天麻素对动脉血管顺应性以及血流动力学的影响

本文旨在研究天麻素对动脉血管顺应性和血流动力学等的作用。采用改良风箱模型来计算动脉管的顺应性和血管中血流惯性。在静脉注射天麻素前后，分别记录和计算出狗的血压，心输出量，外周阻力，血流惯性以及中央和外周动脉血管的顺应性。结果表明天麻素具有降低血压和外周务管阻力，增加动脉血管中血流惯性，以及中央和外周动脉血管的顺应性等作用。因此，天麻素是一种有效的能够改善由血管顺应性下降所致的高血压－老年性高血压的中     

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。     

应用7种解痉挛药物预防去甲肾上腺素诱发的血管痉挛的疗效比较

目的　探讨使用解痉药物预防去甲肾上腺素诱发的血管痉挛。 方法　64只SD大鼠随机分为8组,在其股动静脉区域滴加7种解痉挛药剂预处理30 min（前列腺素E1、硝普钠、硫酸镁、罂粟碱、酚妥拉明、维拉帕米和利多卡因）,生理盐水作为对照组。随后分别滴加去甲肾上腺素0.1 ml（1:1000）,建立血管痉挛模型。通过激光散斑血流成像系统监测股动静脉灌注强度和内径,数据处理为血流灌注。采用单因素方差分析进行组间股血管灌注差异比较。 结果　对照组（生理盐水）局部应用去甲肾上腺素5 min,动脉灌注约降低91%,静脉灌注约降低78%。硝普钠和酚妥拉明组均可预防股动静脉血管痉挛（P<0.05）,罂粟碱仅对股动脉痉挛有预防作用,前列腺素E1仅对股静脉有预防痉挛的作用。 结论　术前使用硝普钠和酚妥拉明预处理血管,可以预防去甲肾上腺素诱发的动静脉痉挛。其中硝普钠预防效果最强,酚妥拉明效果次之。     

慢性肺动脉高压肺血管力学特性的评价

本文以风心病二尖瓣病变合并被动性肺动脉高压为研究对象,借助右心导管技术和利用压力波形面积确定动脉顺应性的改进方法,通过测定肺血管阻力和顺应性,以评价慢性肺动脉高压肺血管力学特性的变化规律。发现慢性肺动脉高压患者肺动脉血管阻力明显升高（P＜0.01）;而反映血管壁固有结构的零压顺应性Co明显下降(P＜0.01),与术前肺动脉平均压呈显著负相关(r＝－0.745P＜0.05);扩血管药物试验提示不同程度肺动脉高压组的肺血管阻力均有显著下降(P＜0.01),轻度肺高压组零压顺应性和平均压顺应性均明显升高(P＜0.01);而重度肺高压组零压顺应性Co无明显变化(P＞0.05)。由此我们认为慢性肺高压肺血管都存在不同程度的重建,肺血管外周血管阻力和顺应性是影响其肺动脉压力水平的主要因素。     

硝苯吡啶对Na~+负荷大鼠血管反应性的影响

钠负荷导致血压升高和增加血管反应性的机理,目前多倾向于接受Folkow的外周阻力取决于血管壁(厚度)/腔(半径)的公式。因钠的滞留使血管壁中层水肿、管腔减小,从而升高外周阻力并对缩血管活性物质产生较强的收缩。近年研究证明钙离子的膜内外转运是平滑肌收缩的基础并与高血压发生有密切关系。本工作通过硝苯吡啶阻断钙通道,探讨钠负荷大鼠血管反应性和钙的关系。     

中风患者脑血管血液动力学参数变化及相关性分析

本文观察了中风患者脑血管血液动力学参数(CVHP)变化并分析了CVHP各指标的相关性联系及对脑血流量的影响。结果表明中风患者CVHP各指标均显著差于对照组(P<0.05～0.01);CVHP各指标均可见显著相关性联系;颈动脉最小血流量(Qmin、最小血流速度(Vmin)、平均血流速度(Vmean)、脑血管外周阻力(R)、脑血管零压顺应性(Co)、颈动脉最大血流量(Qmax)、和最大血流速度(V(max))及平均动脉血压(MBP)对脑血流量的多元回归方程起着主要作用。     

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。     

中分子右旋糖酐及硝普钠对犬实验性急性心包填塞的血流动力学影响

本文通过动物实验探讨中分子右旋糖酐及硝普钠对急性心包填塞的血流动力学影响。结果表明,中分子右旋糖酐单纯扩容可明显提高心包填塞的心输出量(CO)和平均外周动脉压(MSAP)。但同时亦使平均右房压(MRAP)、平均肺动脉压(MPAP)、平均肺动脉楔嵌压(MPWP)和平均心包腔内压(MIPP)明显升高(P均<0.05)。在扩容基础上,适量硝普钠可进一步提高CO(P<0.05),同时可避免单纯扩容所导致的MRAP、MPAP、MPWP及MIPP升高的不利影响,从而使心包填塞的血流动力学获得明显改善。     

心血管系统对加速度负荷反应的计算机模拟

本文报告了一个心血管系统的数学模型。它将动、静脉各分为27段,用参数R(流阻)、L(惯性)、C(顺应性)来表示此段的流体动力学特征,而R、L、C是用各段血管的几何及力学参数确定的。(文中给出了这些参数的均值)。还考虑了静脉的塌陷效应及管壁的粘弹性质造成的能量损失。同样的方法应用到肺动脉、冠状动脉与外周血管,因此建立了心血管     

Elevated arterial blood pressure in cardiac tamponade.

BACKGROUND. In cardiac tamponade cardiac output falls, but peripheral vascular resistance increases, so that systemic blood pressure may be maintained at normal or near-normal levels. We recently observed a patient with cardiac tamponade whose blood pressure was markedly elevated. METHODS. To determine the frequency of elevated blood pressure in patients with cardiac tamponade and their hemodynamic characteristics, we studied 18 consecutive patients with cardiac tamponade from a variety of causes using right heart catheterization. RESULTS. Six of the 18 patients had systolic arterial blood pressures ranging from 150 to 210 mm Hg (mean [+/- SD], 176 +/- 26) and diastolic pressures ranging from 100 to 130 mm Hg (mean, 113 +/- 14). All six had previously been hypertensive. After pericardiocentesis there was a significant decrease in blood pressure (to 139 +/- 13 mm Hg systolic, P less than 0.05; and 83 +/- 6 mm Hg diastolic, P less than 0.01) and peripheral vascular resistance (from 2150 +/- 588 to 1207 +/- 345 dyn.sec.cm-5, P less than 0.01). Cardiac output increased in all six. The other 12 patients, 3 of whom had a history of hypertension, had significant increases in cardiac output and systolic blood pressure (from 119 +/- 13 to 127 +/- 7 mm Hg, P less than 0.05) after pericardiocentesis, whereas peripheral vascular resistance decreased. Both groups had similar degrees of cardiac tamponade, as indicated by measurements of cardiac output and intrapericardial, right atrial, and pulmonary-artery wedge pressures. CONCLUSIONS. Elevated blood pressure may occur in some patients with cardiac tamponade who have preexisting hypertension. Moreover, blood pressure may fall after pericardiocentesis in patients who have elevated blood pressure associated with tamponade.     

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.     

Effects of stress management on blood pressure and other cardiovascular variables.

Blood pressure and impedance cardiography derived measures of heart rate, stroke volume, cardiac output and total peripheral resistance were measured in 16 persons before and after participation in a comprehensive program of stress management that included home monitoring of blood pressure and feedback of finger skin temperature during relaxation. Ten of the subjects were hypertensive and six were normotensive. Baseline measures of systolic and diastolic blood pressure and heart rate decreased significantly after participation in the program. In addition, reactivity to a psychological stressor (oral quiz) was significantly lower as revealed in reduced systolic and diastolic pressure, heart rate and cardiac output at the second assessment. A reduction in sympathetic nervous system activity is postulated as a possible mechanism for the changes observed.     

Cardiovascular differentiation of emotions.

This study examined the cardiovascular mechanisms governing differential blood pressure changes during the emotions of joy, sadness, fear, and anger. Heart rate, blood pressure, stroke volume, peripheral vascular resistance, cardiac output, and indices of myocardial contractility were measured during fear, anger, joy, sadness, physical action, and neutral imagery conditions in 27 right-handed male volunteers screened for imagery ability, alexithymia, anxiety, and depression. Anger imagery, rather than fear, was accompanied by the largest effects on the cardiovascular system. Increased diastolic blood pressure in anger was associated with maintained levels of peripheral vascular resistance and increased cardiac output and heart rate compared with changes during neutral imagery. Sadness produced a distinct pattern with moderate increases in blood pressure and vascular resistance and a decrease in cardiac output compared with changes during neutral imagery. Fear, action, and joy produced similar blood pressure changes in which systolic pressure increased and diastolic pressure was relatively unchanged. The measurement of cardiac output and determination of vascular resistance changes during emotional imagery demonstrate that previously observed emotion-specific blood pressure responses are produced by underlying patterns of cardiovascular activation, which differ between the major categories of emotions.     

Psychophysiological Reactivity in Cardiac Transplant Recipients

To assess the contribution of the heart's autonomic innervation to reactivity to psychological stressors, hemodynamic responsiveness of the denervated human heart was examined in two studies. In Study 1, cardiac output measured by thermodilution. heart rate, and systolic and diastolic blood pressure responses to a 4-min mental arithmetic task were studied in 7 cardiac transplant patients during routine post-transplant cardiac catheterization. In Study II, 6 cardiac transplant patients, 5 normal controls, and 5 renal transplant patients participated in a 78-min psychophysiological stress protocol during which heart rate, systolic and diastolic pressure, and cardiac output (measured noninvasively by impedance cardiography) as well as serum epinephrine and norepinephrine were measured at baseline and while subjects performed mental arithmetic and reaction time tasks. In Study I, transplant patients showed significant increases, relative to baseline, in heart rate, systolic blood pressure, and cardiac output in response to mental arithmetic. The diastolic blood pressure response was marginally significant. In Study II, mental arithmetic produced significant reactivity in systolic blood pressure and marginally significant increases in heart rate and diastolic blood pressure in cardiac transplant patients. Reaction time produced only marginally significant diastolic blood pressure reactivity. Hemodynamic reactivity of the cardiac transplant group generally was lower than that of the two innervated groups, which generally were similar to each other. Although the small number of subjects makes conclusions tentative, these data suggest that: 1) Cardiac transplant patients are capable of significant reactivity to psychological stressors despite the absence of innervation of the heart, and 2) reactivity to these stressors is diminished relative to innervated control subjects. In the absence of cardiac innervation, reactivity is due to the vascular system and cardiac effects mediated by humoral factors.     

Cardiovascular reactivity, Type A behavior, and coronary heart disease: Comparisons between myocardial infarction patients and controls during laboratory-induced stress

Cardiovascular responses to a series of laboratory stressors were examined in middle-aged Type A and Type B men. The subjects were 30 patients with diagnosed myocardial infarction (NYHA Class 1) and 26 age-matched healthy controls. All subjects were nonsmokers in the normotensive range, and none were on medication. Blood pressure, heart rate, forearm blood flow and resistance, and impedance cardiography-determined response variables were obtained during performance and recovery periods of both mental and physical tasks. The patients showed elevated reactivity in systolic blood pressure and cardiac output and prolonged systolic lime ratio during mental stress tasks and elevated total peripheral resistance and lower cardiac output and stroke volume during physical tasks, as compared with control subjects. Thus, the difference in blood pressure reactivity between patients and controls appeared to be primarily dependent on the vascular component during physical tasks, whereas the mental tasks promoted a hemodynamic response pattern more consistent with beta adrenergic activation. Type A men, irrespective of coronary status, showed larger systolic and diastolic blood pressure response to both mental and physical stress than did Type B men.     

The Influence of Pulmonary Blood Flow Rate on Vascular Input Impedance and Hydraulic Power in the Sympathetically and Noradrenaline Stimulated Cat Lung

This study was designed to evaluate the influence of sympathetic nerve stimulation (NS) and α-adrenergic receptor stimulation (αS) on the pulmonary vascular input impedance and hydraulic power output of the right heart during variations of cardiac output (CO). An open chest cat preparation was used and pulsatile pressure and flow in the pulmonary artery were measured by high frequency response transducers. Calculations showed that vascular resistance (VR) was inversely dependent on CO, hut input impedance of the unstimulated lung was not influenced by CO variations. NS or αS increased VR and input impedance significantly, and the relation pulsatile hydraulic power/total hydraulic power (W_p/W_t) increased 40%, indicating that such stimulation has larger relative influence on impedance than on resistance. The reduction of arterial compliance during NS (maximal stimulus) was calculated to be 60%, independent of CO. Input impedance during NS or αS was reduced by CO elevations, probably because the concomitant distension of the arterial bed reduced arterial resistance and inertance. The ratio W_p/CO, which expresses the fraction of pulsatile hydraulic power lost per ml mean arterial flow, was found to be flow dependent both in control and stimulated conditions: W_p/CO was positively correlated to CO in control condition and weakly negatively correlated to CO during stimulation. At high CO the arterial vessels could he stimulated and stiffened without much extra load on the right heart.     

Cardiovascular indices of peripheral and central sympathetic activation

OBJECTIVE: A number of sympathetic nervous system (SNS) parameters have been used in cardiovascular psychophysiology. This study aimed to describe the pattern and redundancy of a set of SNS parameters during peripherally induced changes of cardiac sympathetic activation and reflex modulation of central SNS control. Preejection period (PEP) was assessed as a marker of peripheral sympathetic activation. Low-frequency blood pressure variability (BPV) was assessed as an estimate of central SNS control. METHODS: Peripheral beta-sympathetic stimulation and blockade were achieved with epinephrine and esmolol hydrochloride (beta1-blockade), respectively. Changes in central SNS output were induced by loading and unloading arterial baroreceptors with norepinephrine and nitroprusside sodium, respectively. This single-blinded, crossover study in 24 healthy men also included two placebo control periods. PEP was derived from impedance cardiography and adjusted individually for heart rate. BPV was calculated by power spectral analyses of beat-to-beat heart rate and systolic blood pressure (Finapres system) data. RESULTS: PEP decreased during epinephrine infusion (-40.1 +/- 3.8 ms, p <.0001) and increased during esmolol infusion (+6.6 +/- 3.5 ms, p =.05). PEP was shortened after central SNS activation by nitroprusside (-16.8 +/- 2.9 ms, p < 0.0001). Systolic BPV in the low-frequency range (0.07-0.14 Hz, Mayer waves) increased during nitroprusside infusion (+0.44 +/- 0.19 ln mm Hg(2), p =.03) and decreased during norepinephrine infusion (-0.67 +/- 0.13 ln mm Hg(2), p < 0.0001). Low-frequency BPV did not change significantly during epinephrine or esmolol infusion. CONCLUSIONS: Our data provide empirical evidence of separable peripheral and central sympathetic response components. The combined report of low-frequency BPV and PEP gives distinct information on both central SNS control and the level of sympathetic cardiac activation achieved.     

Circulatory effects of noise

Thirteen patients with mild essential hypertension, mean age 44 years (range 21-59), were studied during "stress" before and after postsynaptic alpha-adrenoceptor blockade and combined postsynaptic alpha- and non-selective beta-adrenoceptor blockade. Loud broad band noise (100 dBA for 10 min) was used as the stress stimulus. Exposure to noise caused a significant increase in systolic (7%, p less than 0.05), diastolic (9%, p less than 0.01) and mean arterial pressure (6%, p less than 0.01). The blood pressure elevation was caused by an increase in total peripheral resistance (12%, p less than 0.05). There was no significant change in heart rate, stroke volume or cardiac output. The blood pressure response during noise stimulation was not affected by postsynaptic alpha-adrenoceptor blockade (prazosin, 2 mg orally). The hemodynamic reaction pattern, however, was totally reversed. Thus, the cardiac output increased significantly (9%, p less than 0.05), while the total peripheral resistance tended to decrease. Combined postsynaptic alpha- and non-selective beta-adrenoceptor blockade (labetalol, 200 mg orally) inhibited the increase in systolic blood pressure caused by noise, while the diastolic and mean arterial pressures still increased significantly (5%, p less than 0.01). Labetalol effectively blocked the stress-induced increase in total peripheral resistance and there was no significant increase in cardiac output after combined alpha- and beta-adrenoceptor blockade. Exposure to noise caused a significant increase in circulating noradrenaline (20%, p less than 0.05). Plasma adrenaline and plasma renin activity were not affected by noise stimulation. These results suggest that blood pressure elevation is essential during "stress" but that the hemodynamic pattern causing blood pressure elevation may vary and may be affected by pharmacological blockade of various parts of the sympathetic nervous system.