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PubMed1999

Use of electrochemical impedance measurements to monitor beta-adrenergic stimulation of bovine aortic endothelial cells.

Due to the high permeability of endothelial cell layers derived from macrovascular vessels, precise determination of their barrier function towards ion movement requires refined experimental techniques. We thus cultured bovine aortic endothelial cells (BAEC) directly on thin gold-film electrodes and measured the electrochemical impedance to study their passive electrical properties in general and during beta-adrenergic stimulation. Impedance spectra (10-2.10(6) Hz) of confluent cell monolayers revealed that the electrical characteristics of the cells can be modelled by a simple resistor-capacitor parallel network. Under control conditions the overall resistance of confluent BAEC monolayers was 3.6+/-0.6 Omega.cm2 (n=30) and the capacitance was 0. 6+/-0.1 microF/cm2. Both quantities are discussed with respect to morphological characteristics of these cells. Stimulation of BAECs with the synthetic beta-adrenoceptor agonist isoproterenol leads to a concentration-dependent, highly specific increase of the cell layer resistance characterized by a concentration for half-maximal response (EC50) of 0.3+/-0.1 microM. The cell layer capacitance, however, remained unaffected. Using impedance measurements at a single frequency, we analysed the response of BAECs to treatment with isoproterenol in comparison with several chemically unrelated compounds known to stimulate the adenosine 3',5'-cyclic monophosphate (cAMP)-dependent signal transduction cascade. These studies confirmed that the enhancement of the cell layer resistance after beta-adrenergic stimulation is mediated by an increase in intracellular cAMP.

Adenylyl Cyclases↗
PubMed2003

Membrane-bound and releasable nucleotidase activities: differences in canine mesenteric artery and vein.

1. At least two enzymatic activities are proposed to degrade the extracellular ATP: (i) ubiquitously expressed membrane-bound enzymes (ecto-nucleotidases); and (ii) soluble (releasable) nucleotidases that are released during stimulation of sympathetic nerves and break down neuronal ATP. No quantitative data have placed the magnitude of these nucleotidase activities into a physiological perspective of neurovascular control. 2. We studied comparatively the membrane-bound and releasable nucleotidase activities in canine isolated inferior mesenteric arteries and veins using 1,N6-etheno(epsilon)-nucleotides (i.e. epsilon-ATP, epsilon-ADP, epsilon-AMP and epsilon-adenosine) as exogenous substrates. The enzymatic activities were estimated by measuring the disappearance of the epsilon-substrate and appearance of epsilon-products by means of HPLC-fluorescence detection during either stimulation of sympathetic perivascular nerves (releasable activity) or in the absence of nerve stimulation (ecto-nucleotidase activity). 3. Incubation of vascular segments with 50 nmol/L epsilon-ATP for 60 min resulted in a decrease of the epsilon-ATP substrate by 63.5 +/- 4.6 and 91.2 +/- 6.2% in the artery and vein, respectively. In contrast, the decrease of the epsilon-ATP during electrical field stimulation (EFS; 16 Hz, 0.3 msec, 2 min) was 39.8 +/- 4.2% in the artery and 13.1 +/- 7.3% in the vein. Therefore, the mesenteric arteries demonstrate a greater releasable ATPase activity and a weaker ecto-ATPase activity than mesenteric veins. 4. The degradation of epsilon-ADP and epsilon-AMP was similar in both blood vessels under either experimental protocol. The epsilon-adenosine was not significantly degraded in the absence or presence of EFS. 5. These data implicate a differential removal of extracellular ATP as a potential mechanism of serving resistance and capacitance in the splanchnic circulation.

Animals↗
PubMed1997

Influence of mibefradil on Ca2+ influx induced by vasoactive hormones or depletion of intracellular calcium stores.

The influence of the new calcium antagonist mibefradil (CAS 116666-63-8, Ro 405967) on calcium influx into rabbit smooth muscle cells (VSMC) was studied. Angiotensin II-stimulated divalent cations entry was blocked by mibefradil at micromolar concentrations (1-10 mumol/l). In the same range of concentrations, the antagonist depressed capacitative calcium influx evoked by thapsigargin- and 2,5-di-tert-butylhydroquinone (BHQ)-dependent depletion of internal depots. The ability to block the receptor-mediated pathway of calcium current into VSMC may explain in part the difference between the mode of pharmacological action of mibefradil as compared to other calcium antagonists.

Angiotensin II↗
PubMed1989

Nicorandil as a hybrid between nitrates and potassium channel activators.

Nicorandil, although structurally a nitrate, differs from classic nitrates in several respects. It preferentially dilates resistive vessels. Its effect on venous return in dogs is not unanimously a decrease but rather an increase. In high doses or concentrations it suppresses myocardial contraction and ventricular automaticity, nearly sparing sinoatrial nodal automaticity and atrioventricular nodal conduction. It shortens the effective refractory period of myocardium. These cardiac effects of nicorandil have been explained by its mechanism of action as a potassium (K) channel activator. However, what part of the vascular effects of nicorandil this mechanism is responsible for has not been determined. BRL 34915 and pinacidil, nonnitrate vasodilators with a K-channel activator action, have essentially the same cardiovascular profile as nicorandil in isolated, blood-perfused canine heart preparations. In anesthetized, open-chest dogs the 2 K-channel activators decreased systemic blood pressure and increased venous return and cardiac output without elevating heart rate, unless the cardiodepressant effect emerged. The increase in venous return or cardiac output survived elimination of baroceptor functions. These results taken together with previous results on nicorandil suggest the following: (1) The property of nicorandil as a resistive vessel dilator highly selective for vasculature originates in its mechanism of action as a K-channel activator. The nonunanimous effect of nicorandil on venous return is a result of the opposing actions as a capacitive (action as a nitrate) and a resistive vessel dilator. Nicorandil, with its hybrid nature, is advantageous over specific K-channel activators and classic nitrates in therapeutic implications.

Animals↗
PubMed1998

Effects of superoxide anions on endothelial Ca2+ signaling pathways.

Although the involvement of free radicals in the development of endothelial dysfunction under pathological conditions, like diabetes and hypercholesterolemia, has been proposed frequently, there is limited knowledge as to how superoxide anions (O2-) might affect endothelial signal transduction. In this study, we investigated the effects of preincubation with the O2(-)-generating system xanthine oxidase/hypoxanthine (XO/HX) on mechanisms for Ca2+ signaling in cultured porcine aortic endothelial cells. Incubation of cells with XO/HX yielded increased intracellular Ca2+ release and capacitative Ca2+ entry in response to bradykinin and ATP in a time- and concentration-dependent manner. This effect was prevented by superoxide dismutase but not by the tyrosine kinase inhibitor tyrphostin A48. In addition, capacitative Ca2+ entry induced by the receptor-independent stimulus 2,5-di-(tert-butyl)-1,4-benzohydroquinone or thapsigargin was enhanced in O2(-)-exposed cells (+38% and +32%, respectively). Increased Ca2+ release in response to bradykinin in XO/HX-pretreated cells might be due to enhanced formation of inositol-1,4,5-trisphosphate (+140%). Exposure to XO/HX also affected other signal transduction mechanisms involved in endothelial Ca2+ signaling, such as microsomal cytochrome P450 epoxygenase and membrane hyperpolarization to Ca2+ store depletion with thapsigargin (+103% and +48%, respectively) and tyrosine kinase activity (+97%). A comparison of bradykinin-initiated intracellular Ca2+ release and thapsigargin-induced hyperpolarization with membrane viscosity modulated by XO/HX (decrease in viscosity) or cholesterol (increase in viscosity) reflected a negative correlation between bradykinin-initiated Ca2+ release and membrane viscosity. Because intracellular Ca2+ is a main regulator of endothelial vascular function, our data suggest that O2- anions are involved in regulation of the vascular endothelium.

Adenosine Triphosphate↗
PubMed1988

Effects of Ca++-antagonists on systemic capacitance vessels and venous return curves of dogs--a study with mean circulatory pressure.

We measured mean circulatory pressure (MCP) in anesthetized, open-chest dogs before and after intravenous administration of Ca++-antagonists to estimate the effects on systemic capacitance vessels and on venous return (VR) curves both with and without continuous intravenous infusion of norepinephrine (NE). Diltiazem (300 micrograms/kg) decreased total peripheral resistance (TPR) and MCP significantly. Nifedipine (5 micrograms/kg), nicardipine (30 micrograms/kg) and verapamil (200 micrograms/kg) decreased TPR significantly without any change in MCP in the absence of NE, but with the exception of verapamil, they decreased MCP in the presence of NE. This indicates that diltiazem relaxed the systemic capacitance vessels, and nifedipine and nicardipine significantly decreased the tone of the systemic capacitance vessels that had been previously elevated by NE, but this action was very slight with verapamil. These Ca++-antagonists rotated VR curves clockwise, decreased resistance to VR (RVR) and increased VR both in the presence and absence of NE. It was suggested that the decrease in the RVR would be at least partially responsible for the increase in the VR.

Animals↗
PubMed2000

Coronary and systemic hemodynamic effects of clevidipine, an ultra-short-acting calcium antagonist, for treatment of hypertension after coronary artery surgery.

BACKGROUND: The aim was to evaluate the use of clevidipine, a new vascular selective, ultra-short-acting calcium antagonist for blood pressure control after coronary artery bypass grafting (CABG). METHODS: The effects of clevidipine on central hemodynamics, myocardial blood flow and metabolism were studied at two different phases after CABG. In phase 1 (n=13), the hypertensive phase, the effects of clevidipine were compared to those of sodium nitroprusside (SNP) when used to control postoperative hypertension. In phase 2 (n=9), the normotensive phase, a clevidipine dose-response relationship was established. RESULTS: At a target mean arterial pressure (MAP) of 75 mmHg, systemic vascular resistance (SVR) and heart rate (HR) were lower, preload, stroke volume (SV) and pulmonary vascular resistance (PVR) were higher, while there were no differences in myocardial lactate metabolism or oxygen extraction with clevidipine compared to SNP. In the normotensive phase, clevidipine induced a dose-dependent decrease in MAP (-19%), SVR (-27%) and PVR (-15%), accompanied by an increase in SV (10%), but no reflex increase in HR or changes in cardiac preload. Clevidipine caused a direct coronary vasodilation, as indicated by a decrease in myocardial oxygen extraction from 54% to 45%. Myocardial lactate metabolism was unaffected by clevidipine. The blood clearance of clevidipine was 0.05 l x min(-1) x kg(-1), the volume of distribution at steady state was 0.08 l x kg(-1) and the initial and terminal half-lives were <1 min and 4 min, respectively. CONCLUSIONS: Clevidipine rapidly reduced MAP and induced a systemic, pulmonary and coronary vasodilation with no effect on venous capacitance vessels or HR. Clevidipine caused no adverse effects on myocardial lactate metabolism. Clevidipine thus appears suitable to control blood pressure after CABG.

Antihypertensive Agents↗
PubMed1999

Nasal nitric oxide does not control basal nasal patency or acute congestion following allergen challenge in allergic rhinitis.

Nasal nitric oxide (NO), a powerful vasodilator, could control the filling of nasal capacitance vessels, thus determining nasal patency and mediating the acute congestion accompanying allergen challenge. We examined the effect of topical N-nitro-L-arginine-methyl-ester (L-NAME; 100 to 200 mg), an NO synthase inhibitor, on nasal NO and on nasal patency assessed by acoustic rhinometry in 7 subjects with nasal allergy, and in 4 subjects we examined the effects of nasal allergen challenge on nasal NO before and after a short course of nasal steroid. After L-NAME, nasal NO fell to 42.1%+/-15.7% of baseline (p < .0001) with no significant change in minimal cross-sectional area. After allergen challenge, acute congestion was associated with a significant fall in nasal NO, which returned to baseline by 4 hours, when the congestion resolved. Repeat challenge after 2 weeks of nasal corticosteroid yielded similar findings. A role for NO in modulating vascular tone was not supported by the present study.

Acute Disease↗
PubMed1983

[Instrumental diagnosis of deep venous thrombosis. Prospective study with non-invasive methods].

The clinical diagnosis of deep vein thrombosis is unreliable and venography remains the best single method of investigation. In the last ten years several non-invasive procedures have been introduced in the vascular laboratories, sometime without adequate assessment of their reliability. We tested sensitivity and specificity of three different non-invasive procedures, namely phleboscintigraphy with 99Technetium, Doppler ultrasound technique and strain-gauge plethysmography in patients with clinically suspected deep vein thrombosis of lower limbs or pulmonary embolism. A total of 288 patients entered the study. Venography was used as the reference standard and was assessed independently, without knowledge of the results of non-invasive methods. In the first 36 patients phleboscintigraphy and Doppler ultrasound were evaluated: sensitivity and specificity of phleboscintigraphy resulted only a little more than 50%; the method was therefore considered unreliable and subsequently abandoned. Doppler ultrasound could be evaluated upon a total of 81 patients, showing an unsatisfactory sensitivity (63%), but a quite reliable specificity (86%). Best results were obtained with strain-gauge plethysmography, using maximal venous outflow and venous capacitance as diagnostic parameters. 209 patients entered this study, and a sensitivity of about 90% with a specificity of about 95% was observed. If we consider only acute proximal deep vein thrombosis, sensitivity approaches 97%, while it is only 60% in distal deep vein thrombosis.

Adolescent↗
PubMed2002

Release from intracellular stores is responsible for calcium signaling with von Willebrand factor in human platelets.

Interaction of von Willebrand factor (VWF) with the platelet promotes hemostasis upon vascular injury. Such interaction raises intracellular free calcium concentration ([Ca2+]i) and induces platelet activation. The platelet [Ca2+]i increase is generally attributed to influx across the plasma membrane. The present study defined the contribution of intracellular calcium stores. Platelet [Ca2+]i was monitored with Fura-PE3. Ristocetin-mediated binding of VWF transiently elevated [Ca2+]i after a lag phase. Studies with 63 healthy donors consistently revealed a VWF-induced platelet [Ca2+]i signal in the absence of extracellular calcium; there was only modest enhancement with extracellular calcium. Blockade of plasma membrane calcium channels did not diminish the signal, whereas depletion or blockade of the intracellular calcium stores abolished it. These findings imply that release from intracellular stores is responsible for the VWF-induced platelet [Ca2+]i increase. Influx across the plasma membrane plays no more than a minor role, probably representing "capacitative entry" to refill the intracellular stores.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed2006

Different mechanisms between thromboxane A2- and leukotriene D4-induced nasal blockage in guinea pigs.

Although thromboxane (TX)A2 is involved in allergic rhinitis, the mechanisms inducing nasal blockage have not been elucidated. We evaluated the roles of nasal mucosal vascular changes following intranasal instillation of the TXA2 analog U-46619 or leukotriene (LT)D4 to induce nasal blockage in a guinea pig model of allergic rhinitis. Both U-46619- and LTD4-induced nasal blockages in sensitized animals were swiftly and completely suppressed by a vasoconstrictor, naphazoline. The nitric oxide synthase inhibitor N(omega)-nitro-l-arginine methyl ester relieved LTD4-induced nasal blockage, but not U-46619-induced nasal blockage. Although both agonists produced vasodilatation of nasal mucosa in vivo, LTD4 caused vasodilatation while U-46619 caused vasoconstriction in vitro. Both LTD4- and U-46619-induced nasal blockages in vivo should depend on vasodilatation of nasal mucosa. LTD4-induced nasal blockage is induced by direct vasodilatation via nitric oxide. In contrast, U-46619-induced nasal blockage may be associated with contraction of a certain vein that should exist at the exit of capacitance vessels, leading to congestion of the nasal mucosa.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1993

Early structural changes in hypertension: pathophysiology and clinical consequences.

The structural upward resetting of heart, vessels, and barostat functions represents what may be the most important long-term cardiovascular alteration in hypertension; the altered geometric design of the systemic precapillary resistance vessels is of profound hemodynamic relevance. This is especially true in primary (essential) hypertension, for which three major etiological elements can be distinguished: polygenetic predisposition, environmental factors, and the structural factor. The physical and biological principles behind the early "structural upward resetting" of heart and vessels in hypertension are outlined and experimentally illustrated. Further, the long-term hemodynamic effects of this per se "normal" structural adaptation are discussed, particularly concerning systemic precapillary resistance, but also concerning the heart, barostat mechanisms of reflex and renal nature, and the venous capacitance vessels. With this background in mind, the primary long-term goal of therapy must be to reverse these structural changes toward normal cardiovascular design and dimensions, whereas in the future preventive measures may be actualized. Thus, treatment should serve not only to reduce the increased load on heart and vessels but also, wherever possible, to reduce the influence of trophic, growth-promoting factors of local and remote nature, as exemplified by model studies in rats.

Animals↗
PubMed1994

Head-up tilt and hemodynamic changes during orthostatic hypotension in patients with supine hypertension.

OBJECTIVES: This study assessed the mechanism(s) of the decrease in upright blood pressure in patients with supine hypertension by using the tilt test and a hemodynamic approach. BACKGROUND: Orthostatic hypotension in patients with supine hypertension creates a pathophysiologic and therapeutic dilemma. METHODS: We studied 28 consecutive patients with history of orthostatic intolerance amounting to recurrent syncope in 13 of them (15 men, 13 women; mean [SD] age 65 +/- 11 years). They all had supine hypertension (systolic blood pressure > 160 mm Hg) and orthostatic hypotension (found to be a decrease in systolic blood pressure > 30 mm Hg during tilt test). Cardiac output, cardiopulmonary volume and systemic resistance were assessed by radionuclide first-pass technique (technetium-99m red blood cell tagging). Total blood volume was determined by radioiodinated serum albumin, and the ratio of cardiopulmonary to total blood volume was used as an index of venous capacitance. RESULTS: Twenty-one patients had accentuated venous pooling defined as a tilt-induced decrease in cardiopulmonary volume/total blood volume ratio > 15% from baseline or a supine ratio < 14% (normal 16% to 18%), or both. Seven of the 28 patients had autonomic insufficiency; 6 of the 7 also had venous pooling; 1 patient had autonomic insufficiency only. Neither clinical history nor changes during tilt differentiated the subgroups. Plasma catecholamine levels increased during head-up tilt in all subgroups, and differences in their increase were not significant between patients with venous pooling and those with autonomic insufficiency. However, radionuclide hemodynamic variables revealed that patients with venous pooling compensated for the decrease in stroke volume by increasing peripheral resistance, whereas patients with autonomic dysfunction did not. CONCLUSIONS: Orthostatic hypotension in patients with supine hypertension may have multiple etiologies. Hemodynamic assessment with determination of cardiopulmonary volume and systemic vascular resistance differentiated between venous pooling and autonomic insufficiency in these patients; head-up tilt and plasma catecholamine levels did not. These findings may have important therapeutic implications.

Adult↗
PubMedDate not supplied

Effect of regional heating of upper body on the liver blood flow in rats.

The changes in rat liver blood flow, caused by hyperthermia, were studied. The liver region of rats was heated with Thermotron IV, an experimental capacitive heating device utilizing 8 MHz RF, and the liver blood flow was measured with radioactive microspheres. Portal venous blood flow slightly decreased during 30 min heating of the liver at 41 degrees C and returned to control level after the heating. When the liver was heated at 43 degrees C, portal venous blood flow decreased initially by about 20%, but gradually returned to control level during the 30 min heating. Hepatic arterial blood flow increased slightly during 30 min heating at 41 degrees C and 43 degrees C. Because almost 85% of the liver blood flow is portal venous blood flow, the change in total liver blood flow paralleled the change in portal venous blood flow. During regional heating of the liver the cardiac output declined significantly, which may account in part for the decrease in splanchnic blood flow, and thus portal venous blood flow. Changes in vascular resistance in the viscera may be another reason for the decrease in portal venous blood flow during heating of the liver region.

Animals↗
PubMed2003

Rho-dependent kinase is involved in agonist-activated calcium entry in rat arteries.

The present study was aimed at investigating whether, besides its pivotal role in Ca(2+)-independent contraction of smooth muscle, Rho-kinase is involved in the mechanisms underlying the Ca2+ signal activated by noradrenaline in arteries. In rat aorta and mesenteric artery, the Rho-kinase inhibitor Y-27632 (10 microM) completely relaxed the contraction evoked by noradrenaline (1 microM) and simultaneously inhibited the Ca2+ signal by 54 +/- 1 % (mesenteric artery) and 71 +/- 15 % (aorta), and the cell membrane depolarisation by 56 +/- 11 % (mesenteric artery). A similar effect was observed in arteries contracted by AlF4-, while in KCl-contracted arteries, Y-27632 decreased tension without changing cytosolic Ca2+. The same effects were observed with another inhibitor of Rho-kinase (HA1077) but not with an inhibitor of protein kinase C (Ro-31-8220). Effects of Y-27632 were not prevented by incubating the artery in 25 mM KCl, with K+ channel blockers or with the Ca2+ channel blocker nimodipine. Y-27632 did not affect either the increase in the production of inositol phosphates activated by noradrenaline, or the release of Ca2+ from non-mitochondrial stores evoked by InsP3 in permeabilised aortic cells, or the Ca2+ signals evoked by thapsigargin or caffeine. The capacitative Ca2+ entry activated by thapsigargin was not impaired by Y-27632, but the entry of Ba2+ activated by noradrenaline in the presence of nimodipine was blocked by 10 microM Y-27632. These results indicate that Rho-kinase is involved in noradrenaline activation of a Ca2+ entry distinct from voltage- or store-operated channels in rat arteries.

Aluminum Compounds↗
PubMed1994

Venoconstriction of hepatic capacitance vessels during hemorrhage in cats: afferent mechanisms.

Cats anesthetized with pentobarbital sodium were hemorrhaged (1 ml.min-1.kg body wt-1) until arterial pressure declined to 55 mmHg. Hepatic volume was recorded by plethysmography. Hemorrhage volume was 21.1 +/- 4.7 (SD) ml/kg, and hepatic volume declined by 4.0 +/- 1.7 ml/kg. These responses were markedly reduced by four procedures that prevented decreases in carotid arterial and central venous pressures and eliminated vagal conduction. When any three of these four procedures were carried out, the remaining stimulus caused a significant increase in the size of the hepatic volume decrease. The results suggest that arterial receptors (baro- and/or chemoreceptors) in the carotid arterial bed or brain and venous baroreceptors in the right atrium and superior and inferior venae cavae are involved in hepatic capacitance responses to hemorrhage. The responses were linearly related to the stimuli, and hepatic blood volume changed by 1.7 +/- 1.1 and 0.030 +/- 0.016 ml/kg for each 1-mmHg change in venous and carotid arterial pressures, respectively. The maximal responses to these afferent stimuli applied individually were not significantly different (-4.2 +/- 1.8 ml/kg) and were not additive, suggesting overlapping redundant systems. The possibility of baroreceptors in superior vena cava has not previously been documented.

Afferent Pathways↗
PubMed1975

[Effect of potassium ions on the reactions of resistive and capacitive vessels in the skeletal muscles and intestines].

L. a. administration of 4.2% KCl was followed by contractile responses of the resistance intestinal vessels, whereas contractile-dilatatory responses were observed in the skeletal muscles. The intestinal capacitance vessels responded with insignificant increase of the venous outflow, while the contractile-dilatatory responses of the resistance vessel were not followed by any increase of the venous outflow in skeletal muscles. After papaverin administration, contractile responses of the resistance intestinal vessels were insignificant, while the contractile-dilatatory responses of the skeletal muscles resistance vessels became contractile only. After noradrenaline injections only contractile responses were observed in the resistance intestinal vessels.

Animals↗
PubMed1995

Neuropeptide Y in human hand veins: pharmacologic characterization and interaction with cyclic guanosine monophosphate-dependent venodilators in vivo.

The dorsal hand vein compliance technique was used to study direct vascular effects of human neuropeptide Y in vivo. Human neuropeptide Y is an endogenous vasoconstrictor peptide that is costored with norepinephrine in sympathetic nerve endings and coreleased with the catecholamine under various physiologic and pathologic conditions. Compared with the alpha 1-adrenergic agonist phenylephrine (geometric mean dose-rate that produces the half-maximal response [ED50]: 1.05 nmol/min; maximum venoconstriction [Emax] +/- SEM, expressed as a percentage of baseline compliance: 91% +/- 3%), human neuropeptide Y was nine times more potent (geometric mean ED50: 0.122 nmol/min; p < 0.001) but markedly less efficacious (Emax: 58% +/- 4%; n = 12; p < 0.001). Venoconstrictor effects of human neuropeptide Y lasted several hours and were unchanged by simultaneous administration of alpha-adrenergic antagonists but were readily reversed by nitroglycerin or bradykinin. The high responsiveness of subcutaneous veins to human neuropeptide Y indicates that human neuropeptide Y may regulate venous compliance and filling of the venous subcutaneous capacitance bed in vivo.

Adult↗