PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Models, Cardiovascular”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 73 records · Page 4Linked to original sources
PubMedDate not supplied

Experimental model of cardiovascular post-resuscitation syndrome--no effect of platelet activating factor antagonism.

The cardiovascular instability seen in the reperfusion phase after resuscitation from cardiac arrest may contribute to secondary brain injury. The aim of the present study was to characterise post-resuscitation cardiovascular instability in an experimental model of cardiac arrest and to test if cardiovascular stability could be improved by pre-treatment with the platelet activating factor (PAF) antagonist BN52021. Ten anaesthetised pigs received pre-treatment with BN52021 before induction of ventricular fibrillation (arrest/BN52021 group), while ten animals received only the vehicle (arrest/vehicle group). After a non-intervention interval of 9 min, resuscitation was attempted. Resuscitated animals were observed for 5 h and compared to a sham arrest group of seven animals. The haemodynamic situation after resuscitation was characterised by a low cardiac output that was inadequate in relation to the oxygen demand, as reflected by a low mixed venous oxygen saturation. The arterial blood pressure was to some extent reduced and the filling pressures in both the right and left heart were increased, but urinary output was not reduced. The severe haemodynamic compromise was not adequately reflected by standard monitoring variables such as arterial blood pressure and urinary output. Pre-treatment with BN52021 was unable to improve any aspect of short-term survival or haemodynamic stability.

Acid-Base Equilibrium↗
PubMed2002

Computational modeling of cardiovascular response to orthostatic stress.

The objective of this study is to develop a model of the cardiovascular system capable of simulating the short-term (< or = 5 min) transient and steady-state hemodynamic responses to head-up tilt and lower body negative pressure. The model consists of a closed-loop lumped-parameter representation of the circulation connected to set-point models of the arterial and cardiopulmonary baroreflexes. Model parameters are largely based on literature values. Model verification was performed by comparing the simulation output under baseline conditions and at different levels of orthostatic stress to sets of population-averaged hemodynamic data reported in the literature. On the basis of experimental evidence, we adjusted some model parameters to simulate experimental data. Orthostatic stress simulations are not statistically different from experimental data (two-sided test of significance with Bonferroni adjustment for multiple comparisons). Transient response characteristics of heart rate to tilt also compare well with reported data. A case study is presented on how the model is intended to be used in the future to investigate the effects of post-spaceflight orthostatic intolerance.

Baroreflex↗
PubMed2000

Angiotensin-converting enzyme inhibitor prevents plasminogen activator inhibitor-1 expression in a rat model with cardiovascular remodeling induced by chronic inhibition of nitric oxide synthesis.

Plasminogen activator inhibitor-1 (PAI-1) may participate in the development of cardiovascular remodeling by inhibiting extracellular matrix turnover and fibrinolysis. However, little is known about physiological regulators of PAI-1 in vivo. Angiotensin II has been shown to stimulate PAI-1 in vitro. We previously reported that long-term inhibition of nitric oxide (NO) synthesis with Nomega-nitro-L-arginine methyl ester (L-NAME) causes cardiovascular remodeling (vascular medial thickening and fibrosis) associated with increased tissue angiotensin-converting enzyme (ACE) activity. In the present study, we examined whether treatment with an ACE inhibitor modulates the cardiovascular PAI-1 expression in this model in vivo. Wistar-Kyoto rats were treated with either no drugs, L-NAME (100 mg/kg x day), or L-NAME plus the ACE inhibitor imidapril (20 mg/kg day). Marked increases in PAI-1 mRNA and protein levels in the aorta and left ventricle were observed after the first and fourth weeks of PAI-1 treatment. PAI-1 immunoreactivity was increased in the endothelium and the media of the aorta and coronary arteries after treatment of L-NAME. This increase in PAI-1 levels was associated with an increase in ACE activity of the aorta and left ventricle. ACE inhibition with imidapril significantly prevented both the increases in PAI-1 levels and the development of cardiovascular remodeling. These findings suggest that the local renin-angiotensin system regulates PAI-1 expression, and that the increased PAI-1 levels may contribute to the cardiovascular remodeling in this model.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1979

Further observations on modelling of the cardiovascular function in the electrical model.

In 1976 the fourth type of the electrical model of the cardiovascular function was constructed, showing formal and electronic changes: inverting system, hysteresis comparator (for the valve function), simulation of the insufficiency and the stenosis of the valves. The analog values were established but they are not yet definitive. The important values are: pressure 100 mm Hg = 100mV; flow 100 ml/sec = 137 microA. The action of the heart is given by changing capacity; the contractility is characterized by systolic capacity (CS). The diastolic capacity (CD) is not yet variable (CD = 4,000 microF) and consequently the diastolic pressure is always near to zero. The pressure curves of the left ventricle and of the aorta of cardiac patients with aortic valve disease were simulated. For comparison purposes only two clinical records and electrical model simulation records are given in this paper. In the patients (only aortic stenosis is given here) left heart catheterization was carried out. A case of coronary heart disease is also shown. The curves (simulated) are satisfactory and reflect the events in the compression chamber. The values of the parameters, which were used in the stimulation, represent the analysis of the clinical curves and a functional characterization of the situation. Besides these simulations the effect of valve changes on the pressure in the left ventricle, aorta and large arteries was also studied. With the aim of extending the integrative view of the use of the electrical model, an attempt of comparing the time course of capacity changes and the time course of inner surface changes of the left ventricle was made. The cinecardioangiographic data, obtained in an invasive way, were used for the purpose of obtaining the inner surface of the left ventricle. From pressure and surface data the cardiac forces (isometric, average and also total force per minute) were calculated and compared with the normal state, taken from the literature. The total force per minute includes the sum of systolic durations per minute and characterizes the energy expenses of the heart. Further data must be obtained by different cardiographic techniques in order to obtain a solid basis for the use of indirect methods, where the electrical model would be helpful as a noninvasive integrative tool in the assessment of the cardiovascular function.

Adult↗
PubMed2004

The calcium channel antagonist benidipine reduces plasma and cardiac endothelin-1 levels in type II diabetic rat model.

Cardiovascular complications are the central feature of type 2 diabetes mellitus, and insulin resistance is an early clinical manifestation of type 2 diabetes mellitus. Calcium channel blockers are widely used to treat cardiovascular diseases in diabetic patients; however, it remains unknown how endothelin-1 (ET-1) is altered and associated with cardiac lesions at the insulin-resistant early stage of type 2 diabetes mellitus, and, if so, whether calcium channel blockers can reverse such alterations. We examined plasma and cardiac expression of ET-1 in male Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a spontaneous model of human type 2 diabetes mellitus. At 8 weeks of age, OLETF rats were treated for 12 weeks with a long acting calcium channel blocker, benidipine (3 mg/kg per day p.o.) (BEN, n = 15), or with vehicle (OLETF, n = 15), and age-matched genetic control, male Long-Evans Tokushima Otsuka (LETO) rats were also used (n = 15). Blood pressure was significantly higher in OLETF than LETO rats, and benidipine treatment of OLETF rats for 12 weeks did not reduce their blood pressure significantly. Plasma and cardiac levels of ET-1 were significantly higher in OLETF compared with LETO rats (both P < 0.01), and were reversed after benidipine treatment. Our results suggest that ET-1 plays a pivotal role in the pathogenesis of cardiac complications at the insulin-resistant stage of diabetes mellitus, and that benidipine treatment may have a beneficial effect on these complications.

Age Factors↗
PubMedDate not supplied

Small animal models of cardiovascular disease: tools for the study of the roles of metabolic syndrome, dyslipidemia, and atherosclerosis.

INTRODUCTION: Cardiovascular disease, the leading cause of death in much of the modern world, is the common symptomatic end stage of a number of distinct diseases and, therefore, is multifactorial and polygenetic in character. The two major underlying causes are disorders of lipid metabolism and metabolic syndrome. The ability to develop preventative and ameliorative treatments will depend on animal models that mimic human disease processes. The focus of this review is to identify suitable animal models and insights into cardiovascular disease achieved to date using such models. CRITERIA FOR ANIMAL MODELS: The ideal animal model of cardiovascular disease will mimic the human subject metabolically and pathophysiologically, will be large enough to permit physiological and metabolic studies, and will develop end-stage disease comparable to those in humans. Given the complex multifactorial nature of cardiovascular disease, no one species will be suitable for all studies. AVAILABLE MODELS: Potential larger animal models are problematic due to cost, ethical considerations, or poor pathophysiological comparability to humans. Rabbits require high-cholesterol diets to develop cardiovascular disease, and there are no rabbit models of metabolic syndrome. Spontaneous mutations in rats provide several complementary models of obesity, hyperlipidemia, insulin resistance, and type 2 diabetes, one of which spontaneously develops cardiovascular disease and ischemic lesions. The mouse, like normal rats, is characteristically resistant to cardiovascular disease, although genetically altered strains respond to cholesterol feeding with atherosclerosis, but not with end-stage ischemic lesions. CONCLUSIONS: The most useful and valid species/strains for the study of cardiovascular disease appear to be small rodents, rats, and mice. This fragmented field would benefit from a consensus on well-characterized appropriate models for the study of different aspects of cardiovascular disease and a renewed emphasis on the biology of underlying diseases.

Animals↗
PubMed2004

Role of endothelin in mediating postmenopausal hypertension in a rat model.

Cardiovascular disease is the leading cause of death in women after menopause. Hypertension, a major cardiovascular risk factor, becomes more prevalent after menopause. The mechanisms responsible for the increase in blood pressure (BP) in postmenopausal women are unknown. We have recently characterized the aged, postestrous-cycling (PMR) spontaneously hypertensive rats (SHR) as a model of postmenopausal hypertension. The purpose of the present study was to determine whether endothelin plays a role in the increased BP in PMR. Premenopausal female SHR, aged 4-5 mo (YF), and PMR, aged 16 mo, were studied. Expression of preproendothelin-1 mRNA was not different in either renal cortex or medulla between PMR and YF (n = 7-8/group). In contrast, ET-1 peptide expression was significantly higher in renal cortex of PMR than in renal cortex of YF, but there was no difference in medullary ET-1. Expression of endothelin ET(A) receptor (ET(A)R) mRNA was lower in renal cortex and medulla of PMR than of YF. Additional groups of rats (n = 6-7/group) were treated for 3 wk with the ET(A)R antagonist ABT-627 (5 mg.kg(-1).day(-1)). BP was significantly higher in PMR than in YF. ET(A)R antagonist reduced BP in PMR by 20% to the level found in control YF. ET(A)R antagonist had no effect on BP in YF. These data support the hypothesis that the increase in BP in PMR is mediated in part by endothelin and the ET(A)R.

Animals↗
PubMed1990

Swine as a model for cardiovascular research: improved cardiopulmonary bypass techniques.

A large-animal model is essential for the assessment of functional parameters in cardiovascular surgical research. To date the canine model has been used successfully because of its availability and tolerance to cardiopulmonary bypass. However, because of decreased availability and increased cost, an alternative animal model is now needed. The swine model has been used in experimental cardiac procedures, but complications during cardiopulmonary bypass have presented a formidable challenge. These complications include enormous fluid shifts from the vascular bed, increased metabolic acidosis, and marked hemoglobinuria. To eliminate these deleterious complications within the swine model, a number of technical alterations were achieved. The priming solution used for the extracorporeal circuit was altered to consist of 1000 mL lactated Ringer's solution. 500 mL 20% mannitol, 500 mL 6% dextran in 5% detrose solution. 50 mEq sodium bicarbonate, and 10,000 IU heparin. The extracorporeal circuit employed the use of membrane oxygenation. Three different blood flow rates (150, 175, and 200 mL/kg min-1) were studied. We conclude that the optimum blood flow rate for cardiopulmonary bypass in swine is in the range of 175-200 mL/kg min-1. Membrane oxygenation results in less damage to blood during cardiopulmonary bypass. The asanguinous hyperosmolar priming solution is beneficial for cardiopulmonary bypass in swine to greatly reduce fluid shifts, prevent metabolic acidosis, and eliminate hemoglobinuria.

Acidosis↗
PubMed1996

Central hypervolemia in the conscious rat: a model of cardiovascular deconditioning.

The aim of the present study as to investigate whether increased central hypervolemia induced by tail suspension (TS) in the rat is an appropriate model of cardiovascular deconditioning (CVD). First, the physiological relationship between central venous pressure (CVP) and extracellular fluid volume (ECFV) was studied. TS (20 degrees) increased CVP (5.8 +/- 0.7 vs. 2.8 +/- 0.8 mmHg; P < 0.01). After 24 h of TS, CVP had returned to control range while ECFV was reduced by 19%. CVP kinetics during 24 h of TS was not affected by either reduction (-20%) or augmentation (/35%) of the ECFV. The normalization of CVP is likely to be a consequence of ECFV reduction, which itself is reduced by increased urinary excretion of water and sodium. Second, recovery from TS was studied. Resumption of the horizontal position was shown to be associated with a significant increase of heart rate (HR) and a slight reduction of blood pressure (BP); there was an apparent delay between increased HR and reduced BP. This imbalance between HR and BP is compatible with CVD. A model of simulated orthostatism (SO) was developed to further investigate the responses of HR and BP. Interestingly, SO (90 degrees rotation) in the normal rat was associated with significant tachycardia and a slight increase of BP. This pattern remained stable for at least 3 h. In rats that were tail suspended for 48 h, episodes of hypotension and bradycardia (5 +/- 1 in 3 h) suggested a defect in adaptation to increased hydrostatic pressure. In conclusion, TS appears to be an appropriate model of CVD. Reduction process. Return to horizontal position in TS rats induced a tachycardia with minimal effects on BP; this pattern is close to that observed in humans assuming upright posture. SO in previously TS rats disclosed episodes of hypotension and bradycardia that deserve further investigation.

Animals↗
PubMed2004

Coronary stent strut size dependent stress-strain response investigated using micromechanical finite element models.

Cardiovascular stents are metal scaffolds that are used in the treatment of atherosclerosis. These devices are typically composed of very thin struts (< or = 100 microm thickness, for coronary applications). At this size-scale the question arises as to the suitability of using bulk material properties in stent design. This paper investigates the use of finite element analysis to predict the mechanical failure of stent struts, typical of the strut size used in coronary stents. 316 L stainless steel in uniaxial loading was considered. To accurately represent the constitutive behavior of the material at this size-scale, a computational micromechanics approach was taken involving an explicit representation of the grain structure in the steel struts, and the use of crystal plasticity theory to represent the constitutive behavior of the individual grains. The development of the finite element models is discussed and results are presented for the predictions of tensile mechanical behavior as a function of strut thickness. The results showed that using this modelling approach, a size effect, already seen experimentally, is produced. This has significant implications for stent design, especially in the context of the desire to produce smaller stents for small bore neurovascular and peripheral artery applications.

Biocompatible Materials↗
PubMed1990

[The marmoset in biomedical research. Value of this primate model for cardiovascular studies].

Because of its small size, low cost of maintenance, breeding capabilities in captivity, the marmoset, a New World monkey, appears well suited for clinical and fundamental investigations. The contribution of this laboratory animal in the main areas of biomedical research is succinctly described: viral oncology, infections diseases, immunology, reproduction, toxicology and teratology, odontology, behaviour and neuro-psychopathology. Emphasis is put upon the exceptional interest of the use of marmoset as a biological model in cardiovascular studies.

Angiotensinogen↗
PubMed2004

Electropharmacological and proarrhythmic effects of a class III antiarrhythmic drug nifekalant hydrochloride assessed using the in vivo canine models.

Cardiovascular effects of Nifekalant were examined using halothane-anesthetized dogs, and its proarrhythmic potential was estimated with chronic complete atrioventricular block dogs. Nifekalant was intravenously administered to the halothane-anesthetized dogs in three doses of 0.03, 0.3, and 3 mg/kg/10 minutes with a pause of 20 minutes (n = 6). The low dose hardly affected any of the cardiovascular parameters. The middle dose, a clinically recommended antiarrhythmic dose, decreased the total peripheral resistance, increased the cardiac output, and prolonged the ventricular repolarization phase and effective refractory period. The high dose increased the left ventricular contraction, transiently decreased the mean blood pressure, and enhanced the atrioventricular conduction, besides potentiation of the changes induced by the middle dose. Increment in the repolarization phase by the high dose was greater than that in the refractoriness, leading to increase of ventricular electrical vulnerability. To the atrioventricular block animals, clinically relevant antiarrhythmic dose of 3 mg/kg p.o. of Nifekalant and its 10-times-higher dose were administered. The high dose prolonged QT interval leading to torsades de pointes in all animals (n = 5), which was not detected by the clinical dose (n = 5). These results suggest that antiarrhythmic dose of Nifekalant can be used safely; however, caution should be paid for patients complicating bradycardia and/or a risk of elevated plasma drug concentration.

Animals↗
PubMed1996

Comparative responses to propofol anaesthesia alone and with alpha 2-adrenergic medications in a canine model.

Cardiovascular and pulmonary effects of propofol, a relatively new nonbarbiturate intravenous anaesthetic, were assessed and compared in 22 male and female dogs. Dogs in group 1 did not receive any premedication prior to 6.6 mg/kg IV propofol, group 2 was premedicated with atropine (0.02 mg/kg IM) and the alpha 2-agonist medetomidine (10 micrograms/kg IM), and group 3 received the same premedication agents as group 2, but the medetomidine effects were reversed by the alpha 2-antagonist atipamezole (30 micrograms/kg IV) after 30 min of anaesthesia. Each dog in groups 2 and 3 received a propofol induction dose of 2.2 mg/kg IV. The anaesthetic duration was shortest with propofol alone and prolonged with medetomidine as a premedication which was reversible with atipamezole. In group 1, the most prominent effects were a temporary drop in diastolic arterial blood pressure (26% and 24%) at 2 and 5 min post-propofol, respectively and a drop in respiratory frequency (41%) 2 min after propofol induction. Similar respiratory depression was observed in groups 2 and 3 (20% and 48%, respectively) at the same time. Apnea was not observed. An increase in systemic arterial blood pressure was observed throughout the trial in groups 2 and 3 until dogs recovered or were reversed with atipamezole. Medetomidine significantly reduces propofol dosage requirements. Safe and effective injectable anaesthesia was produced by propofol in this group of dogs. The frequency of respiratory depression would suggest in clinical usage, the practitioner should be aware oxygen supplementation is the treatment of choice should apnea occur.

Adjuvants, Anesthesia↗
PubMed1996

Modeling of cardiovascular variability using a differential delay equation.

The influence of time delay in the baroreflex control of the heart activity is analyzed by using a simple mathematical model of the short-term pressure regulation. The mean arterial pressure in a Windkessel model is controlled by a nonlinear feedback driving a nonpulsatile model of the cardiac pump in accordance with the steady-state characteristics of the arterial baroreceptor reflex. A pure time delay is placed in the feedback branch to simulate the latent period of the baroreceptor regulation. Because of system nonlinearity model dynamics is found to be highly sensitive to time delay and changes of this parameter within a physiological range cause the model to exhibit different patterns of behavior. For low values of time delay (shorter than 0.5 s) the model remains in a steady state. When time delay is longer than 0.5 s, a Hopf bifurcation is crossed and spontaneous oscillations occur with frequencies in the high-frequency (HF) band. Further increases of time delay above 1.2s cause the oscillations to become more complex, and following the typical Feigenbaum cascade, the system becomes chaotic. In this condition heart rate, and flow show evident variability. The heart rate power spectrum exhibits a peak whose frequency moves from the HF to LF band depending on whether simulated time delay is as short as the vagal-mediated control or long as the sympathetic one.

Baroreflex↗
PubMed1999

Head-out immersion in the non-human primate: a model of cardiovascular deconditioning during microgravity.

BACKGROUND: Orthostatic intolerance is a common complication associated with spaceflight. It has been speculated that this is due to changes in blood volume and alterations in cardiovascular reflexes. The objective of the current study was to develop a model that would allow us to study the cardiovascular system and the regulation of blood volume during short-term microgravity exposure in the primate with the intent of eventually being able to elucidate those factors responsible for the orthostatic intolerance. HYPOTHESIS: Head-out water immersion in the conscious non-human primate simulates the cardiovascular and volume regulatory responses observed in astronauts during exposure to microgravity. METHODS: Four monkeys were chronically instrumented for measuring BP and heart rate and then conditioned to the primate restraint chair. They were then subjected to 72 h of head-out water immersion (two immersions in three monkeys and one immersion in the fourth) in order to simulate the cardiovascular and renal effects of the microgravity environment. RESULTS: During the immersion, there was an increase in arterial BP (ABP) and central venous pressure (CVP) and a reflex decrease in heart rate (HR). Urine flow (UV) increased and water intake decreased, producing a negative water balance. This was not associated with an alteration in food intake. CVP and UV decreased following de-immersion. There was also resetting of the arterial baroreflex control of HR. Significant tachycardia occurred after the immersion that was associated with a decrease in ABP. CONCLUSION: These results are similar to those observed in astronauts during and after spaceflight, suggesting that head-out water immersion of the non-human primate provides a good model for studying cardiovascular and renal adaptations to spaceflight.

Animals↗