的减小,血管的弹性变差,脉压相应地增大;仿真结果与临床监测结果一致。外周阻力增大和血管顺应性减小预示了高血压和动脉粥样硬化等疾病的发生率增大。     

高血压微循环与体循环动力学临床研究系列(下) ——Ⅴ.高血压病血流动力学异常与微循环障碍

本文对原发性高血压(EH)病人30例,正常人30例。观察其外周“压降”发生部位及其上下游血流动力学变化。结果显示:1.EH组外周血压显著下降部位发生于小动脉和微动脉,而正常对照组外周血压显著下降部位仅发生于毛细血管前微动脉,提示EH组总外周阻力血管段延长。2.EH组上游血流动力学异常表现为:(1)动脉血压升高,总外周阻力(TPR)和室壁应力(ESS)等后负荷增加引起左室肥厚(LVH)和舒张功能障碍;(2)动脉顺应性减退,壁剪切应力下降,壁张力增加和壁/腔比率增大。3.EH组微循环障碍表现:微血管压、流、阻异常,微循环储备功能减退,微血管病,加权积分值增加等。     

高血压病人节段性外周动脉压降对皮肤微循环的影响

目的 :研究高血压病人外周动脉节段性压降及其对微循环的影响。方法 :原发性高血压病人 3 0例 ,正常血压 3 0例。袖带血压计测量肱动脉、桡动脉、指动脉血压 ,弹簧压片法测量甲襞毛细血管压 ,并计算节段性压降 (△P)。激光Dopple血流仪测量食指皮肤血流量 ,并计算皮肤血流阻力。结果 :( 1)高血压组和对照组△P分配 :在肱动脉与桡动脉节段之间△P几乎没有变化 ,最大△P均发生于指动脉与毛细血管之间 ;高血压组在桡动脉与指动脉之间提早出现初始△P(P <0 .0 5 ) ,而正常血压组在小动脉水平△P变化无显著性。 ( 2 )高血压组毛细血管压升高与毛细血管前微动脉最大△P呈负相关 (r =-0 .78)。 ( 3 )高血压组毛细血管压升高 ,皮肤血流阻力增加 ,而皮肤静息血流无明显改变。 ( 4 )毛细血管压与肱动脉舒张压 (≥ 10 0mmHg)正相关 (r =0 .5 2 )。结论 :高血压病人外周小动脉段提早出现初始△P ,存在阻力血管段延长 (包括毛细血管前微动脉和小动脉 ) ,这是对上游压—流适应性改变和对下游微循环调控的代偿。皮肤毛细血管压升高是高血压微循环血流动力改变主要参数 ,可作为降压治疗外周效应的评估指标。     

不同高血压状态颈动脉瞬时波强变化及其临床意义

瞬时波强(WI)是一种新的超声检测技术,通过WI可以了解左心室与外周动脉相互之间作用的血流动力学信息。WI的观测指标主要有反映左室收缩性能的W1,反映心脏主动停止搏血功能的W2以及反映外周动脉阻力的NA等三种参数。采用颈动脉WI检查,在原发性高血压血压未控制(HP1)组、血压已得到控制(HP2)组以及正常对照(NC)组之间进行比较分析,发现WI对外周动脉阻力和相应心脏收缩功能的变化较常规超声心动图更敏感。W1和NA有助于原发性高血压疗效的评估和动态随访。     

高血压微循环与体循环动力学临床研究系列——Ⅱ.高血压病人皮肤微循环血流阻力的临床研究

高血压病人30例,正常血压对照30例,采用Laser Doppler血流计测定手指皮肤血流量,间接测定甲襞毛细血管压,并计算皮肤血流阻力,以袖带法测量肱动脉、桡动脉和指动脉血压,计算出平均血压和毛细血管前压降。结果显示:高血压组皮肤微循环中的血流阻力和毛细血管压升高(26.77±14.53对17.74±9.28mmHg/V,P<0.01;68.68±19.42对43.11±10.30mmHg,P<0.01),而皮肤血流改变无显著性差异(2.56±1.01对2.43±0.92,P>0.05);高血压组毛细血管压升高与其上游压降呈负相关关系(r=-0.78,P<0.01),提示皮肤毛细血管压和血流阻力是受其上游“阻力血管”所控制。用血管扩张剂治疗后的病人,血压明显下降而皮肤血流阻力仍处于升高状态。从而提示皮肤血流阻力的“结构成份”增加并借此作为评价“结构阻力”可逆性的客观指标。     

高血压病人阻力动脉重构和微血管功能障碍

目的研究原发性高血压（EH）阻力动脉重构及其微血管整合功能。方法对EH病人30例和正常对照组30例，采用上肢节段性血压、Doppler超声、激光Doppler血流仪等无创性检查方法，评估阻力动脉结构、功能和微循环变化。结果①EH病人阻力动脉段向上延伸（P〈0．05），包括微动脉和小动脉；②阻力动脉重构特征：小动脉管壁增厚（P〈0．01）、壁／腔比值增大（P〈0．01），腔径轻度减少（P〉0．05）；管壁僵硬度增加，脉波传导速度增快（P〈0．001）；血流介导内皮依赖性血管扩张障碍和收缩作用减弱。③同时，皮肤毛细血管压升高（P〈0．01），这与阻力动脉重构引起微循环“调节机制储备”受损和上游高血压跨壁传输作用的两种机制有关。结论高血压病人阻力动脉段向上延伸，伴存动脉结构、机械特性和血管舒缩运动异常，并导致微血管系统整合功能障碍。测定这些改变的相关指标．有助于评估微血管病变程度和降压治疗的外周效应。     

老年大鼠模型视网膜血管改变及视网膜中央动脉血流变化的高分辨率超声图像检测

背景：视网膜对缺血非常敏感,所以眼部血流动力学的改变可直接影响眼的功能,目前评估眼部血液循环可借助多种仪器设备。 目的：应用高分辨率小动物超声影像系统检测视网膜中央动脉的血流动力学变化,结合视网膜血管消化铺片技术检测视网膜血管结构变化,以明确老年大鼠视网膜中央动脉血流动力学的变化规律。 方法：使用高分辨率小动物超声影像系统测量老年大鼠和青年大鼠及视网膜中央动脉的血流参数,包括收缩期峰值血流速度、舒张末期血流速度,计算搏动指数、阻力指数和收缩期舒张期血流速度比值。同时使用视网膜血管消化铺片技术检测视网膜血管形态学改变。 结果与结论：与青年大鼠组相比,老年组大鼠视网膜血管内皮细胞增生,排列紊乱,管径增粗,血管壁不光滑;视网膜中央动脉血流速度、舒张末期血流速度均降低(P < 0.01),计算搏动指数、阻力指数及收缩期峰值与舒张末期血流速度比值则升高(P < 0.01)。说明使用高分辨率小动物超声影像系统检测视网膜中央动脉收缩期和舒张期峰值速度及阻力指数能较敏感地反映血管的老化过程。     

体循环模拟装置的研制

为研究左心室辅助装置而研制出一套体循环模拟装置。它是由血泵、体动脉腔、阻力器和体静脉腔组成。以密闭气腔模拟血管顺应性(Ccmpliance),分别以双密闭气腔和单密闭气腔模拟动脉系统和静脉系统。由波纹管、锥形阀和弹簧构成阻力器模拟外周阻力血管作用。本装置具有升支比较陡峭、降支段有明显重搏波基本符合人体主动脉压力波形以及(?)-CC曲线与正常人体动脉流曲线相似的特点。     

高血压时冠状动脉小动脉及微动脉病变的临床特点

高血压对冠状循环的影响涉及到冠状动脉的各级血管 ,包括心外膜冠状动脉 (直径 2～ 7.5ｍｍ)及其主要分支 ( 1～ 2ｍｍ) ,冠状动脉小动脉 ( 50 0～ 1 0 0 0 μｍ)、微动脉 ( <50 0 μｍ)和心肌组织毛细血管 (平均 8μｍ)。其中 ,冠状动脉主干及其主要分支血管的内弹性膜和中膜平滑肌发达 ,具有较强的收缩力 ,能使管腔明显地缩小或扩大 ,从而调节和分配到心脏各部位的血流。而小动脉和微动脉 (亦称外周阻力血管 )仍属肌性动脉 ,其收缩和扩张可显著影响心肌血流量和冠状动脉阻力的变化 ,其中 <30 0 μｍ的微动脉网是冠状动脉主要的阻力血管床…     

Influence of central and peripheral changes on the hydraulic input impedance of the systemic arterial tree

The input impedance of the systemic arterial tree of the dog has been computed by Fourier analysis. It was shown that a distance between pressure and flow transducers of less than 2 cm results in appreciable errors which manifest themselves mainly in the phase of the input impedance. The input impedance for controls, occlusions at various locations in the aorta, and an increase and decrease of peripheral resistance were studied. For the same experiments, the total arterial compliance was calculated from the peripheral resistance of the diastolic aortic-pressure curve. The characterstic impedance of the ascending aorta was also estimated. The impedance in the control situation may be modelled by means of a 3-element Windkessel consisting of a peripheral resistance and (total) arterial compliance, together with a resistance equal to the characteristic impedance of the aorta. The occlusions of the aorta show that blockage at (and beyond) the trifurcation do not result in a detectable change in input impedance, except for a slight increase of the peripheral resistance. The more proximal an aortic occlusion, the more effect it has on the pattern of the input impedance. When the aorta is occluded at the diphragm, or higher, the single (uniform) tube appears to be a much better model than the Windkessel. Occlusion of one or both carotid arteries increases the mean pressure; consequently not only the peripheral resistance increases but also the total arterial compliance decreases. The Windkessel with increased peripheral resitance and decreased compliance is again a good model. After a sudden release of occlusion of the aorta, the arterial system has a low peripheral resistance and may also be modelled by the Windkessel.     

Viscoelasticity modulates resonance in the terminal aortic circulation.

We used an inertance-viscoelastic windkessel model (IVW) to interpret aortic impedance patterns as seen in the terminal aortic circulation of the dog, and to explain evident oscillatory phenomena in flow measurements. This IVW model consists of an inertance, L, connected in series with a viscoelastic windkessel (VW) where the peripheral resistance, Rp, is connected in parallel with a Voigt cell (a resistor, Rd, in series with a capacitor, C) to account for viscoelasticity. Pressure and flow measurements were taken from the terminal aorta, just downstream of the origin of renal arteries, in three anaesthetised open-chest dogs, under a variety of haemodynamic conditions induced by administering a vasoconstrictor agent (methoxamine) and a vasodilator (sodium nitroprusside). Mean pressure ranged from 40 to 140 mm Hg. The resistance Rp was calculated as the ratio of mean pressure to mean flow. Parameters L, C and Rd were estimated by fitting measured to model predicted flow waves. We found that prominent oscillations observed in flow waves, from midsystole to diastole, are related to resonance that occurs at a frequency, f(o), where reactance of inertance of blood motion matches the reactance of arterial compliance. Estimates of f(o) increased from 2.4 to 10 Hz with increasing pressure and showed a correlation with values of static elastic moduli plotted against mean pressure of dogs' peripheral arteries previously reported by others. Viscous losses, Rd, of arterial wall motion limited the amplitude of resonance peak. We conclude that viscoelasticity, rather than pure elasticity, is a key issue to interpret terminal aortic impedance as it relates to resonance.     

Some Physical Properties of the Pulmonary Arterial Bed Deduced from Pulsatile Arterial Flow and Pressure

This study aimed to quantify changes of vascular compliance and resistance of the proximal and the peripheral pulmonary arterial vessels when vascular smooth muscle was stimulated. These above vascular characteristics were derived from registrations of pulsatile pressure and flow in the pulmonary artery (PA). An in situ cat lung preparation was used, with the right heart by-passed by a pulsatile blood pump. Vascular input impedance was derived from PA pulsatile pressure and flow recordings, and impedance characteristics were used for calculation of the variables of a simple lumped analog representation of the arterial bed. PA smooth muscle was stimulated by infusions of collagen suspension, by general hypoxia and by nor-adrenaline injections. Collagen caused 40% reduction of vascular compliance (C), no changes in proximal arterial resistance (Rl) and 18076 increase in peripheral vascular resistance (R2). Hypoxia caused 5096 reduced C, 20% increased R1 and 70% increased R2. Noradrenaline caused 20:6 reduced C and 30 % increased R1 and R2. These results, together with results derived from simulation of the observed impedance changes in a computer model of the lung arterial bed, indicated that collagen infusion elicited contraction of small and medium-sized arteries, with increased arterial volume as result of increased distending pressure. Hypoxia and noradrenaline, seemed both to cause contraction of the total arterial bed. This effect being most pronounced during hypoxia.     

Renal arterial compliance and conductance measurement using on-line self-adaptive analog computation of model parameters

Dynamic renal arterial flow pattern, arterial compliance, and pre-glomerular conductance were predicted from the measured canine renal arterial pressure pulse pattern using on-line analog computer simulation of renal arterial parameters. The flow was accurately predicted not only under steady-state conditions but also in the presence of marked fluctuations in arterial pressure pattern, mean level, and heart rate. The model has five parameters: largeartery resistance, inertance, and compliance; a pre-glomerular arteriolar conductance; and a non-pulsatile glomerular pressure. The first two were set manually while the last three were automatically adjusted by the method of steepest descents to minimize the absolute error expressed as the instantaneous difference between the measured flow in the artery and the flow predicted by the computer.     

Role of total arterial compliance and peripheral resistance in the determination of systolic and diastolic aortic pressure.

The goal of the study was to define the major arterial parameters that determine aortic systolic (Ps) and diastolic (Pd) pressure in the dog. Measured aortic flows were used as input to the two-element windkessel model of the arterial system, with peripheral resistance calculated as mean pressure over mean flow and total arterial compliance calculated from the decay time in diastole. The windkessel model yielded an aortic pressure wave from which we obtained the predicted systolic (Ps, wk) and diastolic (Pd, wk) pressure. These predicted pressures were compared with the measured systolic and diastolic pressures. The measurements and calculations were carried out in 7 dogs in control conditions, during aortic occlusion at four locations (the trifurcation, between trifurcation and diaphragm, the diaphragm and the proximal descending thoracic aorta) and during occlusion of both carotid arteries. Under all conditions studied the predicted systolic and diastolic pressure matched the experimental ones very well: Ps, wk = (1.000 +/- 0.0055) Ps with r = 0.958 and Pd, wk = (1.024 +/- 0.0035) Pd with r = 0.995. Linear regression for pulse pressure gave PPwk = (0.99 +/- 0.016) PP (r = 0.911). We found the accuracy of prediction equally good under control conditions and in presence of aortic or carotid artery occlusions. Multiple regression between pulse pressure and arterial resistance and total arterial compliance yielded a poor regression constant (r2 = 0.19) suggesting that the two arterial parameters alone cannot explain pulse pressure and that flow is an important determinant as well. We conclude that, for a given ejection pattern (aortic flow), two arterial parameters, total arterial resistance and total arterial compliance are sufficient to accurately describe systolic and diastolic aortic pressure.     

True Arterial System Compliance Estimated From Apparent Arterial Compliance

A new method has been developed to estimate total arterial compliance from measured input pressure and flow. In contrast to other methods, this method does not rely on fitting the elements of a lumped model to measured data. Instead, it relies on measured input impedance and peripheral resistance to calculate the relationship of arterial blood volume to input pressure. Generally, this transfer function is a complex function of frequency and is called the apparent arterial compliance. At very low frequencies, the confounding effect of pulse wave reflection disappears, and apparent compliance becomes total arterial compliance. This study reveals that frequency components of pressure and flow below heart rate are generally necessary to obtain a valid estimate of compliance. Thus, the ubiquitous practice of estimating total arterial compliance from a single cardiac cycle is suspect under most circumstances, since a single cardiac cycle does not contain these frequencies. © 2000 Biomedical Engineering Society. PAC00: 8719Uv, 8719Rr     

Influence of Vessel Distension and Myogenic Tone on Pulmonary Arterial Input Impedance. A Study using a Computer Model of Rabbit Lung

A computer model of the pulmonary arterial (PA) bed of rabbit lungs was designed in order to test experimental observations of changes in PA input impedance and pulsatile hydraulic power (cap.) during increased PA pressure. The computer model was based on a simple 3-component analog representation of single vessels (i.e. resistance, inertance and compliance). 16 generations of arterial vessels, from PA to 60 μm diameter, were combined to calculate PA input impedance. Input impedance was found to mimic closely that observed experimentally. Both venous pressure elevation and arteriolar constriction was found to reduce input impedance and Wp. By combining arteriolar constriction with increased myogenic tone of the larger arteries, Wp was found to show a minimum level at a certain PA pressure, dependent on the degree of arterial stiffening. Wp was found to follow changes in arterial volume and resistance during simulated vasoconstriction. Wp dissipation in arterial vessels was calculated to approx. 50% of total input Wp at physiological pressure conditions, and could be reduced by one half after PA pressure increase from 20 to 50 cm H₂O, despite a concurrent halving of arterial compliance. Arterial vessels smaller than 200 pm diameter were found to have negligible direct influence on PA input impedance.     

Effect of gastric distension on cardiovascular parameters: gastrovascular reflex is attenuated in the elderly

Stretching the stomach wall in young healthy subjects causes an increase in muscle sympathetic nerve activity and in blood pressure, the gastrovascular reflex. We compared healthy elderly subjects with healthy young subjects to find out whether the gastrovascular reflex attenuates in normal ageing and we studied whether there was a difference in autonomic function or gastric compliance that could explain this possible attenuation. Muscle sympathetic nerve activity, finger blood pressure and heart rate were continuously recorded during stepwise isobaric gastric distension using a barostat in eight healthy young (6 men and 2 women, 27 ± 3.2 years, mean ± s.e.m. ) and eight healthy elderly subjects (7 men and 1 woman, 76 ± 1.5 years). Changes in cardiac output and total peripheral arterial resistance were calculated from the blood pressure signal. The baseline mean arterial pressure and muscle sympathetic nerve activity were higher in the elderly group (both P < 0.05) and muscle sympathetic nerve activity increase during the cold pressor test was lower in the elderly group ( P = 0.005). During stepwise gastric distension, the elderly subjects showed an attenuated increase in muscle sympathetic nerve activity compared to the young subjects ( P < 0.01). The older group tended to show a higher increase in mean arterial pressure ( P = 0.08), heart rate ( P = 0.06) and total peripheral arterial resistance ( P = 0.09) The cardiac output rose slightly in both groups without significant difference between groups. The fundic compliance did not differ between groups. We conclude that stepwise gastric distension caused an increase in muscle sympathetic nerve activity in both groups, but the increase in the elderly was attenuated.     

In vitro performance of the novel coronary sinus AutoRetroPerfusion Cannula

Myocardial salvage through coronary sinus intervention has been documented. The AutoRetroPerfusion Cannula is a novel device that is able to perfuse the coronary bed retrogradely through the coronary sinus with arterial blood generated from a peripheral artery with no need for a pump. The cannula consists of a distal end that, once secured in the coronary sinus, opens an umbrella-like membrane to create pressure in the coronary sinus, and at the same time has small channels directed backwards to the right atrium to provide pressure relief. The cannula is introduced from the axillary vein under local anesthesia and the proximal end, which consists of a graft, is anastomosed to the axillary artery to start autoperfusion once the distal end is secured in the coronary sinus and the occluding membrane is open. The AutoRetroPerfusion Cannula was tested in the in vitro mock loop under 50-120 mm Hg of proximal pressure and 50, 100, and 150 ml/min of total flow in the cannula. We were able to achieve the nominal design point of 40-80 mm Hg of distal pressure and 50-150 ml/min of distal flow by adjusting the number, diameter, and length of the small backwards channels.