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 721 records · Page 40Linked to original sources
PubMed1979

[Participation of the contractile activity of the skeletal musculature in systemic circulatory reactions to orthostatic action].

Under orthostatic test (OT) the elimination of the skeletal muscle contractile activity with a myorelaxant sharply elevated the initial hypotension and decreased considerably the compensatory restoration of the arterial pressure (AP) in anesthetized cats. Reaction of the cardiac output in OT changed insignificantly. The AP elevation synchronous with the motor reactions, eliminated by the myorelaxant, was observed. As revealed by the method of artificial circulation (bypass of the left ventricle), the compensatory vasoconstriction of the resistance vessels was eliminated by the myorelaxant under OT. In some experiments myorelaxation evoked a significant elevation of the blood pooling in the capacitance vessels.

Animals↗
PubMed1986

Alpha 1- and alpha 2-adrenoceptor stimulation: changes in venous capacitance in intact dogs.

The peripheral circulatory effects of alpha 1-adrenoceptor stimulation with methoxamine hydrochloride were compared with those of alpha 2-stimulation with UK 14304-18 in 12 intact dogs. Doses of each agent were infused to increase systemic vascular resistance and arterial pressure 50 and then 100% above control. Heart rate was controlled with atropine. At the higher dose, methoxamine increased mean aortic pressure (PAo) from a control of 77.3 +/- 1.6 to 152.9 +/- 3.2 mmHg, mean circulatory filling pressure (MCFP) from 8.0 +/- 0.4 to 13.3 +/- 1.3 mmHg, and central blood volume (CBV) from 21.3 +/- 1.1 to 25.9 +/- 1.5 ml X kg-1, whereas cardiac output did not change. UK 14304-18 increased PAo from 78.1 +/- 2.6 to 148.9 +/- 2.7 mmHg, MCFP from 7.9 +/- 0.4 to 10.6 +/- 0.4 mmHg, and CBV from 21.0 +/- 1.1 to 24.1 +/- 1.5 ml X kg-1, whereas cardiac output decreased from 151.7 +/- 9.4 to 126.3 +/- 5.8 ml X kg-1 X min-1. Mean circulatory filling pressure and CBV were higher with methoxamine than with UK 14304-18. Effective vascular compliance, determined by serial measurements of MCFP during ganglionic blockade after rapid changes in blood volume, decreased from a control value of 1.9 +/- 0.1 to 1.3 +/- 0.3 ml X mmHg-1 X kg-1 with methoxamine, but did not change with UK 14304-18 (1.9 +/- 0.1 ml X mmHg-1 X kg-1). At any given change in blood volume, there was a higher MCFP with alpha 1-stimulation compared with alpha 2-stimulation. Both agents decreased unstressed vascular volume.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1982

Active hepatic capacitance responses to neural and humoral stimuli in dogs.

Active changes in hepatic capacitance were studied in pump-perfused dog livers during hepatic nerve stimulation or during intrahepatic arterial infusion of histamine (0.01-1 mg/l) or epinephrine (0.05 mg/l). Hepatic nerve stimulation at 5 pulses/s (pps) reduced hepatic blood volume by 76 +/- 39 (SD) ml/kg tissue and decreased the apparent hepatic compliance 36% from a control value of 25.6 +/- 9.3 ml.kg-1.mmHg-1, with constant flow perfusion. With a constant hepatic arterial pressure, 5 pps stimulation decreased hepatic arterial flow to 16% of control; the volume expelled was 91 +/- 33 ml/kg. Epinephrine caused hepatic artery constriction, the active expulsion of 71 ml/kg of blood, and a decrease of about 30% in hepatic compliance. Histamine dramatically reduced the hepatic vascular compliance, decreased the portal venous conductance, increased hepatic arterial conductance, and caused the apparent hepatic blood volume to double. Increased hepatic venous pressure, hepatic nerve stimulation, epinephrine, and, especially, histamine caused a significant filtration of fluid from the hepatic vasculature. We conclude that significant active capacitance changes and transsinusoidal fluid filtration can be induced in the canine liver by neural and hormonal stimuli.

Animals↗
PubMed1992

Pharmacologic mechanisms of nitrates in myocardial ischemia.

Nitrates exert both hemodynamic and nonhemodynamic effects that help explain the mechanisms by which these drugs benefit patients with myocardial ischemia. The hemodynamic effects of nitrates include relaxation of conduit arteries, increased arterial compliance, increased venous capacitance, dilation of collateral vessels in the myocardium, and, possibly, increased myocardial compliance. A growing body of evidence suggests that the nonhemodynamic effects of these agents include inhibition of vascular smooth muscle growth and of myocyte hypertrophy and ventricular remodeling. Since endothelial function appears to be abnormal in patients with myocardial ischemia and nitrates replicate many of the effects of endothelium-derived relaxing factor, these drugs may be viewed as a pharmacologic replacement for deficient endogenous activity.

Hemodynamics↗
PubMed1992

Efficacy and safety of felodipine, a new dihydropyridine calcium channel blocker, in elderly hypertensive patients.

Felodipine is a new dihydropyridine calcium channel blocker with a number of properties that enhance its suitability as a first-line antihypertensive drug for the elderly. Felodipine has a 100-fold selectivity for inhibiting the contribution of vascular smooth muscle compared with cardiac muscle. Negative inotropic action appears minimal while selectivity appears to increase with age. Felodipine has a minimal effect on smooth muscle of venous capacitance vessels, thereby greatly reducing the likelihood of orthostatic hypotension. Renal effects are favorable; the glomerular filtration rate is increased in some patients. The extended-release formulation of felodipine produces a smooth 24-hour plasma concentration curve and is effective when prescribed once daily. Felodipine appears to lower blood pressure effectively in the elderly patient with few, generally mild, adverse effects.

Aging↗
PubMed2002

Molecular candidates for capacitative and non-capacitative Ca2+ entry in smooth muscle.

Recent investigations have revealed that mammalian homologues of transient receptor potential (TRP) protein (TRP1-7) are promising candidates for Ca2+ entry mechanisms (or channels) associated with various metabotropic G protein-coupled receptors (GPCRs) in smooth muscle, stimulation of which generates lipid second messengers and depletes internal stores. RT-PCR and immunocytochemical experiments have demonstrated that although the level of expression varies depending on tissues, the major TRP isoforms expressed in smooth muscle are TRP4, 6 and 7. In some vascular preparations, the significant expression of TRP1 mRNA and protein is also detected. Consistent with these findings, recent functional studies using TRP6- and TRP1-specific antisense oligonucleotides and antibodies have suggested that TRP6 is the essential component of alpha1-adrenoceptor activated, store depletion-independent Ca2+ entry channels, while TRP1 is partly involved in Ca2+ entry associated with store depletion or capacitative Ca2+ entry. In addition, coexpression of different TRP isoforms results in the appearance of cation channels showing novel properties reminiscent of some native GPCR-activated Ca2+-permeable non-selective cation channels. Thus, at present, TRP proteins may be the most important clues for elucidating the molecular entities of receptor- and store-operated Ca2+ entry mechanisms in smooth muscle and their roles in smooth muscle functions.

Animals↗
PubMed1991

[Vasomotor activity and vascular geometry].

The circulation may be divided into several anatomical and functional segments placed in series. The vessels of distribution (great arteries) are designed to decrease the cardiac periodicity. The tone of the resistance vessels (arterioles) control the blood pressure. In situ changes of their diameter must be assessed with respect to variations in pressure in order to evaluate the active or passive mechanism of a physiological or therapeutic intervention. The vessels of exchange (capillaries, veinules) which have no smooth muscle in their walls are passively affected by changes in flow and transmural pressure. The capacitance vessels (veins) are partially affected by the blood flow entering this segment and influence the cardiac output by the effects of changes of volume on venous return to the heart.

Blood Vessels↗
PubMed1997

[Hemodynamic effects of amrinone combined with dopamine in patients undergoing living renal transplantation].

Systemic hypertension is a constant feature of chronic renal failure, mediated by renin and exacerbated by salt and fluid loading. Vascular atherosclerosis appears to accelerate in patients on long-term dialysis. Therefore, it is important to control hypertension and keep appropriate renal blood flow during living renal transplantation surgery. Amrinone, a phosphodiesterase inhibitor, produces vasodilation in arterial smooth muscle as well as venodilation in the capacitance bed. By increasing myocardial contractility it increases inotropic effect. Amrinone has potent inodilator effects because of its dual mechanism of action. The current study is aimed to compare hemodynamic effects between amrinone (3-5 mg.kg-1.min-1) (AMR group, n = 4) and nitroglycerin (0.3-1.0 mg.kg-1.min-1) (NTG group, n = 5), combined with dopamine (3-5 mg.kg-1.min-1) in nine patients undergoing living renal transplantation. Increase in cardiac index in AMR group was significantly larger than that in NTG group. Values of systemic and pulmonary vascular resistance in AMR group were significantly smaller than those in NTG group. No significant difference was found in renal function in the post-operative period.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed2001

Arterial elasticity among normotensive subjects and treated and untreated hypertensive subjects.

OBJECTIVE: The aim of this study was to determine arterial elasticity in normotensive and hypertensive individuals. BACKGROUND: In addition to blood pressure, other parameters serve as markers for vascular disease. Arterial elasticity is one parameter that can be determined by a modified Windkessel model of the circulation. This model estimates, from a computerized pulse contour analysis, the proximal (capacitive) elasticity of the large arteries and the distal (reflective) elasticity of the small arteries. METHODS: A prospective, multi-center, controlled clinical study evaluated large-artery and small-artery elasticity indices in four groups: (1) normotensives without a family history of hypertension; (2) normotensives with a family history of hypertension; (3) treated and controlled hypertensives; and (4) untreated and uncontrolled hypertensives. Blood pressure, using a mercury manometer, and arterial elasticity, using a CVProfilor DO-2020 CardioVascular Profiling System (Hypertension Diagnostics, Inc., Eagan, MN, USA), were measured supine in triplicate 3 min apart in a randomized sequence. RESULTS: There were 212 evaluable subjects of mean age 46 years; 57% were women, 51% Caucasian and 33% African-American. Comparing normotensives without a family history and untreated hypertensives, both large-artery and small-artery elasticity indices were significantly different (P < 0.0001). After controlling for age and body surface area, a significant linear trend (P = 0.0001) across the four groups was detected for both large- and small-artery elasticity indices. CONCLUSION: As the hypertension status worsened, large- and small-artery elasticity indices decreased, suggesting a potential for the diagnostic use of arterial elasticity determinations.

Arteries↗
PubMed1988

Distensibility of hepatic venous resistance sites and consequences on portal pressure.

Hepatic venous resistance was measured in cats anesthetized with pentobarbital sodium during changes in hepatic blood flow and in inferior vena cava (IVC) pressure, in an attempt to explain the variable and partial transmission of pressure from IVC to portal vein. Problems with earlier explanations based on a "vascular waterfall" or a "Starling resistor" are discussed. Our data and previously published data can be explained by the hypothesis that hepatic venous resistance decreases as the resistance site is distended by the pressure within the resistance vessels. The product of resistance and distending pressure was a constant. This constant equals the resistance at unit-distending pressure, and it is an index of active contraction of the resistance sites in acute experiments. It is increased during infusions of norepinephrine, and it is higher in innervated than in denervated livers. A distensible hepatic venous resistance is a passive mechanism for partial autoregulation of portal pressure. It also serves as a mechanism for regulation of the splanchnic capacitance response to changes in IVC pressure.

Animals↗
PubMed1983

Comparative vascular effects of stimulation continuously and in bursts of the sympathetic nerves to cat skeletal muscle.

Recent electrophysiological studies indicate that sympathetic vasoconstrictor fibre dicharge in vivo usually occurs in intermittent high frequency bursts, increased activity being established by raised intra-burst frequency or, more commonly, by shortened burst intervals. The present study describes the responses of the resistance and capacitance vessels in cat skeletal muscle to electrical vasoconstrictor fibre stimulation with characteristics simulating the discharge pattern in vivo. Stimulation in bursts (1 s duration) was applied either at varying intra-burst impulse rates (from 5 to 160 Hz) at constant burst interval (5 or 10 s), or at varying burst intervals (from 32 to 2 s) at constant intra-burst frequency (16 or 32 Hz). For comparison, continuous stimulation was made at rates from 0.5 to 16 Hz. Both types of burst stimulation were capable of evoking maintained constrictions in the resistance and capacitance vessels, graded in relation to the total number of impulses/unit time. Stimulation in bursts at varying intervals was as effective as continuous stimulation with maximal constriction reached at 32 Hz bursts at 4 s intervals. The responses to stimulation in bursts at varying impulse rates peaked at 40 Hz, higher intraburst frequencies being less effective, at least in the resistance vessels. The data suggests that the resistance and capacitance vessels are gradedly responsive to sympathetic discharge rates up to about 40 Hz provided excitation occurs in bursts and, that an effective control can be achieved especially by shortening the burst interval. Sympathetic firing in skeletal muscle may thus well exceed 10 Hz, previously believed to be the upper physiological discharge range.

Animals↗
PubMed1993

Leukotrienes C4 and D4 are potent endothelium-dependent relaxing agents in canine splanchnic venous capacitance vessels.

In the present study, the vasomotor effects of the peptide leukotrienes (LTs) LTC4 and LTD4 on isolated canine venous capacitance vessels were evaluated. Both LTs evoked marked concentration-dependent relaxation of norepinephrine-contracted rings of mesenteric and splenic veins and inferior vena cava but had minimal activity in the femoral vein. Relaxation induced by either LT was abolished after physical removal of the vascular endothelium, whereas marked relaxation responses were evoked by glyceryl trinitrate in the same endothelium-denuded rings. The nitric oxide synthase antagonist NG-nitro-L-arginine methyl ester (L-NAME) completely abolished LT-induced mesenteric vein relaxation and unmasked a contractile effect of LTC4. Only partial attenuation of LT-induced relaxation of the inferior vena cava in the presence of L-NAME was observed. In the splenic vein, responses solely to LTC4 were very slightly reduced in the presence of L-NAME. Reduced hemoglobin (10(-6) and 10(-5) M) inhibited LTC4-evoked splenic vein relaxation and, in a concentration of 10(-5) M, inhibited LTD4-evoked relaxation of the splenic vein. On the other hand, methylene blue (10(-6) and 10(-5) M) attenuated splenic vein relaxation produced by both LTs but solely reduced LTC4-evoked inferior vena cava relaxation. Thus, the peptide LTs, the major components of the slow-reacting substance of anaphylaxis, exert a profound endothelium-dependent relaxant effect on venous capacitance vessels, which is only partially dependent on L-arginine and nitric oxide. A role for LT-evoked capacitance venodilation as a mechanism contributing to the reduced venous return and cardiac output associated with systemic anaphylaxis is postulated.

Animals↗
PubMed2004

Contribution of store-operated Ca2+ entry to pHo-dependent changes in vascular tone of porcine coronary smooth muscle.

Vascular smooth muscle contracts on increases of extracellular pH (pH(o)) and relaxes on pH(o) decreases possibly resulting from changes in transsarcolemmal Ca(2+) influx. Therefore, we studied store-operated Ca(2+) entry (SOCE; i.e. capacitative Ca(2+) entry (CCE)) during acidification (pH(o)=6.5) and alkalinization (pH(o)=8.0) in isolated porcine coronary smooth muscle cells (SMCs) by monitoring cytoplasmic Ca(2+) ([Ca(2+)](i)) and divalent cation entry (Mn(2+) quench) with fura-2/AM-fluorometry. Additionally, we evaluated the contribution of SOCE to pH(o)-dependent changes in isometric tension of porcine coronary smooth muscle strips. SOCE elicited in SMCs by the SERCA inhibitor BHQ was strongly modulated by pH(o) showing a decrease upon acidification and vice versa an increase upon alkalinization. BHQ-mediated tension of smooth muscle strips also revealed strong pH(o) dependence. In contrast, L-VOC-dependent tension ([K(+)](o)=20 and 40 mmol l(-1)) was remarkably less affected by pH(o) changes. Moreover, refilling of depleted Ca(2+) stores after repeated M(3)-cholinergic receptor stimulation could be almost completely inhibited by SKF 96365 and was markedly reduced by acidification and considerably enhanced by alkalinization pointing to a major role of SOCE in refilling. We conclude that vascular tone particularly responds to alterations in pH(o) whenever SOCE substantially contributes to the amount of activator Ca(2+) for contraction.

Acetylcholine↗
PubMed1992

Abnormalities of vascular compliance in hypertension, aging and heart failure.

AIM: Diastolic arterial pulse wave analysis and a modified Windkessel model were used to evaluate the vascular response to hypertension, heart failure and aging. RESULTS: Compared to age-matched normal subjects, arterial compliance was reduced in patients with hypertension and heart failure, particularly in the vessels that contribute to resonances or oscillations in the pulse wave. In elderly subjects, the capacitive function of the arteries and compliance of the smaller arteries that contribute to oscillations were both reduced. CONCLUSION: These small-vessel structural or functional abnormalities may serve as a marker for disease and for the response to therapy.

Aging↗
PubMed1975

The effect of lidocaine on peripheral hemodynamics.

Lidocaine was given in increasing step-wise dose concentrations of 1, 2, 3, 4, and 5 mg/minute and the resulting serum concentrations correlated with the effect of this agent on the peripheral vasculature of seven patients. Lidocaine infusion causes an immediate sustained increase in mean calf venous capacitance but little effect on mean diastolic blood pressure. In high concentration levels this agent causes an increase in mean calf blood flow and systolic blood pressure. Its effect on calf vascular resistance is variable, but there is a tendency to reduce resistance, particularly at a high concentration level. The effect of lidocaine infusion rate on serum lidocaine levels was such that the greater the infusion rate, the higher the resultant serum lidocaine levels.

Adult↗
PubMed1992

[Effects of isosorbide dinitrate and diltiazem used alone or combined on arterial hemodynamic and viscoelastic parameters. Experimental data in the rabbit].

An experimental model of simultaneous recording of aortic pressure and flow and vascular diameter at the entrance to a limited territory of systemic circulation has been developed in the rabbit. A system of data acquisitions and treatment has also been perfected to evaluate the different parietal viscoelastic parameters of arterial flow in capacitance and resistance arteries. This model was used to study the pharmacodynamic effects of two vasodilator drugs, isosorbide dinitrate (ISDN) and diltiazem (DILT), administered alone or in association (ISDN + DILT) by slow intravenous infusion over 30 minutes at dosages chosen to induce comparable hypotension of about 10%. Under these conditions, the effects of ISDN, DILT and ISDN + DILT on resistance parameters were slightly different. The ISDN had no marked effect on mean aortic flow (Qm) apart from a slight decrease after 10 minutes infusion (-10.4 +/- 3.8%, p less than 0.05). On the other hand, DILT alone or in association with IDN was associated with a significant increase in Qm (DILT: +8.5 +/- 0.8%, p less than 0.001; ISDN + DILT: +9.7 +/- 2.1%, p less than 0.01). This explains the absence of a significant effect of ISDN on peripheral resistance (PR) or entrance impedance (Zc) of the vascular bed. Conversely, the effects of DILT and ISDN + DILT on these parameters were very marked (DILT:RP = -17.2 +/- 0.9%, p less than 0.001; Zc = -8.2 +/- 0.5%, p less than 0.001; ISDN + DILT: RP = -16 +/- 1.4%, p less than 0.001; Zc = -8.0 +/- 0.4%, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗