Distensibility Of Large Arteries Research Articles

Pulmonary perfusion measured by means of electrical impedance tomography

Electrical impedance tomography (EIT) is a recent imaging technique based on electrical impedance, offering the possibility of measuring pulmonary perfusion. In the present study the influence of several pulmonary haemodynamical parameters on the EIT signal were investigated. First, the influence on the systolic wave of the EIT signal of stroke volume, large pulmonary artery distensibility (both assessed by means of MRI) and the extent of the pulmonary peripheral vascular bed in 11 emphysematous patients (reduced peripheral vascular bed) and 9 controls (normal peripheral vascular bed) was investigated. Second, the influence of hypoxic pulmonary vasoconstriction on was examined in 14 healthy subjects. Finally, the origin of the diastolic wave was examined in three patients with atrioventricular dissociation. Multiple regression analysis showed that was only dependent on the variable emphysema (p < 0.02), but not dependent on stroke volume (p > 0.3) or pulmonary artery distensibility (p > 0.9). The mean value of for emphysematous patients ( arbitrary units (AU)) was significantly lower (p < 0.001) than in the control group . In the group of healthy subjects decreased significantly (p < 0.001) during hypoxia compared with rest measurements . The absence of the diastolic wave in the cardiological patients suggests the influence of reverse venous blood flow on the EIT signal. It is concluded that volume changes in the small pulmonary vessels contribute significantly to the EIT signal. Moreover, the hypoxia induced decrease in indicates the potential of EIT for measuring pulmonary vascular responses to external stimuli. Keywords: pulmonary perfusion, emphysema, hypoxia, electrical impedance tomography

Effect of sympathectomy on mechanical properties of common carotid and femoral arteries.

Sympathetic stimulation is accompanied by a reduction of arterial distensibility, but whether and to what extent elastic and muscle-type arterial mechanics is under tonic sympathetic restraint is not known. We addressed this issue by measuring, in the anesthetized rat, the diameters of the common carotid and femoral arteries with an echo-Doppler device (NIUS 01). Blood pressure was measured by a catheter inserted contralaterally and symmetrically to the vessel where the diameter was measured. Arterial distensibility over the systolic-diastolic pressure range was calculated according to the Langewouters formula. Data were collected in 10 intact (vehicle pretreatment) and 9 sympathectomized (6-hydroxydopamine pretreatment) 3-month-old Wistar-Kyoto rats. Compared with the intact animals, sympathectomized rats showed a marked increase in arterial distensibility over the entire systolic-diastolic pressure range. When quantified by the area under the distensibility-pressure curve, the increase was 59% and 62% for the common carotid and femoral arteries, respectively (P<.01 for both). In the femoral but not in the common carotid artery, sympathectomy was accompanied also by an increase in arterial diameter (+18%, P<.05 versus intact). Therefore, in the anesthetized normotensive rat, sympathetic activity exerts a tonic restraint on large-artery distensibility. This restraint is pronounced in elastic vessels and even more pronounced in muscle-type vessels.

Alteration of arterial distensibility in systemic sclerosis.

To evaluate the distensibility of large arteries in patients with systemic sclerosis (SSc). Prospective case-control study including unselected patients with SSc. One cardiology and two internal medicine units in a teaching hospital. Eighteen patients with SSc and controls matched for age, sex, height, weight and 24-h ambulatory blood pressure (BP). The timing of Korotkoff's sounds (QKD interval), a newly described noninvasive ambulatory method was used to measure arterial distensibility during 24 h. Two endpoints were used: QKD 100-60 (normalized for a heart rate of 100 beats min-1 and a systolic BP of 100 mmHg) and the slope of QKD against pulse pressure. The patients with SSc had a lower slope of QKD against pulse pressure than the controls (median 0.55, range 0-1.21, versus 0.92, range 0.5-1.34, respectively; P = 0.003), and a lower QKD 100-60 (medians/ranges respectively 191 [162-216] and 203 [169-231]: P = 0.01). These results indicate that arterial distensibility of large arteries is decreased in SSc.

Age-related differences in elastic properties of the upper arm vascular bed in healthy adults.

The significance of age-related changes in arterial stiffness has remained largely uncertain in healthy subjects. This appears to be partly due to difficulties in the interpretation of methods for measuring arterial stiffness in vivo. Therefore, a recently developed electrical bioimpedance method was used for studying elastic properties of a vascular bed as a function of age. In 66 healthy subjects, aged 22-82 years, we investigated the vascular bed of an upper arm segment. This vascular bed showed an age-related decrease in the venous blood volume (r = -0.31, p < 0.01) and in the distensibility, the inverse of stiffness, of the larger arteries (r = -0.38, p < 0.001). The distensibility of the arterial bed as a whole at normotensive blood pressure, however, appeared to increase with age (r = 0.32, p < 0.005). The arterial and venous blood volumes, arterial compliance and extravascular fluid volume were significantly higher in the males than in the females. Practically all investigated vascular properties appeared to be related with height, body mass or body mass index. We concluded that comparative studies concerning vascular properties should preferably be performed in subjects matched as to age, gender, height and body mass. In healthy subjects the smaller arteries adjust to the age-related decrease in large artery distensibility by means of an age-related increase in distensibility. These age-related changes in arterial distensibility are caused by changes in the females, and seem to be associated with age-related changes in body mass index rather than with aging per se.

Disparate effects of antihypertensive drugs on large artery distensibility and compliance in hypertension

Distensibility and compliance are large artery properties, that may be important in cardiovascular disease. Distensibility is a determinant of the pulsatile stress on the vessel wall and is thought important in ageing and atherosclerotic disease. Compliance reflects the buffering capacity of the arteries and is a major determinant of the afterload on the heart. In hypertension large arteries are getting stiffer, resulting in a decreased distensibility and compliance. Decrease in blood pressure by itself can improve large artery properties. Despite a decrease in blood pressure, not all antihypertensive drugs improve large artery properties. Compliance is improved by firstline antihypertensive drugs such as angiotensin-converting enzyme (ACE) inhibitors, calcium antagonists, beta-blockers with vasodilating properties, selective beta 1-blockers and some diuretics. Recent data suggest that ACE inhibitors such as perindopril improve distensibility and compliance of large arteries more than diuretics such as amiloride/hydrochlorothiazide. Apart from the indirect effect (decrease in blood pressure), this makes a direct effect of perindopril on large artery properties very likely. ACE inhibitors such as perindopril decrease the afterload on the heart more than diuretics such as amiloride/hydrochlorothiazide by both a more pronounced decrease in systemic vascular resistance and an increase in large artery compliance.

Disparate effects of antihypertensive drugs on large artery distensibility and compliance in hypertension

Disparate effects of antihypertensive drugs on large artery distensibility and compliance in hypertension

Hemodynamic Comparison of Dopexamine and Nitroprusside at High and Low Doses in Patients with Coronary Artery Disease and Impaired Left Ventricular Function

Pure vasodilator drugs are currently the preferred agents for treatment of acute and chronic heart failure of all grades of severity. In contrast, the role of drugs that combine vasodilation with inotropic action remains highly controversial despite their several advantageous physiological actions and long therapeutic history in heart failure. We hypothesize that this uncertainty might be due first to subtle unfavorable hemodynamic effects not detectable by the relatively crude hemodynamic methods by which these agents are usually analyzed, particularly with regard to the quantification of afterload, and secondly to the narrow therapeutic range of these drugs, such that the dose administered is critical. We tested this hypothesis by comparing several refined hemodynamic measurements of dopexamine, an inotropic vasodilator, with a pure arteriovenous dilator (sodium nitroprusside, SNP) on left ventricular (LV) systolic and diastolic function, large arterial behavior, and coupling of the left ventricle to the arterial system at two dose levels in 35 patients with ischemic heart disease. The study protocol was a fixed order of 15-min infusions of saline, dopexamine 1 microg/kg/min, and dopexamine 3 + ++microg/kg/min, or saline, SNP 1 microg/kg/min, and SNP 3 microg/kg/min. Detailed hemodynamic observations were made at the end of each 15-min infusion period. Both drugs produced equivalent arterial vasodilation, as measured by the decrease in systemic vascular resistance index (SVRI), but dopexamine resulted in a significantly greater increase in cardiac index (CI). Myocardial contractility, assessed by several load-independent indexes, increased with dopexamine, as anticipated with an inotropic drug, but did not alter with SNP. Arterial compliance, a measure of the distensibility of large conduit arteries, was increased by SNP but not by dopexamine. Arterial wave reflection was increased by dopexamine, especially at high doses, but reduced by SNP. Increased arterial compliance and reduced wave reflection reduce LV afterload. SNP reduced preload, whereas dopexamine had no effect on this aspect of ventricular function. Vasodilator drugs and those which combine vasodilator and inotropy increase cardiac output (CO) and reduce SVR. Therapy with inotropic vasodilators has no effect on preload and does not reduce the dynamic components of ventricular afterload, although it does reduce its static components. These effects are dose dependent; there is less perturbation of afterload at lower doses. In contrast, vasodilator therapy reduces preload and both static and dynamic parts of afterload.

Effects of antihypertensive agents on local arterial distensibility and compliance.

Distensibility and compliance are important vessel wall properties. Distensibility is related to elastic properties of the arterial wall, and compliance reflects the buffering function of the artery. Distensibility is a determinant of stress on the vessel wall. A decreased distensibility might increase the risk of arterial wall damage. Therefore, a preserved local distensibility might be important in protecting the arterial wall of each particular artery and especially of those arteries that are more susceptible to vascular disease. Local distensibility and compliance of various large arteries can be measured noninvasively with echo tracking techniques. Studies on local distensibility and compliance revealed that with the calcium antagonist verapamil and the angiotensin-converting enzyme inhibitor perindopril arterial compliance increased mainly because of an increase in distensibility, with only a minor effect on arterial diameter. In contrast, the nitrate compound isosorbide dinitrate increased compliance mainly by increasing arterial diameter, without an increase in distensibility. This indicates that an increase in arterial compliance does not automatically imply an increase in arterial distensibility. The effect of antihypertensive drugs may also depend on the vascular territory. The diuretic amiloride/hydrochlorothiazide increased brachial artery compliance but not common carotid artery compliance. During angiotensin-converting enzyme inhibition the effect on arterial compliance was smaller at the carotid than the femoral artery. However, the opposite held for the nitrate compound. These distinctive effects of antihypertensive drugs on arterial distensibility and compliance and on vascular territories may be relevant to pharmacological prevention and management of arterial disease.

Short and long-term effects of smoking on arterial wall properties in habitual smokers

Objectives. This study investigated the short-term effects of smoking on hemodynamic function and distensibility function and compliance of large arteries in habitual smokers. In addition, the effect of smoking was not measured in nonsmokers, but vessel wall properties were compared between smokers and nonsmokers(basal state).Background. Smoking is a well known risk factor for atherosclerosis. Loss of distensibility and compliance of large arteries may play a role in the onset of atherosclerosis.Methods. The distensibility and compliance coefficients of the common cartoid and brachial arteries were determined from the arterial wall displacement during systole and the end-diastolic diameter by using a vessel wall defector and from the pulse pressure as assessed in the upper arm. Cardiac function (cardiac output, stroke volume) was measured with Doppler echocardiography. Systemic vascular resistance was calculated as mean arterial pressure divided by cardiac output.Results. In habitual smokers, smoking one cigarette caused a sharp increase in blood pressure (6%) and heart rate (14%). Cardiac index increased (16%), mainly because of the marked increase in heart rate. Stroke and systemic vascular resistance indexes did not change significantly. Smoking enhanced forearm blood flow after wrist occlusion (17%), but total forearm blood low was unchanged, suggesting an increase in muscle blood flow and a decrease in skin flow. Because of higher blood pressure, the diameter of the elastic common carotid artery increased by 3% (passive phenomenon). Distensibility of the carotid artery decreased (7%), and as a result, carotid compliance was preserved. In contrast, despite blood pressure, the diameter of the muscular brachial artery did not change, suggesting an increased vascular tone. Brachial distensibility and compliance decreased (18% and 19%, respetively). Habitual smokers were comparable to nonsmokers with regard to blood pressure, cardiac function, vascular resistance and vessel wall properties of large arteries. Heart rate was higher in habitual smokers (14%).Conclusions. These data indicate that in habitual smokers, smoking one cigarette causes short-term increases in arterial wall stiffness that might be harmful to the artery and increase the risk for plaque rupture. Except for a higher heart rate, no obvious long-term effect of smoking was observed on hemodynamic variables and arterial stiffness. Because acute cardiovascular events are mainly due to plaque rupture, the short-term of smoking might be a more important risk than long-term for these acute ischemic events.

Endotheuum-Derived Relaxing Factor (Edrf) Increases Large Artery Distensibility in Normal Subjects (Introduced by Ah Henderson)

Endotheuum-Derived Relaxing Factor (Edrf) Increases Large Artery Distensibility in Normal Subjects (Introduced by Ah Henderson)

Arterial compliance and blood pressure.

As a result of the dual function of arteries, the conduit and cushioning functions, arterial pressure has 2 components: the steady component, characterised by mean blood pressure, and the pulsatile component, characterised by pulse pressure. Arterial compliance mostly depends on arterial intrinsic elastic properties, and is a determinant of the propagation speed of the pulse pressure wave. Decreased arterial compliance is responsible for both an increase in the incident pressure wave and the higher effect of reflected pressure waves. This increases systolic pressure and ventricular afterload, and generates left ventricular hypertrophy. Arterial structural changes that accompany the aging process result in a loss of distensibility and compliance. In essential as well as in secondary hypertension, arterial compliance is reduced, and age-related structural changes of the arterial wall are accelerated. Whether the change in arterial compliance is a passive consequence of the increase in blood pressure or is related to changes in the arterial wall structure remains unclear. Calcium antagonists improve the distensibility and compliance of large and small arteries, contributing significantly to the improvement in the management of essential and secondary hypertension.

Effects of diurnal variability and exercise training on properties of large arteries

To examine the diurnal variability in arterial distensibility and compliance and to study the effects of exercise training on these large artery properties. Vessel wall properties of the elastic common carotid and muscular brachial arteries were measured non-invasively with a vessel wall movement detector system in 12 healthy volunteers. Properties of the common carotid, the femoral and the brachial arteries were studied in 15 sedentary males in comparison with 15 male cyclists. Diurnal changes in the carotid and brachial arteries were similar. Blood pressure decreased at night while arterial diameter increased. Distensibility decreased and compliance was preserved at night. The vessel wall properties of the carotid artery did not differ between the sedentary males and the cyclists, but the femoral and brachial arteries were more elastic in the cyclists. The diameter of the femoral artery was larger in the cyclists. We found a diurnal pattern in changes in diameter and distensibility of elastic and muscular large arteries. Compliance, the buffering capacity of larger arteries, was preserved at night. The supplying femoral artery was larger and more distensible in cyclists. Exercise training did not affect the elastic carotid artery, but improved vessel wall properties of the brachial, and maybe also of other, muscular large arteries.

32 Isobaric comparison of large artery geometry and distensibility between hypertensive and diabetic subjects

s: Xth journees de I'Hypertension Arterielle Annual Scientific Meeting of the French Society of Hypertension,Section of the French Society of Cardiology Pairs, France: PDF Only

Almitrine Decreases the Distensibility of the Large Pulmonary Arteries in Man

Almitrine improves blood gas values in patients with COPD, primarily through better ventilation-perfusion matching. The improvement comes largely from a vasomotor effect of the drug. The vasomotor mechanism is unknown. We suspected that decreased distensibility of the large pulmonary arteries was one probable effect of the drug. If present, reduced distensibility would explain many of the hemodynamic alterations produced by almitrine. To test this idea, we measured the diameter of the right pulmonary artery during systole and diastole both before and after almitrine administration in nine patients who were undergoing pulmonary cineangiography. Our calculations of the distensibility of the right pulmonary artery showed that almitrine caused a 60 percent decrease. This significant alteration in the stiffness of the large pulmonary arteries can account for the rise in systolic pressure, a change that would be expected to redistribute pulmonary blood flow upwards and thereby improve ventilation-perfusion balance.

Modifications of the Arterial Mechanical Properties of Normotensive and Hypertensive Rats Without Arterial Pressure Changes

Possible reduction in arterial thickness may be an interesting way to reduce left ventricular afterload in various pathologic conditions. We tested the effects of cicletanine (3 mg/kg) on the systemic hemodynamics and the mechanical properties of the arterial walls in 12-week-old normotensive Wistar Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). The mechanical properties of the arterial walls were assessed using three independent methods: the characteristic impedance of the ascending aorta (Zc), systemic arterial compliance (SAC), and compliance of the carotid artery (CC). Zc and SAC were calculated from phasic records of pressure and flow in the ascending aorta; CC was measured in situ with or without smooth muscle cell activity [potassium cyanide (KCN) poisoning]. After chronic therapy by daily gavage for 15 days, there were no significant changes in either WKY and SRH in terms of arterial blood pressure (BP), cardiac output (CO), and heart rate (HR). In contrast, Zc, SAC, and passive distensibility of the isolated carotid arteries were significantly improved in treated groups. The increase in arterial distensibility reflected modifications in function (smooth muscle tone) of the arterial wall after cicletanine chronic therapy. Although the exact mechanisms of the observed changes in arterial mechanics remain unclear, this study showed that in experimental hypertension cicletanine can affect distensibility of large arteries independently of significant changes in BP.

Unrelated responses of brachial artery hemodynamics and renin-angiotensin system to acute converting enzyme inhibition by enalaprilat in essential hypertension

The simultaneous acute effects of converting enzyme inhibition by intravenous enalaprilat on the circulating renin-angiotensin system and on the brachial artery were studied in 12 hypertensive patients by a double-blind comparison with saline effects in 14 hypertensive patients. The brachial artery was investigated in terms of arterial section (measured by pulsed Doppler technique) and wall rigidity (assessed by pulse wave velocity). Arterial and biochemical parameters were measured in baseline before injection and at 20 to 40 minutes (t 1) and 80 to 100 minutes (t 2) after saline and drug injections. Compared with the saline vehicle, enalaprilat significantly decreased angiotensin enzyme converting activity (p < 0.001), increased plasma renin activity (p < 0.01) and decreased plasma aldosterone concentrations (p < 0.01). The drug reduced blood pressure (p < 0.01) and increased the brachial artery section (p < 0.01), but did not change pulse wave velocity. In the enalaprilat group, significant postinjection relations were observed between: (1) enalaprilat concentration and plasma angiotensin converting enzyme activity (r = −0.72, p < 0.001); (2) plasma renin activity and mean blood pressure (r = −0.46, p < 0.02); (3) plasma enalaprilat concentration and pulse wave velocity (r = −0.50, p < 0.01) and (4) pulse wave velocity and brachial artery section (r = 0.42, p < 0.05). Thus, the brachial artery effects of enalaprilat were not directly related to the blockade of the renin-angiotensin system in plasma. It follows that the negative correlation found between plasma enalaprilat concentration and brachial pulse wave velocity (effect of the drug on the distensibility of large arteries) might be due to factors other than the circulating renin-angiotensin system. The above effect was more potent at time 12 than at time t 1, suggesting that its carrier might be the inhibition of local renin-angiotensin converting enzymes inside the arterial walls.

Cardiac hypertrophy and arterial distensibility in essential hypertension

Echocardiographic determinations, left ventricular mass-volume ratio ( M V ), left ventricular end-systolic stress (ESS), carotidofemoral pulse wave velocity (PWV), and brachial artery compliance (BAC), deduced from pulsed Doppler measurements and from the Bramwell-Hill equation, were evaluated in 20 patients with sustained essential hypertension in comparison with 20 control subjects of the same age and sex. In hypertensive patients, M V ratio, ESS, and PWV were significantly increased while BAC was reduced. In the overall population, ESS was directly correlated with PWV ( r = 0.73), and M V ratio was significantly correlated with PWV ( r = 0.60), BAC ( r = −0.70), and systolic arterial pressure ( r = 0.71). No comparable results were observed with diastolic arterial pressure. PWV was unchanged after cadralazine, a dihydralazine-like substance, and was decreased with the same blood pressure reduction following nitrendipine, a new calcium-blocking agent. These results suggest that: (1) the distensibility of large arteries plays an important role in the maintenance of cardiac hypertrophy in hypertension, and (2) antihypertensive drugs may act differently on arterial distensibility with possible consequences on ESS and reversion of left ventricular hypertrophy.

Arterial Distensibility in Normal and Hypertensive Man

1. The pulse-wave velocity along the brachial radial artery was measured in 38 subjects and volume distensibility values were calculated. 2. Measurements made at each subject's resting blood pressure showed that those with high blood pressure had higher pulse-wave velocity values and hence less distensible arteries. 3. An acute rise in arterial distending pressure was accompanied by a rise in pulse-wave velocity. 4. When pulse-wave velocity was remeasured in all subjects at identical arterial distengin pressures, no difference was found between hypertensive and normal subjects. 5. It appears that poor distensibility of large arteries in hypertensive subjects is a consequence of the elevated distending pressures and not due to irreversible structural changes in the arterial wall.

Some effects of nitroglycerin upon the splanchinic, pulmonary, and systemic circulations.

Splanchnic, pulmonary, and systemic hemodynamics were studied in 18 patients after the sublingual administration of nitroglycerin. The drug, contrary to expectations, produced an over-all vasoconstrictive effect on the splanchnic circulation rather than vasodilatation. There was no evidence of venous pooling in this bed, and indeed the data may indicate a splanchnic supportive role in augmenting venous return to the heart with disengorgement of its own volume. In contrast, there was vasodilatation and pooling of blood in the pulmonary vascular bed. The systemic circulation probably sustains several effects by nitroglycerin, including arterial vasodilatation. A direct change in large artery distensibility probably explains the modest fall in systolic blood pressure seen. Further decline in arterial pressure may depend on venous pooling of a small or large degree. Probably the fall in systemic and specific organ flows is also linked to decreased venous return and the vascular readjustments provoked thereby. Pulsus alternans was produced by nitroglycerin, a previously unreported effect of the drug, but the mechanism by which it arose could not be defined.