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At least 163 records · Page 9Linked to original sources
PubMed1998

Hunting down nucleic acid binding factors in the cardiovascular system.

Transcription regulation of genes active in the cardiovascular system is a complex process, involving DNA and RNA binding proteins. Nucleic acid binding proteins bind to the regulatory DNA and interact with other proteins, including RNA polymerase to initiate and control the level of transcription. The RNA binding proteins have a function in spliceosome formation and in stabilising mRNA. In this review the currently available molecular approaches to analyse regulatory DNA in relation to DNA binding proteins are discussed. Similar techniques that have been developed for RNA binding protein studies are included. In addition to an explanation of the various methods, examples are provided from DNA-protein interactions on genes active in the cardiovascular system, together with strategies for identification and characterisation of new nucleic acid binding proteins active in cardiac or vascular cell types.

Animals↗
PubMed1993

Effects of lower-body negative pressure on blood flow with applications to the human cardiovascular system.

The paper reports a theoretical investigation into the effects of lower-body negative pressure on blood flow through the human cardiovascular system. The human cardiovascular system is modelled as a closed network of arteries, arterioles, capillaries, venules and veins of different lengths and cross-sections. The pumping action is provided by the contraction of the ventricles. The model has been analysed using the finite-element method. The pertinent equations incorporating the effects of lower-body negative pressure for the pressures and flow velocities have been derived, and the quantitative results have been computed. Percentage changes in flow velocities, pressure drops and conductances under the application of lower-body negative pressure in the various segments and organs of the entire cardiovascular system are obtained. The lower-body negative pressure has no effect on the flow rates in carotid, ulnar and coronary arteries, nor on the supply of blood to the upper extremities, kidneys, spleen and liver. The major effects are found in the lower extremities.

Blood Vessels↗
PubMed2006

Simulation of the cardiovascular system using equivalent electronic system.

This paper describes simulation of the cardiovascular system using a complex electronic circuit. In this study we have taken a slightly different approach to the modeling of the system and tried to advance existing electrical models by increasing more segments and parameters. The model consists of 42 segments representing the arterial system. Anatomical and physiological data for circuit parameters have been extracted from medical articles and textbooks. The frequency of heart is 1 Hz and the system operates in steady state condition. Each artery is modeled by one capacitor, resistor and inductor. The left and right ventricles are modeled using AC power suppliers and diodes. The results of the simulation including pressure and volume graphs exhibit operation of the cardiovascular system under normal condition. The results of the simulation have been compared with the relevant experimental observation and are in good agreement with them.

Computer Simulation↗
PubMed1994

Nitric oxide and the cardiovascular system.

Nitric oxide is a simple diatomic molecule that functions as a cellular messenger in a number of organ systems, included among which is the cardiovascular system. Serving several physiologic roles in the cardiovascular system, nitric oxide is an important determinant of basal vascular tone, regulates myocardial contractility, and modulates platelet-vessel wall interactions. From the perspective of cardiovascular pathophysiology, nitric oxide has been implicated in the pathogenesis of essential hypertension, atherosclerosis, and the hypotension associated with shock states. This review will focus in detail on the chemistry, biology, and pathobiology of nitric oxide as it relates to cardiovascular function.

Cardiovascular Diseases↗
PubMed1996

Numerical simulation of the blood flow in the human cardiovascular system.

This paper describes a numerical model of the human cardiovascular system. The model is composed of 15 elements connected in series representing the main parts of the system. Each element is composed of a rigid connecting tube and an elastic reservoir. The blood flow is described by a one-dimensional time-dependent Bernoulli equation. The action of the ventricles is simulated with a Hill's three-element model, adapted for the left and right heart. The closing of the four heart valves is simulated with the aid of time-dependent drag coefficients. Closing is achieved by letting the drag coefficient approach infinity. The resulting system of 32 non-linear ordinary differential equations is solved numerically with the Runge-Kutta method. The results of the simulation (pressure-time and volume-time dependence for the atria and ventricles and pressure forms in the aorta at a heart rate of 70 beats per minute) agree with the physiological data given in the literature. The model's input aortic impedance is 31.5 dyn s cm-5 which agrees with literature data given for aortic input impedance in man 26-80 dyn s cm-5). Long-term stability of the system was achieved. The cardiovascular system presented here can also be simulated at higher and varying heart rates--up to 200 beats per minute. The results of calculations for some pathological changes (e.g. valvular abnormalities) are discussed.

Algorithms↗
PubMed2002

Growth hormone, insulin-like growth factor-1 and the aging cardiovascular system.

There is a large body of evidence that biological aging is related to a series of long-term catabolic processes resulting in decreased function and structural integrity of several physiological systems, among which is the cardiovascular system. These changes in the aging phenotype are correlated with a decline in the amplitude of pulsatile growth hormone secretion and the resulting decrease in plasma levels of its anabolic mediator, insulin like growth factor-1 (IGF-1). The relationship between growth hormone and biological aging is supported by studies demonstrating that growth hormone administration to old animals and humans raises plasma IGF-1 and results in increases in skeletal muscle and lean body mass, a decrease in adiposity, increased immune function, improvements in learning and memory, and increases in cardiovascular function. Since growth hormone and IGF-1 exert potent effects on the heart and vasculature, the relationship between age-related changes in cardiovascular function and the decline in growth hormone levels with age have become of interest. Among the age-related changes in the cardiovascular system are decreases in myocyte number, accumulation of fibrosis and collagen, decreases in stress-induced cardiac function through deterioration of the myocardial conduction system and beta-adrenergic receptor function, decreases in exercise capacity, vessel rarefaction, decreased arterial compliance and endothelial dysfunction leading to alterations in blood flow. Growth hormone has been found to exert potent effects on cardiovascular function in young animals and reverses many of the deficits in cardiovascular function in aged animals and humans. Nevertheless, it has been difficult to separate the effects of growth hormone deficiency from age-related diseases and associated pathologies. The development of novel animal models and additional research are required in order to elucidate the specific effects of growth hormone deficiency and assess its contribution to cardiovascular impairments and biological aging.

Aged↗
PubMedDate not supplied

[Individual adaptation of cardiovascular system in female swimmers, students of middle school].

Long trainings promote perfection of the regulatory mechanisms, that is characterized by an increase of cholinergic effects on the cardiovascular system of children. An optimal ratio of sympathetic and parasympathetic effects is typical of swimmer girls of different age with high level of working capacity in rest, that influences the adequate adaptation of the cardiovascular system to physical exercises. There are limits of adaptibility of the cardiovascular system of swimmer girls which is determined by informative indices of histogram. As influenced by physical exercises the favourable, incomplete favourable and unfavourable directions of the cardiovascular system shifts in swimmer girls are observed. Essential individual variations of the pattern of the functional changes in the cardiovascular system confirm the necessity to organize the training process allowing for the individual peculiarities of the development of children and adolescents.

Adaptation, Physiological↗
PubMed1996

Mutations affecting the formation and function of the cardiovascular system in the zebrafish embryo.

As part of a large-scale mutagenesis screen of the zebrafish genome, we have identified 58 mutations that affect the formation and function of the cardiovascular system. The cardiovascular system is particularly amenable for screening in the transparent zebrafish embryo because the heart and blood vessels are prominent and their function easily examined. We have classified the mutations affecting the heart into those that affect primarily either morphogenesis or function. Nine mutations clearly disrupt the formation of the heart. cloche deletes the endocardium. In cloche mutants, the myocardial layer forms in the absence of the endocardium but is dysmorphic and exhibits a weak contractility. Two loci, miles apart and bonnie and clyde, play a critical role in the fusion of the bilateral tubular primordia. Three mutations lead to an abnormally large heart and one to the formation of a diminutive, dysmorphic heart. We have found no mutation that deletes the myocardial cells altogether, but one, pandora, appears to eliminate the ventricle selectively. Seven mutations interfere with vascular integrity, as indicated by hemorrhage at particular sites. In terms of cardiac function, one large group exhibits a weak beat. In this group, five loci affect both chambers and seven a specific chamber (the atrium or ventricle). For example, the weak atrium mutation exhibits an atrium that becomes silent but has a normally beating ventricle. Seven mutations affect the rhythm of the heart causing, for example, a slow rate, a fibrillating pattern or an apparent block to conduction. In several other mutants, regurgitation of blood flow from ventricle to atrium is the most prominent abnormality, due either to the absence of valves or to poor coordination between the chambers with regard to the timing of contraction. The mutations identified in this screen point to discrete and critical steps in the formation and function of the heart and vasculature.

Animals↗
PubMed2004

Mathematical modeling of cardiovascular system dynamics using a lumped parameter method.

This work reviews the main aspects of cardiovascular system dynamics with an emphasis on modeling hemodynamic characteristics by the use of a lumped parameter approach. The methodological and physiological aspects of the circulation dynamics are summarized with the help of existing mathematical models. The main characteristics of the hemodynamic elements, such as the heart and arterial and venous systems, are first described. Distributed models of an arterial network are introduced, and their characteristics are compared with those of lumped parameter models. We also discuss the nonlinear characteristics of the pressure-volume relationship in veins. Then the control pathways that participate in feedback mechanisms (baroreceptors and cardiopulmonary receptors) are described to explain the interaction between hemodynamics and autonomic nerve control in the circulation. Based on a set-point model, the computational aspects of reflex control are explained.

Animals↗
PubMed1984

The role of central alpha 1- and alpha 2-adrenoceptors in the regulation of vasopressin release and the cardiovascular system.

In order to investigate the role of central alpha 1- and alpha 2-adrenoceptors in the control of vasopressin (ADH) release and the cardiovascular system, norepinephrine (NE) (1.4 microgram/kg), methoxamine (1.4 microgram/kg), yohimbine (60 micrograms/kg), and prazosin (40 micrograms/kg) were administered via the cerebral ventricles in urethane-chloralose-anesthetized dogs after morphine sedation (n = 42). In the control study 0.9% saline was administered. NE resulted in a significant fall in blood pressure, heart rate, and ADH release. Methoxamine tended to activate the cardiovascular system, but did not affect the release of ADH significantly. Prazosin decreased blood pressure significantly with a significant rise in heart rate and ADH release. Pretreatment with prazosin did not block significantly the effect of NE on blood pressure, heart rate, and ADH release. Yohimbine did not affect the cardiovascular system and ADH release significantly. Pretreatment with yohimbine completely blocked the effect of NE on ADH release, and brought about a slight rise in blood pressure and heart rate. In none of the experiments could changes in ADH release be attributed to changes in plasma osmolality. These results indicate that central alpha 1-adrenoceptors might act to activate the cardiovascular system, but have no effects on ADH release in anesthetized dogs. On the other hand, central alpha 2-adrenoceptors might act to reduce ADH release and to depress the cardiovascular system.

Animals↗
PubMed1994

[Control system for a complete artificial heart based on a mean value model of the cardiovascular system].

The reliable use of an artificial heart in patients requires a control strategy that is able to monitor and realistically regulate the different loads of the cardiovascular system. The model outlined in the following article was created in an interdisciplinary environment with heart specialists and automation engineers. A control system for an artificial heart, in the form of a peristaltic pump, was created with the help of a load-dependent mean-value model of the cardiovascular system. The resistance of the arterioles in the systemic vascular system RA was chosen as the parameter for the adaptation of the cardiac output. This parameters can be easily and accurately estimated through the measurement of pressures and flows, and it is a very good indicator for the load of the organism. The results, obtained through simulation of the overall system, show a very fast and accurate adaptation of the cardiac output to the needs of the body at changing loads over a large range of workloads. At the same time, the protection of the lungs from excessive pressure is ensured by balance control of the outputs of the two halves of the artificial heart. The control system outlined here needs only pressure and flow sensors, which can be integrated into the pump housing.

Cardiac Output↗
PubMed2006

CRF receptors in the rodent and human cardiovascular systems: species differences.

CRF has powerful receptor-mediated cardiovascular actions. To evaluate the precise distribution of CRF receptors, in vitro CRF receptor autoradiography with (125)I-[Tyr(0), Glu(1), Nle(17)]-sauvagine or [(125)I]-antisauvagine-30 was performed in the rodent and human cardiovascular system. An extremely high density of CRF(2) receptors was detected with both tracers in vessels of rodent lung, intestine, pancreas, mesenterium, kidney, urinary bladder, testis, heart, brain, and in heart muscle. In humans, CRF(2) receptors were detected with (125)I- antisauvagine-30 at low levels in vessels of kidneys, intestine, urinary bladder, testis, heart and in heart muscle, while only heart vessels were detected with (125)I-[Tyr(0), Glu(1), Nle(17)]-sauvagine. This is the first extensive morphological study reporting the extremely wide distribution of CRF(2) receptors in the rodent cardiovascular system and a more limited expression in man, suggesting a species-selective CRF receptor expression.

Animals↗
PubMed1985

Cardiovascular system of the conjoined twins.

The cardiovascular system of the dicephalus (2 spines, one pelvis) conjoined twins is being described. The heart consists of 2 atria and 3 ventricles. Various malformations are evident in the layout systematic and pulmonary circulation. The vascular system can be divided into 3 zones: an upper one--with an almost symmetrical duplication, a middle one--with an atypical pattern, and a lower one--with a normal pattern.

Cardiovascular Abnormalities↗
PubMed2000

Adverse effects of corticosteroids on the cardiovascular system.

OBJECTIVE: To review the potential adverse effects of glucocorticoid therapy on the cardiovascular system and to provide insight into the mechanisms of these effects. DATA SOURCES: Case reports and studies demonstrating adverse effects of glucocorticoid therapy on the cardiovascular system were examined from a MEDLINE search. Animal data and in vitro studies were identified to provide insight on the mechanisms of these effects. DATA SYNTHESIS: Undesirable effects identified were dyslipidemia, hypertension and left ventricular free wall rupture after myocardial infarction. Elevations of total plasma cholesterol, triglycerides, low density lipoprotein cholesterol and high density lipoprotein cholesterol are often reported. The elevation of various lipid subfractions is likely mediated by increased plasma insulin levels, impaired lipid catabolism and increased lipid production in the liver. Hypertension was shown to be more prevalent in patients treated with high doses of glucocorticoid. The mechanisms are complex, but final pathways include increased systemic vascular resistance, increased extracellular volume and increased cardiac contractility. Glucocorticoids were demonstrated to increase the incidence of left ventricular free wall rupture by delaying myocardial scar formation in the postmyocardial infarction period. CONCLUSIONS: The major adverse effects of glucocorticoids on the cardiovascular system include dyslipidemia and hypertension. These effects may predispose treated patients to coronary artery disease if high doses and prolonged courses are used. Accordingly, corticosteroids should be employed judiciously in patients with other risk factors for cardiovascular disease, and attention should be paid to risk modification. Low dose and alternate day therapy may reduce the incidence of complications in corticosteroid therapy. The mechanisms of these adverse effects are complex and have not yet been fully explained.

Animals↗
PubMed1980

Investigations of autonomic diabetic neuropathy of the cardiovascular system.

One-hundred and nine patients consecutively admitted to our hospital underwent a standardized sustained hand grip test, the Valsalva maneuver, and the Schellong test in a study of autonomic diabetic neuropathy of the cardiovascular system. The correlation between autonomic diabetic neuropathy of the cardiovascular system and the duration of diabetes, the age of the diabetic patient, the forms of treatment, and other neuropathic or vascular complications of diabetes was studied. Autonomic diabetic neuropathy of the cardiovascular system is a complication of long-term insulin-dependent diabetes and is dependent on the duration of the disease. The responses to the Valsalva maneuver in 17 poorly controlled diabetics before and after establishing good control of the diabetes showed no change in the Valsalva ratio. Short-term changes in diabetic control seem to have no effect on the Valsalva ratio as an indicator of autonomous nervous system involvement. The so-called "10 second Valsalva ratio" is a simple and reproducible method of evaluating the Valsalva maneuver.

Adult↗
PubMed1994

Parathyroid hormone-related protein in the cardiovascular system.

PTH-related protein (PTHrP) is expressed in a stretch-responsive manner in several types of smooth muscle. We previously demonstrated the production of PTHrP in adult rat heart muscle. In this study, we demonstrate the production of PTHrP in the cardiovascular systems of several mammalian species, including human. We demonstrate PTHrP by immunohistology, using a panel of murine monoclonal antibodies to PTHrP epitopes that span the entire length of the human PTHrP amino acid sequence, quantitate the concentration of PTHrP in the rat cardiovascular system by region-specific RIAs, and measure the relative levels of PTHrP messenger RNA (mRNA) by competitive polymerase chain reaction. Immunohistology studies demonstrated the presence of PTHrP in the cardiovascular systems of humans, rats, pigs, and rabbits. The most robust expression was found in atria, followed by the large vessels, then ventricles. No difference was seen between the left and right sides of the heart. Double staining procedures revealed that PTHrP and atrial naturietic peptide were coexpressed in some cells. Using RIAs and polymerase chain reaction, we demonstrated that atria contained a higher concentration of PTHrP than ventricles and that the relative PTHrP concentrations correlated to its mRNA concentrations in these two tissues. The concentrations of PTHrP in the smooth muscle surrounding the aorta and vena cava were comparable to those in atria. However, in these large vessels, the higher PTHrP levels did not correspond to its mRNA levels. Whereas the immunoreactive concentrations of PTHrP were similar in the atria, aorta, and vena cava, the mRNA levels in the aorta and vena cava were 3-fold lower than those in the atria. Certain PTHrP epitopes appeared to be differentially expressed in specific cardiovascular tissues. A comparison of region-specific assays showed that immunoreactivity measured by immunoassays to PTHrP-(38-64) and PTHrP-(109-141) were 3- to 5-fold greater than that determined by an immunoassay to PTHrP-(1-34). Our observations demonstrate that the atria, aorta, and vena cava contain the greatest amounts of PTHrP in the cardiovascular system. The discrepancy between the concentrations of PTHrP and its mRNA present in the aorta and vena cava suggest that the two may be regulated differently in these tissues. The widespread distribution of PTHrP suggests an important function for the protein in the cardiovascular system, possibly functioning as the calcium counterpart for the atrial natriuretic-sodium regulatory axis.

Animals↗