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At least 685 records · Page 38Linked to original sources
PubMed1985

Capacitive effects on canine coronary artery diastolic pressure-flow relationships.

The extent of capacitive effects on coronary diastolic pressure-flow relationships was investigated by proposing a theoretical model and by actually measuring the time constants of the coronary and systemic circulation. The dynamic pressure-flow relationship obtained by an aortic declining pressure perfusion and the static pressure-flow relationship obtained by constant pressure reservoir perfusion were compared to support the theoretical model, which revealed that the capacitive effects could be quantified by the alpha value, i.e. the ratio of the time constants of the coronary and systemic circulations. In 10 anesthetized dogs, the two independent methods disclosed that capacitive effects are limited and diastolic outflow pressure in the coronary circulation is the static zero-flow pressure intercept determined by the vascular tonus and intramyocardial pressure.

Animals↗
PubMed1991

[Changes in the intraorganic blood vessels of the stomach and duodenum in peptic ulcer].

It was established that the ulceration zones showed hyperemia which increases the volume density of venous vessels, disturbs the permeability of their walls, causes trophic disorders with subsequent phlebosclerosis, limitation of capacitance, appearance of venous hypertension and further changes of the vessel wall structures and neighbouring tissues. Compensatory reaction of the arterial intraorganic bed (vascular spasm) deteriorates trophic disorders. Simultaneous increase of the volume density of arterial vessels in the "intact" zone favours reparative and compensatory capacities of the latter. Repeat ulcer formation and chronic course of the disease furthers development of hemo- and microcirculatory disorders, progressing of angio- and perivascular sclerosis, reorganization of the intramural gastric and duodenal vascular bed.

Acute Disease↗
PubMed1990

[The regional circulation of the parotid gland in Sjögren's disease].

Morphological methods, rheography and coagulography were used to study regional circulation in the parotid salivary gland (PSG) in 20 patients with the primary dry syndrome (Sjögren's disease). It has been established that in the presence of immune inflammation with the predominance of traits characteristic of delayed-type hypersensitivity, the vascular bed of the PSG undergoes transformation (changes in the tone, elasticity of vessels, blood flow rate, dystonia of resistive and atonia of capacitance microvessels, lymphostasis, and so forth). The changes in regional circulation are not infrequently coupled with a high concentration of fibrinogen and low fibrinolytic activity of the blood tending towards hypercoagulation.

Adult↗
PubMed1986

Augmentation of venous return by adrenergic agonists during spinal anesthesia.

To test the effectiveness of adrenergic agonists in correcting the vascular sequelae of spinal anesthesia, we used venous reservoir volume (RV) and mean arterial pressure (MAP) as indices of the changes in venous capacitance and arterial resistance produced by adrenergic agonists in dogs anesthetized with pentobarbital and undergoing cardiopulmonary bypass (CPB). A CPB-based technique was chosen both to prevent drug and reflex effects on the heart from influencing the results and to provide a convenient means by which to monitor venous capacitance. Total spinal anesthesia significantly decreased both RV and MAP relative to steady-state CPB values. Return of these hemodynamic alterations to baseline was attempted using pure alpha- and beta-adrenergic agonists, and a mixed adrenergic agonist (phenylephrine, isoproterenol, and ephedrine, respectively). Isoproterenol increased RV, but further decreased MAP. Phenylephrine increased MAP but not RV. Ephedrine increased both MAP and RV. We conclude that a mixed adrenergic agonist such as ephedrine more ideally corrects the noncardiac circulatory sequelae of spinal anesthesia than does either a pure alpha- or beta-adrenergic agonist.

Adrenergic alpha-Agonists↗
PubMed1985

[Doppler ultrasound and strain gauge plethymography in the diagnosis of the post-phlebitic syndrome].

Certain non-invasive techniques like Doppler CW and strain gauge plethysmography are highly effective ways of evaluating the natural history of postphlebitic syndrome. 40 patients of both sexes, average age 51.5 +/- 6.9 with a history of deep venous thrombosis (28 documented phlebographically) were subjected to Doppler tests with assessment of venous blood pressure and bilateral strain gauge plethysmography. 34 of the 40 suspected PPS cases were confirmed, though not all cases were at the same stage. Persistent deep venous thrombosis was found in five of the extremities and the last one examined revealed a primary varicose syndrome. A comparison of the Doppler and phlebography results showed both to be highly sensitive techniques (100% accuracy). When the contralateral limbs were examined, the Doppler technique revealed 7 cases of PPS and 21 primary varices. In contrast strain gauge plethysmography identified all 28 cases of increased venous capacitance as primary varices, thus confirming the inability of this technique to distinguish between the various varicose conditions. Assuming the presence of a vascular diagnosis laboratory where both techniques are available, strain gauge plethysmography is recommended as the examination of choice. This technique is simple and fast to perform and can provide extensive information whether at rest (filling and emptying volumes and times; venous tone and distensibility, venous blood pressure at rest) or in movement (venous pressure when standing, muscular pumping index). Hence plethysmography can reveal any canalisation present even in the earliest stages though it cannot pinpoint the precise site of the deep obstruction. The longer, more complex Doppler CW procedure should be reserved for secondary investigations. This technique is preferable to plethysmography when a more accurate assessment of the degree, site and extension of the venous recanalisation is needed. Doppler CW also provides information on any valvar sequelae since it records the direction of the blood flow in the presence of a substitution syndrome (increased venous flow in the surface vessels). Finally if used in a rational manner the two techniques can be combined to eliminate contrast medium techniques, which would only be adopted as a preoperative measure.

Adult↗
PubMed2000

The effect of propofol on angiotensin II-induced Ca(2+) mobilization in aortic smooth muscle cells from normotensive and hypertensive rats.

UNLABELLED: We studied the effect of propofol (5.6-560 micromol/L; 1-100 microg/mL) on the mechanisms involved in Ca(2+) mobilization elicited by angiotensin II (AngII) in Wistar Kyoto (WKY) and spontaneously hypertensive (SHR) rats. We studied the variations in intracellular Ca(2+) ([Ca(2+)](i)) concentrations in cultured aortic vascular smooth muscle cells (VSMCs) isolated from 6-wk-old WKY and SHR rats loaded with the Ca(2+)-sensitive fluorescent dye, Fura-2, using fluorescent imaging microscopy. In the absence of external Ca(2+), AngII (1 micromol/L) induced a transient [Ca(2+)](i) mobilization from internal stores that was larger in SHR than in WKY rats. Ca(2+) influx was assessed after external Ca(2+) (1 mmol/L) reintroduction. Propofol (1-100 microg/mL) added 5 min before the experiments did not alter AngII-induced Ca(2+) release from internal stores in either strain. By contrast, Ca(2+) influx elicited by AngII was significantly decreased by propofol. This effect occurred at a smaller concentration of propofol in the SHR than in the WKY rats. When Ca(2+) stores were depleted by exposure of cells to thapsigargin, an inhibitor of the sarcoendoplasmic reticulum Ca(2+)-ATPase, reintroduction of Ca(2+) to the medium induced a capacitative Ca(2+) influx of similar magnitude than that elicited by AngII. This influx was also significantly decreased by propofol at 100 microg/mL ( WKY: 27 +/- 3% of control values, n = 107; SHR: 16 +/- 3%, n = 47; P < 0.001). In conclusion, propofol decreased AngII-induced Ca(2+) influx through voltage-independent channels, without altering Ca(2+) release from internal stores in aortic VSMCs. The hypertensive rats were found to be more sensitive to the effect of propofol than the normotensive rats. This suggests that the response of VSMCs to AngII may be altered by propofol. IMPLICATIONS: In rat aortic vascular smooth muscle cells, propofol reduced angiotensin II-elicited Ca(2+) entry through capacitative Ca(2+) channels without altering Ca(2+) release from intracellular stores. Spontaneously hypertensive rats were more sensitive to these effects of propofol than normotensive rats. The response of vascular smooth muscle cells to angiotensin II may be altered by propofol.

Anesthetics, Intravenous↗
PubMed2004

Vasodilatory mechanism of unoprostone isopropyl on isolated rabbit ciliary artery.

PURPOSE: To clarify the vasodilatory mechanism of unoprostone isopropyl (unoprostone), a PG F2alpha related compound used for treatment of glaucoma, we have investigated the effect of this drug and its metabolites on isolated rabbit ciliary artery in vitro. METHODS: Under the dissecting microscope, ciliary arteries were prepared from albino rabbit eyes and mounted in a myograph system. The effects of unoprostone isopropyl and other agents were investigated using isometric tension recording methods. RESULTS: Unoprostone induced a dose-dependent relaxation in ciliary arteries that were pre-contracted with high-K solution, 10 microM histamine or 10 microM PG F2alpha. Neither unoprostone metabolite M1 or M2 had a relaxant effect on the precontracted vessels. Relaxation was unaffected by inhibition of adenylyl cyclase with SQ 22536, guanylyl cyclase with ODQ, or maxi-K channels with iberiotoxin. Pretreatment with unoprostone did not affect histamine-induced transient contractions in Ca2+ -free solution. However, SKF96365, a general Ca2+ channel blocker, evoked relaxation similar to unoprostone with respect to amplitude and rate of onset. CONCLUSIONS: Unoprostone, but not its metabolites M1 and M2, relaxed pre-contracted rabbit ciliary artery. The mechanism of vascular smooth muscle relaxation by unoprostone differs from that of IOP reduction and does not depend on adenylyl cyclase, guanylyl cyclase, or maxi-K channels. Relaxation may be mediated by inhibition of Ca2+ entry, possibly through capacitative Ca2+ channels.

Adenine↗
PubMed1995

The H2O2-generating enzyme, xanthine oxidase, decreases luminal Ca2+ content of the IP3-sensitive Ca2+ store in vascular endothelial cells.

OBJECTIVE: Xanthine oxidase inhibits agonist-stimulated Ca2+ signaling in calf pulmonary artery endothelial cells by an H2O2-dependent mechanism. We investigated the effect of xanthine oxidase on luminal Ca2+ content of the inositol-1,4,5-trisphosphate (IP3)-sensitive Ca2+ store. METHODS: Luminal Ca2+ content was estimated from the net release of Ca2+ activated by 2,5-di-t-butylhydroquinone (BHQ), an inhibitor of microsomal Ca2+ pumps. RESULTS: Initially, xanthine oxidase depleted the IP3-sensitive Ca2+ store of releasable Ca2+, but with more prolonged incubation, the enzyme also depleted non-IP3-sensitive stores. In addition, xanthine oxidase inhibited capacitative Ca2+ influx. Similar results were observed when thapsigargin was substituted for BHQ. CONCLUSIONS: Depletion of luminal Ca2+ content within the IP3-sensitive Ca2+ store contributes to xanthine oxidase inhibition of Ca2+ signaling in vascular endothelial cells.

Animals↗
PubMed1992

The inhibitory effect of halothane on mesenteric venoconstriction and related reflex responses during acute graded hypoxia in rabbits.

Systemic hypoxia is a common abnormality encountered frequently in the clinical setting that produces compensatory cardiopulmonary changes affecting heart rate, blood pressure, peripheral vascular resistance, and respiratory drive. These changes are known to be inhibited or reversed by inhaled anesthetics. More recently, chemoreflex-mediated constriction of capacitance veins has been identified as a mechanism that contributes significantly to the hemodynamic adjustments during hypoxia. However, the effects of anesthetics on this response have not been clarified. The current study was designed to quantify sympathetically mediated mesenteric venoconstriction as well as heart rate and blood pressure responses to acute graded hypoxia; to identify the inhibitory effects of inhaled halothane on these responses; and to estimate the contribution of the peripheral chemoreceptors in mediating these changes. Changes in mesenteric vein diameter were measured in alpha-chloralose anesthetized rabbits in situ with simultaneous changes in heart rate and blood pressure during 40-s periods of 10%, 5%, 2.5%, and 0% inspired O2 administered sequentially before, during, and after 1% or 1.25% inhaled halothane. Sympathetic efferent nerve activity also was measured, and, in a separate group of animals, measurements were preceded by carotid chemoreceptor denervation. Hypoxia-mediated venoconstriction, bradycardia, and hypertension were attenuated almost equally by both 1% and 1.25% inhaled halothane (the higher dose produced only slightly greater inhibition). These responses were inhibited significantly in chemoreceptor-denervated animals, and the subsequent 1% inhaled halothane added only minimal additional attenuation. Increases in chemoreflex-mediated sympathetic efferent nerve activity also were reduced significantly by (1.25%) inhaled halothane. These results indicate that halothane impairs capacitance vein responses and other hemodynamic adjustments during hypoxia. Inhibition of these compensatory changes appears to be mediated, at least in part, via attenuation of peripheral chemoreflex responses and suppression of the resultant reflex increases in sympathetic efferent nerve activity.

Acute Disease↗
PubMed2006

Physiological mechanisms dissociating pulmonary CO2 and O2 exchange dynamics during exercise in humans.

During moderate exercise (below the lactate threshold, (thetaL)), muscle CO(2) production ( Q(CO2)) kinetics are monoexponential, with a time constant (tau) similar to that of O(2) consumption. Following a delay incorporating the muscle-lung vascular transit time, Q(CO2) is expressed at the lungs (V(CO2)) with an appreciably longer tau, reflecting the influence of intervening high-capacitance CO(2) stores. Above (thetaL), kinetics become complex, resulting from the conflation of the differing rates of HCO(3)(-) breakdown and degrees of compensatory hyperventilation with that of the underlying aerobic component. During incremental exercise, the increased rate of relative to pulmonary O(2) uptake (V(CO2)) can be used to quantify (thetaL) validly if aerobic and hyperventilatory sources can be ruled out, i.e. (thetaL) is then attributable to the decrease in muscle and blood [HCO(3)(-)]. In many cases, however, very rapid incrementation of work rate and/or prior depletion of CO(2) stores (by volitional or anticipatory hyperventilation) can yield a 'false positive' non-invasive estimation of (thetaL) ('pseudo-threshold') resulting from a slowing of the rate of wash-in of transient CO(2) stores.

Anaerobic Threshold↗
PubMed1986

Atrial natriuretic peptide decreases circulatory capacitance in areflexic rats.

The short-term hemodynamic response to atrial natriuretic peptide appears to be partly mediated by decreased venous return, which could result from increased circulatory capacitance or decreased blood volume. To determine if rat atrial natriuretic peptide 99-126 (0.5 microgram/kg/min IV for 30-70 minutes) dilated capacitance vessels or decreased blood volume, mean circulatory filling pressure (measured during brief circulatory arrest by inflating an intraatrial balloon) and blood volume (51Cr-erythrocytes) were measured in anesthetized rats. Mean circulatory filling pressure, central venous pressure, and blood volume decreased by 0.4 mm Hg, 0.5 mm Hg, and 3.4 ml/kg, respectively. To determine the total circulatory pressure-volume relationship without influence from autonomic reflexes, mean circulatory filling pressure and blood volume were measured in spinal-cord-transected rats before and immediately after infusing or withdrawing 5 ml blood. Atrial natriuretic peptide decreased mean circulatory filling pressure, central venous pressure, and blood volume by 0.9 mm Hg, 1.7 mm Hg, and 8.0 ml/kg, respectively, and displaced the pressure-volume relationship toward the pressure axis by decreasing extrapolated unstressed volume. Similar results were obtained in spinal-cord-transected rats that had initial vascular tone restored to a greater level by norepinephrine infusion. In anephric rats, atrial natriuretic peptide decreased central venous pressure by 0.3 mm Hg and blood volume by 1.6 ml/kg. The results indicate that short-term infusion of atrial natriuretic peptide reduced circulatory capacitance in rats and suggest that this reduction resulted from diminished blood volume due to urinary fluid loss followed by passive vascular recoil and active venoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia, General↗
PubMed1992

Physiologic control. Anatomy and physiology of the airway circulation.

Both for the nose and the lower airways there is an extensive subepithelial capillary network. That for the nose is fenestrated, and this is true for the tracheobronchial tree of rats, guinea pigs, and hamsters, and for that of human asthmatics. However, healthy humans, dogs, and sheep have capillaries without fenestrations except for those close to neuroepithelial bodies and submucosal glands. Deeper in the mucosa there is a capacitance system of vessels, conspicuous in the nose but present also in the lower airways of rabbits and sheep and, to a lesser extent, in those of dogs and humans. Both for the nose and the lower airways, parasympathetic nerves are vasodilator, sympathetic nerves are vasoconstrictor, and sensory nerves are able to release dilator neuropeptides. Most inflammatory and immunologic mediators are vasodilator. A conspicuous difference between the nasal and lower airway vasculatures is the presence of arteriovenous anastomoses only in the former. Countercurrent mechanisms also exist in the nose to increase its efficiency in air conditioning, but they have not been established for the trachea. The pulmonary vasculature could be part of such a system for the bronchi. Distension of the airway vasculature thickens the mucosa, probably both by vascular distension and by edema formation. The latter can lead to exudation into the airway lumen. These processes have not been well quantitated, and the balance sheet of capillary and capacitance vessel volumes, interstitial liquid volume, and exudate volume needs to be worked out in physiologic and pathologic conditions.

Air↗
PubMed1976

Pharmacological basis of the treatment of orthostatic disorders with ergot alkaloids.

Ergot alkaloids increase the tone of isolated canine vein strips dose-dependently in concentrations considerably lower than noradrenaline, but the maximal responses are only about one third of those to noradrenaline. This action can be blocked by prior administration of phentolamine. It is therefore concluded that the long-lasting stimulant action of ergot alkaloids on vascular smooth muscle is mediated mainly by alpha-adrenoceptors. Using the autoperfused hind limb of the cat, it has been shown that dihydroergotamine increases dose-dependently the tone of the capacitance vessels in a manner very similar to electrical stimulation of the sympathetic nerve with increasing frequencies. However, in contrast to sympathetic nerve stimulation, dihydroergotamine elicits only a very weak increase in arteriolar resistance.

Animals↗
PubMed1989

The improvements to a network flow approach to reconstruction of the vascular cross sections from two orthogonal projections.

It is computationally very convenient to view the problem of reconstructing a binary cross section of the coronary arteries from two projections as a flow problem in a capacitated network. The network approach is introduced. In order to speed up this approach some improvements are presented. The improved algorithm is demonstrated by reconstructing several test patterns.

Algorithms↗
PubMedDate not supplied

Structural factors: the vascular wall. Consequences of treatment.

Like all tissues, blood vessels readily adapt their structure upon sustained functional changes. For example, pressure increases soon induce a largely proportional wall (w) thickening, where arteries, veins, and true resistance vessels respond alike. The latter also show a modest structural narrowing of average inner radius (ri), where the increased w/ri ratio results in a geometrically based vascular hyperreactivity. In primary hypertension, this type of precapillary resistance vessel adaptation implies an important "upward structural autoregulation" of systemic resistance, which is thereby kept increased also when vascular smooth muscle activity is entirely normal. Further, the systemic vascular hyperreactivity introduces a positive feedback interaction with functional pressor influences. By this mechanism, even marginal increases in "functional drive" may, if only sustained, steadily enhance the structural w/ri increase until it dominates hemodynamics. Similar alterations of the renal preglomerular vessels cause an early upward resetting of the renal barostat function, while wall thickening of large arteries helps to reset the baroreflexes. Also, the capacitance vessels show some structural adaptation that reduces venous compliance and contributes to blood volume centralization. Due to this overall structural resetting of hypertensive cardiovascular systems, the pharmacological problem of normalizing blood pressure is not one of merely damping an increased vascular smooth muscle activity. The task is more formidable, because effector cell activity must be kept even subnormal, despite counterregulatory mechanisms. These mechanisms almost all have been redesigned to maintain the high pressure state, with the long-range goal that true regression toward normality should ultimately ensue.

Aging↗
PubMed1986

Calcium antagonists and left ventricular function: effects of nitrendipine in congestive heart failure.

Calcium antagonists can affect the arterial vasculature, the venous capacitance vessels and the myocardium. The net effect of these agents on left ventricular (LV) performance depends on the interaction of effects on these 3 vascular components, and the state of LV function at the time that the drugs are administered. A calcium antagonist with profound arterial vasodilator effect might favorably influence LV performance even if it had negative inotropic properties. To demonstrate the direct effect of nitrendipine, a 1,4 dihydropyridine, on LV performance, the acute hemodynamic response to oral nitrendipine was studied in 8 patients with congestive heart failure. Administration of 10 to 20 mg of nitrendipine reduced preload, caused a decrease in both pulmonary wedge pressure and systemic vascular resistance, produced a modest decrease in blood pressure and an increase in stroke volume. In addition, plasma norepinephrine levels were significantly decreased. Plasma renin activity also tended to decrease. These data confirm that the drug can favorably alter performance of the failing left ventricle and further suggest that the vasodilator effect is not accompanied by reflex neurohumoral stimulation.

Adrenergic beta-Antagonists↗