Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Vascular Capacitance”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed1994

Altered pulmonary microvascular reactivity to norepinephrine in canine pacing-induced heart failure.

Pulmonary hypertension in congestive heart failure causes medial hypertrophy in pulmonary vessels and thickening of the endothelial basement membrane. In this study, the functional consequences of such pulmonary vascular adaptations were evaluated. Heart failure was induced in dogs by rapid ventricular pacing (240 beats per minute) for 28 days, at which time left ventricular shortening fraction was decreased by 57% compared with that at baseline. Lung lobes from paced (n = 56) and control dogs (n = 68) were isolated and perfused with autologous blood. Total, arterial (Ra), and venous (Rv) vascular resistances were significantly increased and vascular capacitance decreased in lobes from paced animals compared with controls. Increments in Ra and Rv after intra-arterial boluses of norepinephrine were measured before and after sequential addition of the alpha 1- and alpha 2-receptor antagonists prazosin (16 mumol/L) and yohimbine (0.1 mumol/L) in the presence or absence of propranolol (5 mumol/L). Norepinephrine (1 to 40 micrograms) had little effect on Ra in the absence of propranolol, a pattern that persisted in control lobes after propranolol. However, when lobes from paced animals were pretreated with propranolol, norepinephrine increased Ra, Rv was increased after norepinephrine in control lobes, an effect that was enhanced in the paced group. In both groups, the increment in Rv was greater after propranolol. Irrespective of propranolol pretreatment, prazosin significantly attenuated, if not abolished, the response to norepinephrine. The enhancement in venous vascular reactivity in lobes from paced animals remained when venous pressure was elevated to 20 cm H2O. In control lobes under conditions of elevated tone or when endothelium-dependent relaxing factor was blocked, responses to norepinephrine did not mimic those observed in the paced group. Microvascular permeability, as measured by the capillary filtration coefficient, was not altered in the paced group. We conclude that the pulmonary adaptations to 4 weeks of rapid ventricular pacing include functional changes in pulmonary hemodynamics and vascular reactivity but not in microvascular permeability.

Adrenergic beta-Antagonists↗
PubMed1994

Pressure-induced local venous constrictor responses in human fingers.

Particularly in humans, systemic veins are often exposed to extensive changes in transmural pressure at altered body positions, when centrally conveyed constrictor reflexes provide compensation to maintain a proper venous return. The present aim was to explore whether also purely local mechanisms, of e.g. myogenic and/or axon reflex nature and operating at the venular-small vein levels, may contribute to offset venous pooling at local pressure increases. For such purposes the capacitance vascular responses were recorded plethysmographically in human fingertips, as most of the blood content is here contained in venules and small veins. Local increases in transmural pressure, induced by graded venous outflow obstructions, first induced by a corresponding passive-venous distension which within a few seconds was followed by a venoconstrictor response that could return the local blood content to nearly control level within 25-35 s. On sudden release of venous obstruction this 'active' response was unmasked as a prompt volume 'undershoot' that subsided in another 15-30 s. These microvascular responses could be powerful enough almost to offset the venodistension caused by transmural pressures up to 90-100 mmHg, and at brisk pressure increases they could be quite rapid in onset. As general reflex influences seemed to be excluded. these results in humans suggest that also the capacitance microvessels, like the precapillary resistance ones, can display myogenic responses to offset pressure increases. As the venular-small vein compartment contains up to 40% of the total blood volume such local responses, if generalized, may importantly contribute to venous control in humans.

Adult↗
PubMed1992

Cardiovascular response in canine endotoxic shock: effect of ibuprofen pretreatment.

Ibuprofen pretreatment increases arterial pressure and reduces mortality in endotoxic dogs. The increase in arterial pressure may be caused by increases in arterial resistance, arterial sphincter tone, or both. Thus it is not clear if ibuprofen pretreatment prevents the hemodynamic effects of endotoxemia or merely masks such effects by producing concomitant increases in arterial resistance. Accordingly, this study was performed to determine the effects of ibuprofen pretreatment on arterial pressure-flow relations and other measures of cardiovascular function in a canine model of endotoxic shock. In 19 pentobarbital-anesthetized and splenectomized, closed-chest dogs, biventricular stroke volumes were measured with electromagnetic flow probes, and intrathoracic vascular and pleural pressures were measured with catheters. Instantaneous venous return curves (see Pinsky MR, J Appl Physiol 56:765, 1984) were generated during positive-pressure ventilation, and steady-state arterial pressure-flow relations, left ventricular function, peripheral vascular compliance, oxygen consumption/oxygen delivery ratio, and arterial blood lactate levels were measured during two sequential volume loading and removal (20 ml/kg) sequences. All but two dogs received a bolus infusion of Escherichia coli endotoxin (2 mg/kg) between the two fluid challenge runs. Eleven of the 17 endotoxic dogs also received ibuprofen (15 mg/kg) immediately before the initial fluid challenge. Ibuprofen pretreatment abolished all hemodynamic effects of endotoxin, whereas in the untreated group endotoxin caused decreases in calculated arterial outflow pressure and in peripheral vascular capacitance. Oxygen consumption remained constant despite changes in oxygen delivery in the nonendotoxic dogs and in the ibuprofen-pretreated dogs, whereas oxygen consumption covaried with oxygen delivery in the endotoxic dogs not pretreated with ibuprofen. Arterial lactate levels were higher after endotoxin infusion (2.1 +/- 0.5 to 3.1 +/- 0.6 mmol/liter; P less than 0.05 pre- to postvolume) but were not different between treatment groups. These data suggest that ibuprofen alters many, but not all, of the hemodynamic effects of endotoxin infusion in the dog.

Acidosis↗
PubMed2000

Effects of endothelin-1 and homologous trout endothelin on cardiovascular function in rainbow trout.

The cardiovascular effects of endothelin (ET)-1 and the recently sequenced homologous trout ET were examined in unanesthetized trout, and vascular capacitance curves were constructed to evaluate the responsiveness of the venous system to ET-1. A bolus dose of 667 pmol/kg ET-1 doubled ventral aortic pressure; produced a triphasic pressor-depressor-pressor response in dorsal aortic pressure (P(DA)); increased central venous pressure, gill resistance, and systemic resistance; and decreased cardiac output, heart rate, and stroke volume. These responses were dose dependent. Bolus injection of trout ET (333 or 1,000 pmol/kg) produced essentially identical, dose-dependent cardiovascular responses as ET-1. Dorsal aortic infusion of 1 and 3 pmol. kg(-1). min(-1) ET-1 and central venous infusion into the ductus Cuvier of 0.3 and 1 pmol. kg(-1). min(-1) produced similar dose-dependent cardiovascular responses, although the increase in P(DA) became monophasic. The heightened sensitivity to central venous infusion was presumably due to the more immediate exposure of the branchial vasculature to the peptide. Infusion of 1 pmol. kg(-1). min(-1) ET-1 decreased vascular compliance but had no effect on unstressed blood volume. These results show that ETs affect a variety of cardiovascular functions in trout and that branchial vascular resistance and venous compliance are especially sensitive. The multiplicity of effectors stimulated by ET suggests that this peptide was extensively integrated into cardiovascular function early on in vertebrate phylogeny.

Animals↗
PubMed1980

Changes in blood volume and extravascular water content in isolated perfused rat lungs during ventilation hypoxia.

Isolated rat lungs were perfused with homologous blood at constant volume inflow. The effect of ventilation hypoxia on pulmonary vascular resistance, preparation weight and reservoir volume (vascular capacitance) were studied. In some experiments also wet/dry weight ratio of the preparation was estimated (extravascular water content). There was no difference in this last parameter between hypoxic and normoxic lungs, thus alveolar hypoxia had no effect on tissue water content as previously described in intact rats. With forward perfusion small and transient changes in either direction were seen in preparation weight and reservoir volume, even though inflow pressure exceeded 5 kPa during alveolar hypoxia. With backward perfusion marked weight increases were seen, and if inflow pressure in this situation was above 3.5 kPa, the weight change was irreversible, thus indicating outward fluid filtration. It is concluded that the vessels responding to alveolar hypoxia are located on the arterial side of the pulmonary vasculature.

Animals↗
PubMed1991

[Vascular effects of adenosine-triphosphate].

This study assessed the effects of adenosine triphosphate (ATP) on systemic vascular resistances during the hypothermic cardiopulmonary bypass phase of cardiac surgery. Twenty patients scheduled for cardiac surgery were randomly divided into an ATP group (n = 10), and a placebo group (n = 10). Anaesthesia was similar for all the patients (diazepam, fentanyl and pancuronium). During the heart arrest phase, and as soon as the arterial pressure, the level in the venous return reservoir, and the pump flow rate had all been in steady state for 5 min, ATP or placebo was injected into the venous line of the oxygenator. Injection speed was doubled every three minutes, twice. The following ATP doses were administered: 0.012, 0.025 and 0.05 mg.kg-1.min-1. The level in the venous return reservoir was kept constant. Mean arterial pressure (MAP) and pump flow rate (DP) were assessed every half minute. Systemic vascular resistances were calculated with the relationship MAP/DP. Changes in vascular capacitance were directly proportional to changes in DP as the heart had been excluded, and all the blood returned to the pump, the blood volume being kept constant. MAP and DP remained unchanged in the placebo group. In the opposite ATP induced a dose-related systemic vasodilation: MAP decreased from 82.8 +/- 12.5 mmHg (control) to 66.0 +/- 14.8 mmHg, 59.8 +/- 10.6 mmHg, and 49.0 +/- 4.7 mmHg with 0.012, 0.025 and 0.05 mg.kg-1.min-1 ATP respectively. The MAP returned to preinfusion control levels when the ATP infusion was discontinued (90.0 +/- 17.8 mmHg). The DP, and therefore venous return, did not change, neither during ATP infusion, nor after its discontinuation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1983

Ventricular systolic time intervals by simultaneous echocardiographic recording of the semilunar valves during the first days of life: a study of normal newborn infants.

A modified ultrasonic method was used to image simultaneously the semilunar valves in order to study comparative neonatal right and left ventricular systolic time intervals (STI) and phasic respiration. We obtained 72 serial M-mode echocardiograms from 24 normal term infants during the first 3 days of life. Right and left ventricular pre-ejection period (RPEP, LPEP), ejection times (RVET, LVET), and STI ratios (RPEP/RVET, LPEP/LVET) did not vary with respiratory variation during the first days of life; aortic (Q-Ac) and pulmonic valve (Q-Pc) closure intervals were uninfluenced by respiration. Widening of Ac-Pc interval beyond 15 msec was present in 56% by day 3. The RPEP/LVET was greater than LPEP/LVET on the first day--a finding previously described in infants with dextro-transposition of the great arteries. Relatively fixed duration of right ventricular systole (Q-Pc) and the absence of inspiratory widening of the Ac-Pc interval, despite decreasing pulmonary vascular resistance, may be related to differences of right ventricular compliance and pulmonary vascular capacitance in the newborn infant.

Aortic Valve↗
PubMed2006

Dual-channel photoplethysmography to monitor local changes in vascular stiffness.

OBJECTIVES: Monitoring arterial distensibility changes is important to understand the cardiovascular status of patient. Pulse transit time (PTT), which is an inverse equivalent of pulse wave velocity (PWV), has shown its potential in such studies. However, its methodological approach in using an electrocardiogram and a peripheral photoplethysmography (PPG) is limited due to the inclusion of pre-ejection period (PEP) in its computation. Previous studies have suggested the using the transit time difference between two peripheral measuring sites (PTT-D) instead. However, it requires two medical instruments and may not be efficient in terms of equipment utility, especially in prolonged clinical studies. METHODS: Postural changes are known to cause complex haemodynamics adaptation and thereby affecting transit time measurements. A customised dual-channel PPG system based on discrete electronic devices was constructed to evaluate against conventional peripheral-based PTT. 10 healthy adults (7 male; mean age 27.0 yr) were recruited to assess the differences observed in PTT and PTT-D during two postural change test activities. RESULTS: PTT-D derived from the customised PPG system registered 43.3+/- 5.6 ms and - 31.1+/- 3.8 ms relative changes for the two regulated activities while conventional PTT recorded 43.6+/- 10.3 ms and -31.0+/-m 6.5 ms respectively. The former may have similar results but have significantly lower variance (< 0.05). CONCLUSIONS: Findings herein suggest that PTT-D derived from the customised PPG system shows potential. It can be used as an alternative to conventional peripheral-based PTT and possibly as a direct assessment of arterial distensibility or PWV variations as it does not include PEP in its time-related computations.

Adult↗
PubMed1978

Fortuitous rupture of aortic aneurysm: a catastrophic event affording time for surgical cure.

The rupture of an aortic aneurysm is generally a fatal event, but occasionally the rupture will occur into an adjacent vascular structure, thereby preventing exsanguination and affording temporary survival. Three cases are presented illustrating the fortuitous nature of the rupture of an aortic aneurysm into a vascular structure. The first patient had an atherosclerotic abdominal aortic aneurysm that ruptured into the inferior vena cava and was successfully repaired. The second case demonstrates the formation of a fistula from the aorta to the left pulmonary artery in a patient with a syphilitic thoracic aortic aneurysm. In the third patient a dissecting aneurysm of the aortic root that communicated with the right ventricle after coronary bypass surgery was successfully repaired. Rarely, aortic aneurysms will rupture fortuitously into vascular capacitance structures. These three cases emphasize the need for early accurate diagnosis and the institution of appropriate surgical measures.

Aged↗
PubMed2004

Effect of antihypertensive monotherapy and combination therapy on arterial distensibility and left ventricular mass.

BACKGROUND: Angiotensin-converting enzyme (ACE) inhibitors and calcium channel blockers (CCBs) increase arterial compliance and decrease left ventricular mass in hypertensive patients. This study examined whether combined therapy has greater arterial and cardiac effects than doubled doses of the individual drugs. METHODS: This prospective, randomized, open-label study enrolled 106 patients aged >/=18 years with mild-to-moderate hypertension. Patients were randomized to 5 mg of amlodipine or 20 mg of benazepril for 2 weeks; then, depending on randomization assignment, they were force-titrated to 10 mg of amlodipine or 40 mg of benazepril monotherapy, or to combination amlodipine (5 mg) and benazepril (20 mg) treatment for 22 weeks. Arterial distensibility was assessed using the DynaPulse ambulatory system, and left ventricular mass was assessed by echocardiography. RESULTS: Combination therapy (0.71% +/- 0.51% mL/mm Hg) increased arterial distensibility more than amlodipine (0.28% +/- 0.69% mL/mm Hg; P =.008) or benazepril (0.39% +/- 0.62% mL/mm Hg; P =.03) monotherapies. Left ventricular mass decreased more with combination treatment (65 +/- 56 g) than with amlodipine (28 +/- 4 g; P <.02); the difference from benazepril (42 +/- 50 g) was not significant. CONCLUSIONS: Combined ACE inhibitor and CCB treatment was more efficacious than high doses of the individual agents in increasing arterial compliance and reducing left ventricular mass. These findings indicate that appropriately selected combinations of antihypertensive drugs might have enhanced cardioprotective effects.

Adult↗
PubMed2006

A model of the interaction between autoregulation and neural activation in the brain.

In this paper a model is proposed that predicts the response of the cerebral vasculature to changes in arterial blood pressure, arterial CO2 concentration and neural stimulation. Cerebral blood flow (CBF) is assumed to be controlled through changes in arterial compliance, and hence arterial resistance and volume, through three feedback mechanisms, which act in a linear additive manner, based on CBF, arterial CO2 and neural stimulus. Together with arterial, capillary and venous compartments, a tissue compartment is included, which contributes partly to the initial rise found in the deoxyhaemoglobin response to neural activation. Dynamic simulations of the model under different conditions show that there is significant interaction between the autoregulation and activation processes, and that the level of autoregulation has a strong influence on the CBF and deoxyhaemoglobin responses to neural activation. Overshoot in the deoxyhaemoglobin response is eliminated completely in the absence of this regulation. The feedback mechanism time constants significantly affect the CBF and deoxyhaemoglobin responses. Changes in arterial blood pressure (ABP) are found to have a strong influence on the neural activation response, with the amplitude of the response decreasing significantly at high baseline ABP. Dynamic changes in ABP also have a significant and potentially confounding impact on the measured deoxyhaemoglobin response to neural activation.

Algorithms↗
PubMed1997

Right latissimus dorsi cardiomyoplasty improves left ventricular energetics.

BACKGROUND: The mechanism by which cardiomyoplasty appears to enhance left ventricular (LV) function is not well understood. We applied the time-varying elastance model to study the effect of cardiomyoplasty on LV function, ventriculovascular coupling, and LV energetics in an acute canine model. METHODS: Right latissimus dorsi cardiomyoplasty was performed in 5 dogs. The end-systolic pressure-volume relation was generated by using brief caval occlusions. End-systolic elastance, effective arterial elastance, stroke work, internal work, total mechanical work, and stroke work efficiency (stroke work/total mechanical work) were calculated from these pressure-volume data. Myocardial oxygen consumption and overall mechanical efficiency (stroke work/myocardial oxygen consumption) were predicted using the myocardial oxygen consumption-total mechanical work relation. RESULTS: Skeletal muscle contraction significantly increased end-systolic elastance, an index of contractility. Although stroke work did not change significantly, the increase in end-systolic elastance led to a 29% decrease in total mechanical work, a 50% decrease in internal work, and an increase in stroke work efficiency from 53% to 66%. This was consistent with the observed 29% decrease in effective arterial elastance/end-systolic elastance, an indicator of ventriculovascular coupling that is related inversely to stroke work efficiency. Predicted myocardial oxygen consumption decreased by at least 22%, and predicted overall mechanical efficiency increased at a minimum from 16.1% to 18.4%. CONCLUSIONS: These results support the theory that cardiomyoplasty unloads the LV by decreasing LV volumes and increasing contractility. These effects appear to improve LV energetics by decreasing total mechanical work without significantly affecting stroke work, resulting in improved stroke work efficiency. The decrease in total mechanical work strongly suggests a decrease in myocardial oxygen consumption and an increase in overall mechanical efficiency.

Animals↗
PubMed1998

New closed-form expressions for the estimation of arterial windkessel compliance.

New closed-form mathematical expressions, in the time- and frequency-domain, are derived for estimating the arterial windkessel compliance. The proposed expressions assume the three-element windkessel to model the arterial system and require the measurements of the entire waveforms of arterial pressure and flow. The resistance parameters are estimated using the recently proposed energy-balance method, then compliance is analytically calculated in order to minimize the pressure error in the compliant element. The derived expressions remain valid even when the windkessel compliance is assumed to be pressure-dependent. Also, it is shown that the method, either time- or frequency-domain formulation, provides parameter estimates, which minimize the arterial pressure square error. The method has been applied to simulated data as well as to pressure and flow data measured in the ascending aorta of three anaesthetized dogs under different circulatory conditions.

Algorithms↗
PubMed2004

Flow-tissue interaction with compliance mismatch in a model stented artery.

The insertion of an endovascular prosthesis is known to have a thrombogenic effect that is also a consequence of the interaction between the flowing blood and the stented arterial segment; in fact the prosthesis induces a compliance mismatch and a possible small expansion along the vessel that eventually gives rise to an anomalous distribution of wall shear stresses. The fluid dynamics inside a rectilinear elastic vessel with compliance and section variation is studied here numerically. A recently introduced perturbative approach is employed to model the interaction between the fluid and the elastic tissue; this approximate technique is first validated by comparison with a complete solution within a simple one-dimensional model of the same system. Then it is applied to an axisymmetric model in order to evaluate the flow dynamics and the distribution of wall shear stress in the stented vessel. Compliance mismatch is shown to produce more intense negative wall shear stresses in the stented segment while rapid variations of wall shear stress are found at the stent ends. These effects are enhanced when the prosthesis is accompanied by a small increase of the vessel lumen.

Animals↗
PubMed2004

Effects of stent stiffness on local haemodynamics with particular reference to wave reflections.

The placement of a rigid stent within an elastic vessel produces wave reflection sites at the entrance to and exit from the stent. The net haemodynamic effects of these reflections depend critically on the degree of stiffness of the stent and on its length and position within the diseased vessel, variables that have been found to affect the clinical performance of a stent. Here these effects are examined analytically, using a segmented tube model. The results indicate that the presence of the stent within the larger diseased vessel has the effect of producing higher pressure at the vessel entrance than that at exit. This pressure difference, when superimposed on the underlying pressure distribution within the vessel, has the net effect of actually aiding rather than impeding the flow, but the extent of this depends on the length and position of the stent. A short stent placed near the entrance of the diseased vessel may be favoured clinically for producing the least perturbation in the underlying haemodynamics and thus reducing the chance of restenosis, while a long stent placed near the exit may be favoured for producing a positive pressure difference and thus aiding the flow.

Blood Flow Velocity↗
PubMed1988

Why is flushing limited to a mostly facial cutaneous distribution?

Despite the systemic nature of many agents that provoke flushing reactions, the erythema is most prominent in the "blush area." To elucidate the physiologic basis for such a limited distribution, two types of flushing challenges were studied in normal volunteers. Nicotinic acid provokes flushing through a direct action of vasodilator prostaglandins on vascular smooth muscle. The flushing reaction provoked by oral thermal challenge is mediated via neural mechanisms. Both agents led to increases in cutaneous blood flow at both malar and forearm sites. Both absolute and proportional increases were consistent with the view that the greater vascular capacitance in the visible, superficial cutaneous vasculature in the blush area accounts for the limited distribution of flushing in response to a systemic stimulus.

Adult↗