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PubMed1987

'Sodium sensitivity' in man.

Increased cell membrane permeability to sodium is proposed as the initial event leading to high blood pressure in susceptible subjects when sodium intake is increased. All cells, including circulating cells, would be affected, but a key role for endothelial cells in the pathophysiology of the diastolic blood pressure elevation is proposed. Involvement of capillary endothelium could increase capillary permeability to proteins, and thereby would contribute to the altered fluid distribution on the high sodium diet which has been observed. If movement of fluid into the interstitium raised interstitial fluid pressure, venous capacitance would fall and right atrial pressure would rise. Several mechanisms would cause vascular smooth muscle tone to increase. Altered fluid distribution correlates with the rise in diastolic blood pressure from reduced sodium to high sodium diet, but arteriolar constriction would reduce capillary flow so altered fluid distribution occurs first. Arteriolar constriction could serve as a negative feedback to the raised atrial filling pressure by reducing raised capillary flow, which would decrease both altered fluid distribution and interstitial fluid pressure rise. Consequently, diastolic blood pressure would be chronically raised in 'sodium sensitive' subjects taking increased amounts of sodium in the diet. The relationship of the findings to "essential" hypertension and to premorbid cardiovascular sequelae, and the key role of capillary endothelium in the development of "essential" hypertension is discussed.

Adult↗
PubMedDate not supplied

Haemodynamic dose-response effects of intravenous amrinone in left ventricular failure complicating acute myocardial infarction.

The haemodynamic dose-response effects of intravenous amrinone were measured in 16 male patients, aged 40-65 years, with radiographic and haemodynamic evidence of left ventricular failure 4-18 h after acute myocardial infarction. After a l-h control period to confirm stable haemodynamic baseline variables, patients were randomised to either low-dose (200-400-800 micrograms/kg/h) or high-dose (800-1600-3200 micrograms/kg/h) intravenous amrinone. Each of the three infusions was given consecutively over 30 min (total infusion time 90 min) in each group, and haemodynamic measurements were made at the end of each infusion step. No arrhythmias or other untoward side effects, including haematological changes, were observed during the infusions. In both groups, intravenous amrinone reduced the pulmonary artery-occluded pressure (PAOP) (p less than 0.01), increased the cardiac output (p less than 0.05), and reduced the systemic vascular resistance (p less than 0.05). The reductions in PAOP and systemic arterial diastolic pressure and the increase in heart rate were directly dose-related, but the changes in cardiac output and systemic vascular resistance were not. These results suggest that peripheral vasodilation, particularly of venous capacitance vessels, as well as positive inotropic stimulation, may play a role in the haemodynamic changes induced by intravenous amrinone in acute ischaemic left ventricular failure.

Adult↗
PubMed2001

A mathematical model of the fetal cardiovascular system based on genetic algorithms as identification technique.

The development of fetal cardiac surgery, considered the ultimate goal in the treatment of congenital cardiac malformations, needs to be supported by detailed knowledge of the blood circulation in the fetal cardiovascular system. The hemodynamic behavior in distal territories is usually inferred from vessel resistance indices, which give limited physiological information. This study presents a mathematical model of the human fetal global cardiovascular system, developed to clarify the relationships and differences existing between upper and lower body circulation. We modelled the heart with two time-varying capacitances, each representing the respective ventricle's pressure-volume relationship. The fetal vascular system was represented using two six-element Windkessel models, for the upper and lower body respectively. We obtained the identification of the set of circuital and elastance function parameters of the model using Genetic Algorithms (GAs), which follow the laws of evolutionary theory. We compared the results of our numerical study on the model identified with data collected from measurements and literature, to validate the proposed global cardiovascular system model of the human fetus. This model is intended as an instrument to investigate the differences in blood distribution between the different vascular districts in the upper and lower fetal body and the role of the aortic isthmus, the small tract of vessel connecting upper and lower fetal vascular beds; it may also represent a useful tool in the assessment of dynamic balance during mechanical assistance of circulation.

Algorithms↗
PubMed1987

Beta-2 adrenoceptor control of the venous circulation in intact dogs.

The effects of beta-2 adrenoceptor stimulation on the peripheral circulation in 10 dogs were evaluated. All studies were done during ganglion blockade with hexamethonium. Venous capacitance was assessed by measuring mean circulatory filling pressure, venous compliance and unstressed vascular volume. Beta-2 stimulation was achieved with terbutaline (27 micrograms/min) after beta-1 blockade with metoprolol (0.75 mg/kg). At a dose of terbutaline that decreased mean aortic pressure from 80.4 +/- 3.5 to 58.9 +/- 1.9 mm Hg (P less than .01), there was no change in cardiac index (155.8 +/- 10.5 vs. 161.1 +/- 9.1 ml/kg/min) despite an increase in heart rate from 118.6 +/- 5.2 to 132.6 +/- 5.0 beats/min. Right atrial pressure, left ventricular end-diastolic pressure and dP/dt did not change. Systemic vascular resistance decreased from 0.52 +/- 0.02 to 0.39 +/- 0.03 mm Hg . min . kg . ml (P less than .01). Arterial compliance increased from 0.067 +/- 0.003 to 0.088 +/- 0.007 ml/mm Hg/kg and the volume of blood shifted out of the larger arteries was 1.8 +/- 0.4 ml/kg. Mean circulatory filling pressure did not change but venous compliance decreased from 1.90 +/- 0.04 to 1.47 +/- 0.06 ml/mm Hg/kg and unstressed vascular volume increased from -14.5 +/- 0.5 to -8.4 +/- 0.5 ml/kg. Central blood volume increased from 22.8 +/- 1.1 to 27.4 +/- 2.2 ml/kg. There was an increase in total blood volume from 81.1 +/- 2.7 to 90.5 +/- 3.7 ml/kg. To determine the extent to which changes in the spleen were responsible for these observations, five dogs were studied 2 weeks after splenectomy.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

The influence of H1- and H2-receptor blockade on responses of resistance and capacitance vessels to noradrenaline in working skeletal muscles in cats.

The effects of an H1- and H2-histamine receptor blockade upon the responses to noradrenaline (NA) of pre- and post-capillary segments of the microcirculation of the hind leg of cats were investigated. The responses to the resistance and capacitance vessels to noradrenaline injected in the coll. of femoral artery were reflected as changes in peripheral vascular resistance and in tissue volume respectively and determined during the following exercise before and after the H1 and H2-histamine receptor blockade. Muscular exercise was induced by sciatic nerve stimulation. The results show that H1- and H2-histamine receptor blockade applied together unmasked the vasodilator effects in both NA and that muscle exercise potentiated these effects in both pre- and post-capillary sections. This suggests that histamine may inhibit the response of the resistance and capacitance vessels in the working skeletal muscles to noradrenaline.

Animals↗
PubMed1997

[The importance of the endothelium in heart failure].

The endothelium is involved in cardiac and vascular dysfunction characteristic of heart failure. Vascular dysfunction has been related either to an impaired endothelium dependent vasodilation of both capacitance and resistance vessels, or to an increase in the plasmatic levels of endothelium derived contracting factors, such as endothelin-1. While the former seems to respond favourably to ACE-inhibitors, physical training and L-arginine; the latter will soon be treatable with endothelin-1 A e B receptor antagonists or with inhibitors of its converting enzyme. Cardiac dysfunction may be explained not only by the loss of the positive inotropic effect induced by low concentrations of nitric oxide (produced by the constitutive NO-synthase in the normal endothelium), but also by the negative inotropic effect induced by the high concentrations of nitric oxide, produced as a consequence of the stimulation of the inducible NO-synthase. It is therefore conceivable that cardiac dysfunction would also improve with the administration of drugs presently used to correct endothelium dependent vasodilatation disturbances.

Endothelin-1↗
PubMed1984

Acute hemodynamic and hormonal response to indoramin in congestive heart failure.

Acute hemodynamic and hormonal responses to a single dose of indoramin, an alpha 1-antagonist, were evaluated in 11 subjects with severe chronic congestive heart failure. A hemodynamic effect began within 1 hr of indoramin and persisted during the 6 hr of hemodynamic monitoring. Decreased right and left ventricular filling pressures were associated with increased stroke index and decreased pulmonary and systemic vascular resistances. Heart rate did not increase despite a fall in systemic arterial pressure. Forearm blood flow, forearm venous capacitance, and plasma norepinephrine levels were unchanged, whereas plasma renin activity rose from 12.7 +/- 17.4 to 16.6 +/- 20.4 ng/ml/hr. The only side effect was drowsiness in five of the 11 subjects. Our data demonstrate the acute effectiveness of indoramin in reducing ventricular preload and systemic vascular resistance in heart failure.

Adult↗
PubMed1975

[Plethysmographic and in vitro studies of the vasodilator effect of furosemide (Lasix)].

The beneficial effect of furosemide in treatment of chronic and particularly of acute congestive heart failure has been attributed to its potent diuretic action. In recent studies [16], it has been postulated that the effect of this diuretic agent is primarily vascular in origin. The results of venous occlusion plethysmographic experiments (modificated Whitney-gauge technique) carried out in this study on the forearm of 6 healthy men, show that furosemide (40 mg. i.v.) does not influence arterial blood flow (4-5 ml/100 ml tissue - min). In contrast furosemide induces a prompt significant (p less than 0.001) and sustained (about 45 min) increase in venous capacitance (deltaV/100 ml tissue = 15%) and a corresponding decrease in E'. The direct effect of furosemide on vascular muscle tone was studied in vitro on portal vein and aortic strip preparations from 76 male rats. In 18 experiments mechanical and electrical activity (using three pressure electrodes) were simultaneously recorded. The results of the in vitro experiments show: 1. Only extremely high furosemide concentrations (greater than 500 mg/l) induce slight relaxation of aortic strips. 2. Furosemide causes in contrast a marked dose-dependent per cent decrease of the integrated isometric tension in portal vein preparations: 14 mg/l reduce the initial tension (= 100%) to 80%; 35 mg/l to 65%; 70 mg/l to 50% and 100 mg/l to 35%. 3. The venodilating furosemide effect is significantly (p less than 0.001) increased by reduction in external Na+-concentration [Na+]0 to 120 mM though further reduction in the [Na+]0 to 90 mM does not cause additional changes in the relaxation slope. 4. The simultaneous records of electrical activity demonstrate that the relaxing effect of furosemide is based on decreased spike frequency in shortened bursts as well as on pronounced impairment of conduction velocity without relevant changes in pacemaker frequency. These in vitro results are discussed from the point of view that a furosemide induced decrease in Na+-permeability may determine the changes obtained in electrical and mechanical behaviour of portal veins of the rat.

Adult↗
PubMed1977

[Vascular component of the systemic circulatory response to orthostasis].

Under the orthostatic test (OT) pronounced compensation of the initial lowering of the arterial pressure (AP) and insignificant restoration of cardiac output arose in anesthetized cats. An important role of the baroreceptor reflexes from the carotid sinus in the mechanism of AP compensation was established. The response of the resistance anc capacitance vessels to OT was studied by the method of extracorporeal circulation. Quantitative evaluation of the blood pooling in the vascular system under OT was made. Compensatory response of the AP under OT was determined mainly by the reflex vasoconstriction of the resistance vessels, but not by the venomotor reactions.

Animals↗
PubMed1984

How do changes in diameter at the precapillary level affect cardiovascular function?

A survey is given of the various high-pressure precapillary vascular sections and of how they affect local and overall cardiovascular functions, with special emphasis put on the important "precapillary resistance vessels." The complex interactions between hemodynamic effects dependent on (a) vessel design, (b) transmural pressure, (c) "passive" wall distensibility, and (d) "active" smooth muscle responses are outlined in principle and experimentally illustrated with respect to systemic resistance control. Particular attention is devoted to the influence of the sympathetic vasoconstrictor fibers on precapillary vascular functions, concerning aspects such as speed, precision, range, and differentiation of the neurogenic effects, because these fibers represent the most powerful and widespread of the vascular control mechanisms involved in cardiovascular homeostasis. How these fibers in well-innervated vascular circuits can command up to the maximum contractile capacity of both the precapillary resistance and postcapillary capacitance vessels is illustrated, as well as the way in which these sets of vessels respond to even single nerve impulses with twitchlike, rapid contractions.

Animals↗
PubMedDate not supplied

[Vascular mechanisms of adaptation to head-down tilt body posture].

Using occlusion plethysmography and rheography, the state of peripheral circulation of 18 test subjects during 25 exposures to head-down tilt was investigated. The test subjects were subdivided into two groups: nine subjects actively changed their body position by 90 degrees and nine others were passively transferred to the head-down position at an angle of -12 degrees. It was found that regular training facilitated the development of vascular mechanisms which assisted adaptation to the head-down tilt: it decreased the tone of resistance vessels of the arms and legs and that of capacitance vessels of the legs; it increased the tone of cerebral resistance and capacitance vessels. The tone of leg capacitance vessels varied, depending on the type of training: passive tilting increased their compliance and active tilting decreased it. The final result of the tone redistribution in the peripheral vascular bed during training was a smaller increase of head blood content and a smaller fluid outflow from the legs.

Adaptation, Physiological↗
PubMed1996

Role of calcium-dependent K+ channels in the regulation of arterial and venous tone by nitric oxide in pigs.

Effects of inhibition of calcium-dependent potassium channels (K+Ca channels) on the regulation of arterial and venous tone by nitric oxide (NO) were studied in anaesthetized pigs following vagotomy and blockade of autonomic ganglia. Selective inhibition of K+Ca channels by charybdotoxin (CTX, 2 microg/kg iv) or iberiotoxin (IbTX, 1 microgram/kg) significantly augmented mean total peripheral resistance (TPR) to levels 30-60% above control. Venous and pulmonary vascular tone were assessed by changes in effective compliances of the venous (EVC) and pulmonary (EPC) vascular beds as calculated from changes in central venous and diastolic pulmonary arterial blood pressure during haemorrhagia (-5 ml/kg) and hypervolaemia (+5 ml/kg). Blockade of K+Ca channels significantly decreased both EVC (-20 to -30%) and EPC (-30 to -50%). Both CTX and IbTX significantly diminished the vasodilation caused by the NO-donor S-nitroso-N-acetylpenicillamine (SNAP) both during control conditions and following experimental vasoconstriction induced by systemic inhibition of NO-synthesis by NG-nitro-L-arginine methyl ester (L-NAME) or infusion of vasoconstrictor agonists. Dilator effects of the adenosine 3',5'-cyclic monophosphate (cAMP)-dependent agonist adenosine were only slightly reduced. However, blockade of K+Ca channels did not increase vasoconstriction induced by L-NAME significantly. These results suggest that activation of vascular K+Ca channels is an important mechanism by which NO attenuates the constrictor tone of resistance and capacitance vessels in vivo.

Angiotensin II↗
PubMed1986

Computer simulation of cardiopulmonary resuscitation: computer analysis of a simple electrical model of the circulation.

Extensive research is being conducted to study the mechanism of blood flow during cardiopulmonary resuscitation (CPR). Recently, work has been published using a simple electrical model of the circulation to simulate the hemodynamics of CPR. This analog was a hard-wired circuit consisting of the heart and great vessels modeled as a resistive-capacitive network, pressure as voltage, blood flow as current, blood inertia as inductance and vascular valves as diodes. Such a model is useful for examining the physiology of various methods and techniques of CPR administration. In this investigation, a general purpose circuit simulation program, SPICE Version 2G.6, was used to analyze previously published CPR models. With minor modifications, the program was fully able to simulate the hard-wired circuits. The program is very flexible, allowing for easy model modification and a wide range of parameter values. In addition, the program offers the advantages of increased accuracy and low cost. Suggested future applications are for rapid evaluation of new CPR concepts.

Aorta↗
PubMed1999

NOS inhibition potentiates norepinephrine but not sympathetic nerve-mediated co-transmission in resistance arteries.

OBJECTIVE: The in vitro interaction between sympathetic nerves and basal nitric oxide release was studied in a resistance artery, since these interact powerfully in large vessels. METHODS: The pharmacological interaction between L-NAME and vasoconstriction to field stimulation of sympathetic nerves or exogenous norepinephrine was studied in rabbit cutaneous resistance arteries in wire myographs. RESULTS: Relaxation of norepinephrine-induced tone by acetylcholine, but not sodium nitroprusside, was blocked by N omega-nitro-L-arginine methyl ester (L-NAME: 100 microM), indicating that the agonist-induced release of nitric oxide could oppose the vasoconstrictor effect of norepinephrine and confirming that L-NAME had no effect on endothelium-independent vasodilatation. L-NAME increased norepinephrine potency indicating basal NO release. With short bursts of electrical field stimulation purinergic transmission was dominant at low frequencies and adrenergic at high frequencies. L-NAME had no effect on nerve-mediated responses, even after blocking the purinergic component with alpha,beta-methylene ATP (3 microM), suggesting that the influence of spontaneously released nitric oxide does not extend to the vascular smooth muscle cells under adrenergic nervous control. CONCLUSION(S): This resistance artery exhibits a highly effective nitric oxide-mediated vasodilatation to acetylcholine. It has basal release of nitric oxide which antagonises exogenous norepinephrine. However, basal nitric oxide did not influence adrenergic nerve transmission, which contrasts with previous studies of larger arteries and veins. We speculate that in small resistance arteries there may be a spatial limitation to the zones of vascular smooth muscle influenced by the adrenergic nerves and by basal nitric oxide from the endothelium, respectively. The role of endogenous nitric oxide in modulating vascular tone may thus be less in resistance arteries than in conducting arteries or capacitance vessels and purinergic transmission appears to be particularly resistant.

Acetylcholine↗
PubMed2003

Capacitative calcium entry as a pulmonary specific vasoconstrictor mechanism in small muscular arteries of the rat.

(1) The effect of induction of capacitative Ca2+ entry (CCE) upon tone in small (i.d. 200-500 microm) intrapulmonary (IPA), mesenteric (MA), renal (RA), femoral (FA), and coronary arteries (CA) of the rat was examined. (2) Following incubation of IPA with 100 nm thapsigargin (Thg) in Ca2+-free physiological salt solution (PSS), a sustained contraction was observed upon reintroduction of 1.8 mm Ca2+, which was unaffected by either diltiazem (10 microm) or the reverse mode Na+/Ca2+ antiport inhibitor KB-R7943 (10 microm). An identical protocol failed to elicit contraction in MA, RA, or CA, while a small transient contraction was sometimes observed in FA. (3) The effect of this protocol on the intracellular Ca2+ concentration ([Ca2+]i) was assessed using Fura PE3-loaded IPA, MA, and FA. Reintroduction of Ca2+ into the bath solution following Thg treatment in Ca2+-free PSS caused a large, rapid, and sustained increase in [Ca2+]i in all the three types of artery. (4) 100 nm Thg induced a slowly developing noisy inward current in smooth muscle cells (SMC) isolated from IPA, which was due to an increase in the activity of single channels with a conductance of approximately 30 pS. The current had a reversal potential near 0 mV in normal PSS, and persisted when Ca2+-dependent K+ and Cl- currents were blocked; it was greatly inhibited by 1 microm La3+, 1 microm Gd3+, and the IP3 receptor antagonist 2-APB (75 microm), and by replacement of extracellular cations by NMDG+. (5) In conclusion, depletion of intracellular Ca2+ stores with Thg caused capacitative Ca2+ entry in rat small muscular IPA, MA, and FA. However, a corresponding contraction was observed only in IPA. CCE in IPA was associated with the development of a small La3+- and Gd3+-sensitive current, and an increased Mn2+ quench of Fura PE-3 fluorescence. These results suggest that although CCE occurs in a number of types of small arteries, its coupling to contraction appears to be of particular importance in pulmonary arteries.

Animals↗
PubMed1989

Cardiovascular effects of propofol in the anaesthetized dog.

This study was designed to investigate if propofol produced cardiovascular effects by direct actions or by indirect actions secondary to depression of the central nervous system. Experiments were performed on chloralose anaesthetized dogs in which all neurogenic cardiovascular reflexes were abolished by bilateral vagotomy and common carotid ligatures, in combination with i.v. bretylium and propranolol. Bolus doses of propofol followed by infusions at rates up to 160 mg kg-1 h-1 produced blood concentrations of propofol from 1.99 to 112 micrograms ml-1. Infusions of hydroxyethyl starch given to maintain central venous pressures and pulmonary artery occlusion pressures at control values were used as an index of changes in capacitance. Blood concentrations of propofol less than 10 micrograms ml-1 caused an increase in mean capacitance of 8.0 (SEM 1) ml kg-1 with no significant changes in systemic vascular resistance, pulmonary vascular resistance or inotropic state of the heart. We conclude that anaesthesia with propofol may be accompanied by decreased cardiac output secondary to reduction in preload by a direct venodilator effect. Our experiments indicate that cardiac output and arterial pressure are preserved well at normal anaesthetic blood concentrations of propofol if the preload is maintained.

Anesthesia, Intravenous↗
PubMed1992

Mechanisms of interaction between the sulfhydryl precursor L-methionine and glyceryl trinitrate.

BACKGROUND: L-Methionine potentiates systemic hemodynamic effects of intravenous glyceryl trinitrate (GTN) in tolerant and nontolerant patients to a similar extent as N-acetylcysteine (NAC). This potentiation of GTN action by L-methionine has been attributed to enhanced intracellular formation of nitrosothiols, known to be potent stimulators of soluble guanylyl cyclase. This study was performed to analyze directly the effects of L-methionine on GTN-induced dilation of large epicardial arteries and the venous capacitance system of the dog in the tolerant and nontolerant states. Cultured rat aortic vascular smooth muscle cells and purified guanylyl cyclase were used to study potential intracellular and extracellular mechanisms responsible for this interaction. METHODS AND RESULTS: In awake nontolerant dogs, L-methionine (100 mg/kg) potentiated the tachycardic response to GTN (5.0 and 15 micrograms/kg/min) and enhanced the hypotensive action of GTN (1.5 and 5.0 micrograms/kg/min) in anesthetized, nonreflexic dogs. In nontolerant and tolerant dogs, however, L-methionine did not alter the dose-response of large epicardial artery dilation to intravenous GTN challenges and did not modify nitrate tolerance of the low pressure system of the dog. The infusion of L-methionine (100 mg/kg) significantly increased plasma methionine levels (from 52 +/- 12 to 1,141 +/- 239 microM), cystine levels (from 12 +/- 4 to 26 +/- 7 microM), but not homocystine levels. In vitro, the L-methionine conversion product L-cysteine (0.1-1.0 mM) but not homocysteine significantly enhanced the augmentation of purified guanylyl cyclase activity by GTN (100 microM). Incubation of cultured rat aortic smooth muscle cells with L-methionine (10 microM or 1 mM) did not result in a significant increase of free intracellular sulfhydryl group content. CONCLUSIONS: The L-methionine conversion product L-cysteine mediates tolerance independent the potentiation of GTN action. This may result from an L-cysteine-induced formation of a vasoactive metabolite of GTN (nitric oxide) or nitrosothiol. This effect occurs primarily in the resistance vessel circulation, not in large epicardial arteries and veins. The lack of effect of L-methionine on sulfhydryl group content in large conductance vessels indicates that hepatic L-methionine metabolism constitutes the significant source of L-cysteine. These findings strongly suggest that administration of sulfhydryl-group precursor L-methionine does not represent a therapeutic alternative to a nitrate-free interval to restore nitrate sensitivity in tolerant large epicardial arteries and veins.

Animals↗
PubMed1984

Pulmonary blood flow. A potential factor in the pathogenesis of pulmonary edema.

The purpose of this study is to examine the hemodynamics of the pulmonary circulation and the potential role of pulmonary blood flow in the pathogenesis of cardiogenic pulmonary edema. To do so, the pulmonary circulation was isolated and controlled such that, within a closed circuit, pulmonary blood flow and left atrial pressure (LAP) could be regulated independently: the first by a constant flow pump, the second by a variable height reservoir. The effect of pulmonary blood flow on pulmonary artery pressure and intravascular blood volume was then determined at different LAPs. Contrary to our expectations, the results indicate that (1) pulmonary vascular resistance does not change appreciably as flow increases, (2) the microcirculation comprises the major capacitance vessels of the lung, and (3) increased pulmonary flow in the normal lung causes little change in intravascular pulmonary blood volume, whereas, by contrast, major changes in pulmonary blood volume occur as LAP rises. Next, the effect of pulmonary blood flow on edema formation in the lungs was examined. Below a critical level of LAP (15 mm Hg in these experiments), pulmonary blood flow up to 5 L/min did not produce pulmonary edema. Above this level, however, such an effect was clear. Thus, at an LAP of 20 mm Hg, edema did not develop if pulmonary flow was low (0.7 L/min) but did if flow was increased to 2 L/min. As well, if the LAP was 17.5 mm Hg and pulmonary flow 3.5 L/min, severe pulmonary edema also resulted.

Animals↗