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 811 records · Page 45Linked to original sources
PubMedDate not supplied

The role of beta receptors in the peripheral vasculature of calves with a total artificial heart.

Drugs given to a total artificial heart (TAH) calf isolate their vascular effects independent of the myocardium. During experiments, the TAH maintains full ejection, constant heart rate, and percent systole, and uses no vacuum. Cardiac output (CO) varies solely and directly with preload. Six calves received an infusion of isoproterenol, a beta agonist, and three calves received propranolol, a beta antagonist. The isoproterenol was resumed after beta blockade. Isoproterenol alone caused a significant increase in CO, an effect that was attenuated but not eliminated with beta blockade. Both isoproterenol and propranolol decreased AoP, but only isoproterenol increased preload. Beta receptors play a significant role in decreasing venous capacitance with increased preload and CO, independent of the myocardium.

Animals↗
PubMed1990

A theoretical description of arterial pressure-flow relationships with verification in the isolated hindlimb of the dog.

We developed and tested a new two-compartment serial model of the arterial vasculature which unifies the capacitance (downstream arterial compliance) and waterfall (constant downstream pressure load) theories of blood flow through the arteries. In this model, blood drains from an upstream compliance through a resistance into a downstream compliance which empties into the veins through a downstream resistance which terminates in a constant pressure load. Using transient arterial pressure data obtained from an isolated canine hindlimb preparation, we tested this model, using a stop-flow technique. Numerical parameter estimation techniques were used to estimate the physiologic parameters of the model. The downstream compliance was found to be more than ten times larger than the upstream compliance and the constant pressure load was significantly above venous pressures but decreased in response to vasodilation. Our results support the applicability of both the capacitance and waterfall theories.

Animals↗
PubMed1994

Calcium entry activated by store depletion in human umbilical vein endothelial cells.

We have used the patch clamp technique combined with simultaneous measurement of intracellular Ca2+ to record ionic currents activated by depletion of intracellular Ca(2+)-stores in endothelial cells from human umbilical veins. Two protocols were used to release Ca2+ from intracellular stores, i.e. loading of the cells via the patch pipette with Ins(1,4,5)P3, and extracellular application of thapsigargin. Ins(1,4,5)P3 (10 microM) evoked a transient increase in [Ca2+]i in cells exposed to Ca(2+)-free extracellular solutions. A subsequent reapplication of extracellular Ca2+ induced an elevation of [Ca2+]i. These changes in [Ca2+]i were very reproducible. The concomitant membrane currents were neither correlated in time nor in size with the changes in [Ca2+]i. Similar changes in [Ca2+]i and membrane currents were observed if the Ca(2+)-stores were depleted with thapsigargin. Activation of these currents was prevented and holding currents at -40 mV were small if store depletion was induced in the presence of 50 microM NPPB. This identifies the large currents, which are activated as a consequence of store-depletion, as mechanically activated Cl- currents, which have been described previously [1,2]. Loading the cells with Ins(1,4,5)P3 together with 10 mM BAPTA induced only a very short lasting Ca2+ transient, which was not accompanied by activation of a detectable current, even in a 10 mM Ca(2+)-containing extracellular solution. Also thapsigargin does not activate any membrane current if the pipette solution contains 10 mM BAPTA (ruptured patches). The contribution of Ca(2+)-influx to the membrane current during reapplication of 10 mM extracellular calcium to thapsigargin-pretreated cells was estimated from the first time derivative of the corresponding Ca2+ transients at different holding potentials. These current values showed strong inward rectification, with a maximal amplitude of 1.0 +/- 0.3 pA at -80 mV (n = 8; membrane capacitance 59 +/- 9 pF).(ABSTRACT TRUNCATED AT 250 WORDS)

Calcium↗
PubMed2001

Relationship between extra and intracellular sources of calcium and the contractile effect of thiopental in rat aorta.

To evaluate the relationship between the vasocontractile effect of thiopental and the extra and intracellular sources of Ca2+, we analyzed both the contractile effect of the barbiturate on rat aortic rings and its ability to modify the intracellular calcium concentration in cultured rat aorta smooth muscle cells. Thiopental (10-310 microg/mL) contracted aortic rings only in the presence of extracellular Ca2+, and this effect was not blocked by verapamil or diltiazem. On the contrary, Ca2+ (0.1-3.1 mM) evoked contractions only when thiopental (100 microg/mL) was present. Although in calcium-free solution thiopental (100 microg/mL) did not contract aortic rings, it abolished the contractile effect of either phenylephrine (10(-6) M) or caffeine (10 mM). Finally, thiopental augmented the intracellular calcium concentration in cultured smooth muscle cells incubated either in the presence or absence of calcium. In conclusion, thiopental's vasocontractile effect depends on extracellular calcium influx, which is independent of L-calcium channels. The increase in intracellular Ca2+ concentration elicited by thiopental in Ca2+-free solution and its ability to block the effect of phenylephrine and caffeine suggest that this barbiturate can deplete intracellular pools of calcium. Therefore, the calcium entry pathway associated with the contractile effect of thiopental may correspond to the capacitative calcium entry model.

Animals↗
PubMed1984

[Effect of sodium nitroprusside and nitroglycerin on the resistance and capacitance system in cardiac surgery interventions].

The whole-body arterial and venous dilating properties of nitroglycerin (NTG) and sodium nitroprusside (SNP) were investigated during extracorporeal circulation and normal circulation in patients undergoing coronary bypass surgery. SNP was found to lower preload and afterload for the time of drug administration. During extracorporeal circulation and normal circulation, an average volume of 340 ml was stored in the capacitance vessels when the mean arterial pressure was lowered for 20 mm Hg. When the reduction in preload was compensated by a volume load (blood transfusions), this resulted in a pure impedance reduction by SNP. NTG showed more complex effects. Even with the continuous infusion of NTG only a short-termed, self-limiting afterload reduction occurred during extracorporeal circulation. During normal circulation, the reduction in preload was more extensive with NTG than with SNP, an average volume of 600 ml was stored in the capacitance vessels when the mean arterial pressure was lowered for 20 mm Hg by NTG. While the volume storage by SNP was reversible after termination of the infusion, this was not the case with NTG, where the volume was stored for 1-2 hours. The volume storage by NTG became smaller with an increased filling of the capacitance system. Additionally, the venous resistance of the cardiopulmonary bypass showed different effects on the volume storage by SNP and NTG. In conclusion, the different effects of NTG and SNP cannot be explained by a single, homogenous compartment model of the peripheral circulation but by affecting two different compartments of the capacitance system.

Blood Volume↗
PubMed1977

Comparative effects of adrenaline and felypressin (octapressin) on consecutive sections of the vascular bed in canine adipose tissue.

Blood flow and tissue volume were recorded in the isolated canine subcutaneous adipose tissue, enclosed in a plethysmography. Adrenaline and felypressin (octapressin) were infused intra-arterially at doses producing a blood flow reduction of approximately 60%. Adrenaline (4.6-23 ng/min) caused an initial reduction in tissue volume, indicating a constriction of capacitance vessels. Octapressin (0.46-9.2 ng/min) had no effect on tissue volume. Neither adrenaline or octapressin caused appreciable filtration or absorption, suggesting that the pre- to postcapillary resistance ration remained unchanged. In contrast to sympathetic stimulation and noradrenaline, adrenaline significantly reduced the capillary filtration coefficient (CFC) by 34%, the change in CFC being related to the flow reductions, while octapressin did not reduce CFC sffect of adrenaline on precapillary sphincter sections and on capacitance vessels is greater than that of octapressin in doses producing similar flow reductions.

Adipose Tissue↗
PubMed1987

Peripheral vascular effects of ketanserin and nifedipine during cardiopulmonary bypass.

Ketanserin, a selective S2-serotonergic receptor antagonist with alpha 1-adrenergic receptor-blocking properties, as well as nifedipine, a classic calcium channel blocker, is used as an antihypertensive agent during and following cardiac surgery. In a double-blind prospective study, using hypothermic cardiopulmonary bypass as a study model, ketanserin (10 mg i.v.) and nifedipine (2 mg i.v.) were evaluated with respect to their effects on the peripheral circulation. The results showed that ketanserin and nifedipine dilate the arterial side of the vasculature, but that ketanserin, unlike nifedipine, also dilates the venous capacitance vessels; nifedipine even caused a short-lasting venous vasoconstriction. Since venous tone is increased during and following cardiopulmonary bypass, antihypertensive treatment with ketanserin might be advantageous under these circumstances.

Aged↗
PubMed2004

Protein kinases in vascular smooth muscle tone--role in the pulmonary vasculature and hypoxic pulmonary vasoconstriction.

Hypoxic pulmonary vasoconstriction (HPV) is an adaptive mechanism that in the normal animal diverts blood away from poorly ventilated areas of the lung, thereby maintaining optimal ventilation-perfusion matching. In global hypoxia however, such as in respiratory disease or at altitude, it causes detrimental increases in pulmonary vascular resistance and pulmonary artery (PA) pressure. The precise intracellular pathways and mechanisms underlying HPV remain unclear, although it is now recognised that both an elevation in smooth muscle intracellular [Ca2+] and a concomitant increase in Ca2+ sensitivity are involved. Several key intracellular protein kinases have been proposed as components of the signal transduction pathways leading to development of HPV, specifically Rho kinase, non-receptor tyrosine kinases (NRTK), p38 mitogen activated protein (MAP) kinase, and protein kinase C (PKC). All of these have been implicated to a greater or lesser extent in pathways leading to Ca2+ sensitisation, and in some cases regulation of intracellular [Ca2+] as well. In this article, we review the role of these key protein kinases in the regulation of vascular smooth muscle (VSM) constriction, applying what is known in the systemic circulation to the pulmonary circulation and HPV. We conclude that the strongest evidence for direct involvement of protein kinases in the mechanisms of HPV concerns a central role for Rho kinase in Ca2+ sensitisation, and a potential role for Src-family kinases in both modulation of Ca2+ entry via capacitative Ca2+ entry (CCE) and activation of Rho kinase, though others are likely to have indirect or modulatory influences. In addition, we speculate that Src family kinases may provide a central interface between the proposed hypoxia-induced generation of reactive oxygen species by mitochondria and both the elevation in intracellular [Ca2+] and Rho kinase mediated Ca2+ sensitisation.

Animals↗
PubMed2002

Hepatic sinusoidal vasodilators improve transplanted cell engraftment and ameliorate microcirculatory perturbations in the liver.

After transplantation, hepatocytes entering liver sinusoids are engrafted, whereas cells entrapped in portal spaces are cleared. We studied whether hepatic sinusoidal dilatation will increase the entry of transplanted cells in the liver lobule, improve cell engraftment, and decrease microcirculatory perturbations. F344 rat hepatocytes were transplanted intrasplenically into syngeneic dipeptidyl peptidase IV (DPPIV)-deficient rats. Animals were treated with adrenergic receptor blockers (phentolamine, labetalol), a calcium channel blocker (nifedipine), and splanchnic vasodilators (nitroglycerine, calcitonin gene-related peptide [CGRP], glucagon). Transplanted cells were localized by histochemistry. The hepatic microcirculation was studied with in vivo videomicroscopy. Changes in cell translocations were analyzed by injection of (99m)Tc-labeled hepatocytes. Pretreatment with phentolamine and nitroglycerine increased transplanted cell entry in liver sinusoids, whereas labetalol, nifedipine, CGRP, and glucagon were ineffective. Increased deposition of transplanted cells in sinusoids resulted in greater cell engraftment. In vivo microscopy showed disruption of sinusoidal blood flow immediately after cell transplantation with circulatory restoration requiring more than 12 to 24 hours after cell transplantation. However, in nitroglycerine-treated animals, sinusoidal blood flow was perturbed less. Nitroglycerine did not meaningfully increase intrapulmonary cell translocations. In conclusion, these findings indicate that hepatic sinusoidal capacitance is regulated by alpha-adrenergic- and nitroglycerine-responsive elements. Sinusoidal vasodilatation benefited intrahepatic distribution of transplanted cells and restored hepatic microcirculation after cell transplantation. This shall facilitate optimization of clinical cell transplantation and offers novel ways to investigate vascular mechanisms regulating hepatic sinusoidal reactivity.

Adrenergic alpha-Antagonists↗
PubMed1997

Analog transmission line model for simulation of systemic circulation.

A simple four-tube arteries-microvessels-veins system which simulates a more realistic loading for human circulation was built using transmission line network. Hemodynamic data from literature are used in the fluid-circuit analogy, and the flow leakage and viscoelastic properties of the blood vessels have been considered. The effect of veins on the input impedance spectrum was found to be negligibly small above 0.5 Hz. The predicted input impedance spectra agree reasonably well with the published measurements both in shape and magnitude. Parametric analysis shows that the changes of vascular properties in the lower body affect the first minimum, and the changes in the upper body influence the second minimum. The blood flow in and out of kidney and liver dominates the aortic impedance from 0 to 5 Hz. Decreasing capacitance (i.e., increasing arterial stiffness due to aging), reducing the lumen area, or decreasing the length of blood vessels result in an increase in the impedance modulus, and the first minimum shift to a higher frequency which agree well with experiments. In the current model, the pressure, flow waveform, and local impedance can be predicted at any location along the circulatory tree. The characteristic of arterial pulse propagation resembles published measurements.

Arteries↗
PubMed1975

Circulatory responses to stimulation of the carotid body chemoreceptors in the cat.

Cardiovascular responses to carotid body chemoreceptor stimulation were followed in the 'curairzed', vagotomized, artificially ventilated cat. Stimulation of the chemoreceptors by perfusion of the carotid sinus regions with venous blood induced a reflex vasconstriction in skeletal muscle, kidney, intestine and skin, and, in most cases, an increased heart rate. A comparison of the chemoreceptor reflex responses with those obtained by direct electrical stimulation of the regional vasomotor fibres indicated that in chemorecptor reflexes the vasomotor fibre activity increased to the same extent in skeletal muscle and intestinal resistance vessels and, probably, in the nutritional skin vessels but to a smaller extent in the renal vessels and the skeletal muscle capacitance vessels. The renal vessels and the muscle capacitance vessels seemed, however, to respond more during chemoreceptor stimulation than when the barorecptors were unloaded, indicating that anexcitation of the bulbar vasomotor centre is more effective than the withdroawal of an inhibitory restraint in activating the vasomotor fibres to these vascular sections.

Animals↗
PubMed1983

Vascular and secretory effect of adrenoceptor agonists and peptides in the nose.

With two methods which in cats simultaneously recorded changes of blood flow through the mucosa of a nasal cavity and changes of the nasal patency in the same cavity, it was found that alpha-adrenoceptor agonists and the peptide, angiotensin constricted both the resistance and the capacitance vessels. Beta-adrenoceptor agonists and the peptide VIP dilated the vessels. Further, a filter paper method in dogs demonstrated that a large increase in nasal secretion was obtained with alpha-adrenoceptor stimulation in combination with methacholine, more than that with methacholine alone. Beta-adrenoceptor agonists seem to elicit a very scanty secretion. The peptide, substance P was also found to evoke a nasal secretion.

Airway Resistance↗
PubMed1995

The bovine central adrenomedullary vein: a target for endothelins.

This study reports on morphological and contractile properties of the bovine central adrenomedullary vein (bCAMV). Up to several layers of circularly orientated smooth muscle cells (SMC) were observed, however, without forming a continuous, closed sheath. Discrete bundles of eccentrically arranged, longitudinal SMC were also conspicuous. Chromaffin cells were in most cases located outside the SMC layers, while sometimes being in close apposition to the endothelium in areas without SMC. Circularly mounted preparations of the endothelium-denuded vessel responded selectively to high K+, endothelins (ETs) and neuropeptide Y (NPY). The threshold for ET-1 was 0.13 nM and the half maximally effective concentration (EC50) was 3 +/- 1 nM (n = 9). The order of potencies was ET-1 > or = ET-2 >> ET-3, suggesting a vascular receptor (ETA). Concentrations at and above EC50 frequently developed long-lasting oscillations during the spontaneous relaxation of the ET-1 evoked tension. This response was partly (21%) independent of extracellular Ca2+. A marked tachyphylaxis developed to ET-1 (3-30 nM), resulting, on the other hand, in facilitation of the subsequent constrictor responses to high K+ and NPY. Propranolol and phentolamine alone, or in combination, were without effects on the basal tension and on the above-mentioned responses to high K+, ET-1 or NPY, making a contribution from adrenoceptor activation unlikely. No response was obtained with exogenous catecholamines, acetylcholine or serotonin, nor with a series of peptides known to occur in the adrenal medulla. This study shows that bCAMV is not a passive capacitance vessel but appears unique among mammalian veins in being selectively regulated by ETs.

Adrenal Medulla↗
PubMed1992

Vascular control of the pig nasal mucosa: distribution and effect of somatostatin in relation to noradrenaline and neuropeptide Y.

By means of immunohistochemistry and radioimmunoassay (RIA), we have investigated the possible occurrence of somatostatin (SOM)-like immunoreactivity (-LI) in the autonomic innervation of the pig nasal mucosa. SOM-immunoreactive (-IR) fibres were present around nasal arteries, arterioles and venous sinusoids. Double-labelling experiments revealed that SOM-LI was co-localized with the noradrenaline (NA) markers tyrosine hydroxylase and dopamine-beta-hydroxylase as well as with neuropeptide Y (NPY) in a subpopulation of neurons in the superior cervical sympathetic ganglion and in perivascular nerve terminals. Furthermore, SOM-LI was also present in perivascular fibres containing vasoactive intestinal polypeptide (VIP) and NPY of presumably parasympathetic origin. The parasympathetic fibres that were associated with glands contained peptide histidine isoleucine (PHI), VIP and NPY but not SOM, suggesting that in the nasal mucosa SOM-IR is restricted to perivascular nerves. As revealed by RIA, the content of SOM-LI in biopsies of both nasal mucosa and superior cervical sympathetic ganglion was about 12 pmol/g and the reverse phase HPLC characterisation of SOM-LI shown two separate peaks for SOM-28 and SOM-14. In thiopentone anaesthetized pigs (n = 10), local intra-arterial (i.a.) infusion of SOM (1-14) induced dose-dependent, long lasting and parallel reduction of the nasal arterial blood flow, the volume of the nasal mucosa (reflecting capacitance vessel function) and decrease of the laser Doppler flowmeter signal (reflecting superficial nasal mucosal blood flow). These functional responses were not modified after pretreatment with the alpha-adrenoceptor antagonist phenoxybenzamine (1 mg kg-1 i.a.) whereas the effects of NA were almost abolished. SOM (6.10(-6) mol, i.a.) did not influence the nasal vascular responses to single impulse stimulation of the nasal sympathetic nerve supply providing no evidence for prejunctional activity in spite of clear-cut vascular effects. It is concluded that SOM-LI is co-localized with NA and NPY in sympathetic nerves and with VIP/NPY in parasympathetic perivascular nerves of the pig nasal mucosa. Since SOM evokes vasoconstriction via non-adrenergic mechanisms, this peptide should also be considered when discussing mediator candidates for the neural regulation of the nasal vascular bed.

Animals↗
PubMed2003

Free fatty acid overload attenuates Ca2+ signaling and NO production in endothelial cells.

Hyperlipidemia represents a major risk factor for development of vascular dysfunction and atherosclerosis. Although the unfortunate role of low-density lipoprotein has been clearly demonstrated, the mechanistic pathways through which triglyceride-derived free fatty acids (FFAs) contribute to vascular disorders are not completely understood. Thus, the present study was designed to elucidate the effects of FFAs on cultured endothelial cells. The Ca(2+) signaling, endothelial nitric oxide synthase (eNOS) activity, and production of superoxide anions (.O(2)(-)) were monitored in cells treated with bovine serum albumin-conjugated FFA. FFA-loaded cells showed enhanced intracellular Ca(2+) release in response to ATP, histamine, or the SERCA inhibitor thapsigargin. This effect corresponded to an overall increase in intracellularly stored Ca(2+). In contrast, autacoid-triggered elevation of cytosolic free Ca(2+) concentration was blunted in FFA-loaded cells due to inhibition of capacitative Ca(2+) entry. In agreement with the reduced Ca(2+) signaling, the Ca(2+)-dependent activity of eNOS was reduced under basal conditions and if cells were stimulated with ATP, histamine, or thapsigargin. The attenuated eNOS activity was associated with.O(2)(-) release in FFA-loaded cells. These data indicate that FFAs significantly affect endothelial Ca(2+) signaling, eNOS activity, and.O(2)(-) release and, thus, might contribute to vascular dysfunction in atherogenesis.

Adenosine Triphosphate↗