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PubMed2005

A population-based study of arterial stiffness index in relation to cardiovascular risk factors.

We investigated the relation of arterial stiffness, considered an independent predictor of cardiovascular events, to cardiovascular risk factors in a population-based study of 1023 subjects. An Arterial Stiffness Index (ASI) was developed to evaluate arterial stiffness based on an analysis of the pulse wave amplitude pattern acquired from measurements of brachial blood pressure. In control subjects (n = 266) without any major risk factors, the ASI was 46 +/- 11, and increased with age (r = 0.346). The ASI was significantly higher in women ranging from 50 to 54 years of age than in age-matched men. The ASI rose in correlation with the number of risk factors. Subjects with two risk factors showed a significantly higher ASI than those without any risk factors (54 +/- 26 vs. 46 +/- 11). The ASI was significantly increased in diabetic subjects with hypertension in comparison to those without hypertension. Furthermore, hyperlipidemic subjects with hypertension showed significantly higher values than those without hypertension. ASI could be a useful predictor of cardiovascular events in hypertensive subjects with multiple risk factors.

Adult↗
PubMed1999

[Physiology of coronary circulation and angioplasty: utopia or clinical reality?].

Small pressure transducer and Doppler quartz placed at the tip of angioplasty guide wire give the opportunity to measure coronary flow physiology parameters, the physiopathologic impact of an epicardic coronary stenosis and the efficacy of its treatment. This gives the opportunity to over ride the coronary imaging limitations. Doppler and pressure investigate a different and complementary aspect of the pressure-flow relation and may be used together in some special cases. Myocardial fractional flow reserve (FFRmyo) and relative coronary reserve concepts allow to evaluate patients with heterogeneous coronary reserve. Clinical application field is very broad and can be applied to each step of coronary angioplasty from the evaluation of intermediate lesions and the indication of angioplasty to the guidance of the procedure to the evaluation of the result, through the stenting indication and the stent placement optimization. Numerous studies has emphasized the role of physiologic coronary assessment in the cathlab. The time and economic gain of such an attitude has to be confirmed by future trials but it is clear now that it is not possible to continue to take decision on the sol visual aspect of a lesion.

Angioplasty, Balloon, Coronary↗
PubMed2000

[Dependence of constrictor and dilator humoral responses of arteries and veins in the small intestine on calcium ions entering vascular myocytes].

Verapamyl administered to the intestine circulation in the dose evoking no shifts in the arterial and venous resistance or in the vascular capacity, decreased 2- or 3-fold both the constrictor and dilatory responses of the arterial vessels. Against the background of Verapamyl, noradrenaline and isoproterenol did not practically change either capacity or resistance in the veins. Responses of veins to angiotensin II increased 10-fold and more, whereas they were absent after administration of atropine into the intestine circulation. Constrictor and dilatory responses of veins need to a greater extent than the arteries penetration of external calcium ions to their myocytes.

Animals↗
PubMed2001

[Comparison of two indices of arterial distensibility: temporal apparitions of Korotkoff sounds and pulse wave velocy. A Doppler echocardiography and ambulatory blood pressure monitoring study].

Arterial distensibility, one of the factors influencing afterload, plays a role in the development of left ventricular hypertrophy. The QKd, the delay before the perception of the Korotkoff sounds, is an index of arterial distensibility available from ambulatory blood pressure monitoring. The pulse wave velocity (PWV), another index of arterial distensibility, can be measured by Doppler echocardiography. The aim of this study was to compare these two indices with haemodynamic parameters of arterial distensibility and to determine their relationship to left ventricular geometry and function. Sixty-two consecutive patients, with and without cardiac disease, underwent simultaneous Doppler echocardiography and ambulatory blood pressure monitoring. A correlation was observed between QKd and PWV (N = 53, p = 0.007, r = 0.37). The QKd and PWV were correlated to the absolute index of arterial distensibility (systolic index/pulse pressure) (N = 51, p < 0.001, r = 0.48). QKd was correlated with indices of left ventricular function such as EF (N = 55, p < 0.001, r = 0.66) or the systolic pressure/end systolic dimension ratio (N = 54, p < 0.001, r = 0.75). When the ejection time was subtracted from QKd, only the end systolic pressure/end systolic dimension remained significantly correlated (N = 37, p = 0.005, r = 0.40). The authors conclude that PWV and QKd were correlated and were also correlated with indices of arterial distensibility. QKd is a composite index of left ventricular function and arterial distensibility. Doppler echocardiography and ambulatory blood pressure monitoring provide a non-invasive assessment of the aorta/LV couple.

Aged↗
PubMed2001

[Autoregulation of coronary vessels following the acute blood loss and its combination with preexisting immobilization stress].

A 6-hour immobilization stress and a 2-hour posthaemorrhagic hypotension caused elevation of the coronary flow, deterioration of coronary autoregulation, decreasing of the coronary dilation reserve, and diminishing of the left ventricular pressure. In the "stress + haemorrhage" group, the changes of the coronary vessels autoregulation ability were less obvious. Concentration of NO3-/NO2- in the blood serum was elevated after stress. Inhibition of the NO-synthase decreased the coronary flow. Thereupon, a pre-existing immobilization stress alters the coronary vessels tone.

Animals↗
PubMedDate not supplied

The influence of dialytic modality on arterial stiffness, pulse wave reflections, and vasomotor function.

BACKGROUND: Measurements of aortic stiffness [aortic pulse wave velocity (PWV) and augmentation index (Alx)] have been established as powerful predictors of survival on hemodialysis (HD). Abnormal endothelial-dependent and endothelial-independent vascular reactivity and increased arterial stiffness are commonly described in HD patients. There is, however, a lack of information on the comparative impact of different renal replacement therapies (RRTs) on PWV and Alx, and how these different methods might influence endothelial-dependent abnormal vasodilatation. OBJECTIVE: To describe in a cross-sectional design arterial compliance and distensibility in continuous ambulatory peritoneal dialysis (CAPD) versus HD versus renal transplant (RTx) patients, compared with age- and blood pressure-matched essential hypertensive controls. The PWV and aortic Alx were determined from contour analysis of arterial waveforms recorded by applanation tonometry in 40 CAPD, 41 HD, 20 RTx patients (with normal serum creatinine), and 20 controls with essential hypertension (all normotensive under treatment). Endothelial-dependent and endothelial-independent vascular reactivities were assessed by changes in Alx following challenges with inhaled salbutamol and sublingual nitroglycerin respectively. RESULTS: CAPD patients had significantly stiffer arteries than all other categories. The PWV was 8.29 +/- 1.09 m/ second in CAPD patients, significantly higher (p < 0.05) compared to HD subjects (7.19 +/- 1.87 m/s). Both dialysis subgroups had significantly higher PWV values compared to RTx patients (6.59 +/- 1.62 m/s) and essential hypertensive controls (6.34 +/- 1.32 m/s), p < 0.05. The Alx had a profile similar to PWV in different RRTs. All groups with the exception of CAPD subjects had a significant decrease in Alx following salbutamol. Moreover, the vasodilatation induced by either nitroglycerin or salbutamol was significantly blunted compared to HD. Overall, both dialysis categories had more abnormal responses compared to RTx patients and essential hypertensive controls. CONCLUSION: CAPD is associated with stiffer arteries and more profoundly abnormal endothelial-dependent vasomotor function, compared to matched HD subjects. These differences in arterial physical properties might explain differences seen in cardiac structure and function between the RRTs.

Adult↗
PubMed2004

Perioperative influences on fluid distribution.

Surgery triggers neuroendocrine, metabolic, and immunologic responses, with considerable effects on normal fluid distribution. Of clinical significance to the nurse is the distribution of fluids from the vascular space during the immediate postoperative period, and their return to the circulation approximately 48 to 72 hours later. Understanding the physiological and clinical significance of fluid shifts during the perioperative period allows the nurse to provide effective patient care.

Adaptation, Physiological↗
PubMed1995

[The dependence of ortho- and antiorthostatic hemodynamic reactions on the initial (controllable) tonus of the arterial vessels in rats].

Ortho- and antiorthostatic responses of the hemodynamics were compared by numerous parameters in anesthetised rats. In particular, in antiorthostatism the decrease of diastolic pressure as well as systolic one was greater at a lower initial arterial pressure. The data obtained suggest that, in orthostasis, the constrictor vascular compensatory responses are mainly revealed at a high initial arterial pressure. This mechanism of the compensation is less obvious in antiorthostatism.

Angiotensin II↗
PubMed1996

Vascular hyporesponsiveness in aorta from portal hypertensive rats: possible sites of involvement.

Vascular hyporesponsiveness in portal hypertension has been proposed to be due to postreceptor defect. The present study was aimed to investigate possible sites of involvement in such hyporesponsiveness. Portal hypertension was induced by partial portal vein ligation (PVL). Concentration-response curves to KCI and phenylephrine in both groups showed that the Emax values were significantly lower in the PVL group. The EC50 values were not different between the two groups. In Ca++ free condition, phenylephrine induced a phasic contraction, which was significantly smaller in the aorta from PVL rats. Cumulative readdition of CaCl2 (1.0-2.5 mM) induced tension increases, which were all significantly lower in the PVL group. Basal contents of [3H]inositol phosphates in the aorta were similar between the two groups. Phenylephrine induced concentration-dependent increase of [3H]inositol phosphates in the aorta from both groups. The responses at 10(-8), 10(-7), 10(-6) and 10(-5) M were significantly smaller in the PVL group than in the sham-operated group. Both okadaic acid and phorbol 12,13-dibutyrate induced slowly developing contractile responses in the aorta. The responses were similar between the two groups at all time points. Our results suggested that in the aorta from PVL rats, vascular hyporesponsiveness was observed, together with decreased contractile responses due to: voltage- and receptor-dependent calcium influx as well as intracellular calcium release, and decreased receptor-coupled inositol phosphate formation. Contractile responses due to activation of protein kinase C or phosphatase inhibition were not impaired.

Animals↗
PubMedDate not supplied

[Changes in venous tonus in rats with heart failure during acute and chronic perindopril administration].

The effect of chronic administration of perindopril (given per os daily for 21 days) and a single i.v. injection of perindoprilate (0.5 mg/kg) on the mean circulatory filling pressure (MCFP), mean arterial pressure (MAP), and heart rate (HR) was evaluated in conscious rats with heart failure caused by embolization of the coronary vessels with microspheres 21 days prior to the experiment. In the group of rats with cardiac failure perindoprilate reduced MAP by 10% and MCFP by 15%, but did not change AP and MCFP in animals which had been subjected to a sham-operation. Perindopryl reduced AP by 41% and MCFP by 20% in rats with heart failure, and by 37% and 13%, respectively, in rats which had undergone a sham-operation. It is concluded that the venous vessels in rats with heart failure possess increased sensitivity to perindopril.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1997

Non-invasive assessment of systemic elastic behaviour in hypertensive patients: analysis of possible determinants.

Knowledge about the viscoelastic behaviour of the arterial wall has been proved to have physiological importance and clinical usage. Our purpose was to study the changes of the systemic arterial wall's elastic properties non-invasively, in patients with established essential and with borderline hypertension, and to evaluate its possible determinants. Three groups of normotensive, borderline and established essential hypertensive patients were evaluated. Arterial pulse wave velocity (PWV) was measured and arterial compliance (Cm) was derived in all patients. Pulse wave velocity was obtained from the pressure values of digitized carotid and radial arteries. Arterial compliance (Cm = dD/dP with P pressure and D diameter) was calculated using a formula derived from the Bramwell and Hill equation: Cm = (1,334 x D)/(2 rho x PWV2), where for D humeral diameter was used as measured by high resolution echograph, and rho is the blood density (rho = 1.06). Pulse wave velocity was significantly higher in established essential hypertensive patients with respect to normotensive patients (p < 0.05). Arterial compliance was significantly diminished in established and in borderline hypertensive patients with respect to normotensive patients (p < 0.05), which implies early alterations in hypertensive cardiovascular disease. Multiple regression analysis of the cofactors showed that age and diastolic pressure are independent determinants of Cm. Impairment of the arterial wall's intrinsic elastic properties was demonstrated in established essential hypertension, independent of age and diastolic pressure.

Adolescent↗
PubMedDate not supplied

Influence of prior exercise on stroke volume to pulse pressure ratio in young subjects with hypertension or dilated cardiomyopathy.

The objectives of this study were, first, to compare stroke volume to brachial artery pulse pressure ratios (SV/PP) as noninvasive, indirect estimates of total arterial compliance, in young subjects with primary hypertension or dilated cardiomyopathy and age-matched normal subjects and, second, to determine the influence of prior submaximal exercise on this ratio, and on calf and total peripheral vascular conductance in these subjects. We studied young patients (< 40 years old) with primary hypertension (n = 12) or dilated cardiomyopathy (n = 12) and healthy normotensive subjects (n = 12) matched for age and body size. Doppler estimated stroke volume, brachial artery pulse pressure, and calf blood flow were determined during supine rest before and 60 min after exercise. Normotensive and hypertensive subjects returned 1 month later to determine the reproducibility of the SV/PP value. At rest, the SV/PP value was inversely related to left ventricular mass index (r = -0.55, p < 0.001) and was similar in normotensive and hypertensive subjects, but was significantly lower (p < 0.05) in cardiomyopathy. The SV/PP value was reduced 60 min after exercise in both normotensive (p < 0.05) and hypertensive (p < 0.05) subjects, but not in cardiomyopathy patients. In contrast, total and calf vascular conductance increased after exercise in all three groups. These aftereffects indicate that these estimates of compliance and conductance are dynamic, and can be modulated acutely and independently by exercise.

Adult↗
PubMed1998

Microcirculation in lower limbs during laparoscopic cholecystectomy.

To study the influence of venous hypertension, which develops in lower limbs under pneumoperitoneal pressure, on microcirculation, plethysmographic measurements were performed in patients before and during laparoscopic and traditional (open) cholecystectomy. During laparoscopy, isovolumetric venous pressure (estimate of capillary pressure), and filtration coefficient (estimate of patent capillary surface) decreased, which was not the case during open surgery. These results indicates that venous hypertension during laparoscopic surgery does not extend to the microcirculation; vasoconstriction is a result of protective mechanisms, which disable excessive fluid filtration in microcirculation. Parameters of macrocirculation (ambient venous pressure, compliance of calf tissue) changed intraoperatively in both groups similarly, irrespectively of the surgical technique.

Blood Pressure↗
PubMed2000

Ryanodine receptor and capacitative Ca2+ entry in fresh preglomerular vascular smooth muscle cells.

BACKGROUND: A multiplicity of hormonal, neural, and paracrine factors regulates preglomerular arterial tone by stimulating calcium entry or mobilization. We have previously provided evidence for capacitative (store-operated) Ca2+ entry in fresh renal vascular smooth muscle cells (VSMCs). Ryanodine-sensitive receptors (RyRs) have recently been identified in a variety of nonrenal vascular beds. METHODS: We isolated fresh rat preglomerular VSMCs with a magnetized microsphere/sieving technique; cytosolic Ca2+ ([Ca2+]i) was measured with fura-2 ratiometric fluorescence. RESULTS: Ryanodine (3 micromol/L) increased [Ca2+]i from 79 to 138 nmol/L (P = 0.01). Nifedipine (Nif), given before or after ryanodine, was without effect. The addition of calcium (1 mmol/L) to VSMCs in calcium-free buffer did not alter resting [Ca2+]i. In Ca-free buffer containing Nif, [Ca2+]i rose from 61 to 88 nmol/L after the addition of the Ca2+-ATPase inhibitor cyclopiazonic acid and to 159 nmol/L after the addition of Ca2+ (1 mmol/L). Mn2+ quenched the Ca/fura signal, confirming divalent cation entry. In Ca-free buffer with Nif, [Ca2+]i increased from 80 to 94 nmol/L with the addition of ryanodine and further to 166 nmol/L after the addition of Ca2+ (1 mmol/L). Mn2+ quenching was again shown. Thus, emptying of the sarcoplasmic reticulum (SR) with ryanodine stimulated capacitative Ca2+ entry. CONCLUSION: Preglomerular VSMCs have functional RyR, and a capacitative (store-operated) entry mechanism is activated by the depletion of SR Ca2+ with ryanodine, as is the case with inhibitors of SR Ca2+-ATPase.

Animals↗
PubMed2005

Evidence for capacitative and non-capacitative Ca2+ entry pathways coexist in A10 vascular smooth muscle cells.

It is generally thought that receptor-operated Ca2+ entry is related to store-operated or capacitative Ca2+ entry mechanism. Recent evidence suggests that non-capacitative Ca2+ entry pathways are also involved in receptor activated Ca2+ influx in many different kinds of cells. In this study, we studied whether alpha1-adrenoreceptor (alpha1-AR)-activated Ca2+ entry is coupled to both capacitative and non-capacitative pathways in A10 vascular smooth muscle cells by fura-2 fluorescence probe and conventional whole-cell patch clamp techniques. We found that both thapsigargin (TG) and phenylephrine (Phe) induced transient increase in cytoplasmic Ca2+ concentration ([Ca2+]i) in Ca2+-free medium, and subsequent addition of Ca2+ evoked a sustained [Ca2+]i rise. When the membrane potential was held at -60 mV, both TG and Phe activated inward currents, which were inhibited by GdCl3(Gd3+), 0Na+/0Ca2+ solution and 1-{beta[3-(4-mehtoxyphenyl)propoxy]-4-methoxypheneth-yl}-1H- imidazole hydro-chloride (SK&F96365), but not by nifedipine. When Ca2+ store was depleted by TG in Ca2+-free solution, Phe failed to further evoke [Ca2+]i rise. However, when capacitative Ca2+ entry was activated by TG in the medium containing Ca2+, 10 microM Phe further increased [Ca2+]i. At the same concentration, TG activated an inward cation current, subsequent addition of Phe also further induced an inward cation current. Furthermore, the amplitudes of [Ca2+]i increase and current density induced by Phe in the presence of TG were less than that induced by Phe alone. Our results suggest that both capacitative and non-capacitative Ca2+ entry pathways are involved in Ca2+ influx induced by activation of alpha1-AR in A10 vascular smooth muscle cells.

Adrenergic alpha-Agonists↗
PubMed1998

Effects of volatile anesthetic agents on in situ vascular smooth muscle transmembrane potential in resistance- and capacitance-regulating blood vessels.

INTRODUCTION: This study was designed to compare the inhibitory effect of inhaled volatile anesthetic agents on in situ sympathetic neural versus nonneural regulation of vascular smooth muscle transmembrane potentials as correlates of vascular smooth muscle tone in resistance- and capacitance-regulating blood vessels. METHODS: Vascular smooth muscle transmembrane potentials were measured in situ with glass microelectrodes in neurally intact, small (200-300 m OD) mesenteric arteries and veins of rats before, during, and after inhaled halothane, isoflurane, or sevoflurane (0.5 or 1.0 minimum alveolar concentration [MAC]). Such transmembrane potentials and their anesthetically induced changes were compared, respectively, with those measured in similar vessel preparations after local sympathetic neural denervation with 6-hydroxydopamine. RESULTS: In neurally intact vessels, transmembrane potentials (in millivolts, mean +/- SD) before inhalation of the anesthetic agent were -39 +/- 2.8 (artery) and -43 +/- 4.6 (vein). At 1.0 MAC, halothane, isoflurane, and sevoflurane induced respective hyperpolarizations (in millivolts, mean +/- SD) of 9 +/- 3.1, 6 +/- 2.7, and 9 +/- 4.0 in arteries and 6 +/- 4.4, 2.8 +/- 3.0, and 8.7 +/- 5.6 in veins. Sympathetic denervation significantly attenuated these hyperpolarizations (except for venous response to isoflurane). At 0.5 MAC, transmembrane potential responses to all three volatile anesthetic agents were small and not consistently significant in either the intact or denervated vessels. CONCLUSIONS: In resistance-regulating arteries in situ, inhaled halothane, isoflurane, and sevoflurane (1.0 MAC) attenuate both sympathetic neural and nonneural regulation of vascular smooth muscle transmembrane potentials (and tone). In capacitance-regulating veins in situ, sevoflurane (1.0 MAC) also attenuates both regulatory mechanisms, whereas halothane and isoflurane primarily attenuate nonneural mechanisms. At 0.5 MAC, none of these agents significantly affected either mode of regulation of vascular smooth muscle transmembrane potentials in arteries or veins.

Administration, Inhalation↗