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At least 1,333 records · Page 74Linked to original sources
PubMed1988

A physical model for the cardiovascular and the respiratory systems.

We propose a two degrees of freedom oscillating system to simulate the working of both respiratory and cardiovascular apparatus and to investigate the physico-mathematical characteristics of a possible decoupling between the physiological systems. We suppose a double mathematical pendulum with forced and damped oscillations, with the first frequency equal to four times the second one; not only, does the system not give resonance or beatings, but it also simulates with reasonable approximation the ratio between natural relative frequencies. The two Langragian equations, that have form: (formula; see text) cannot be solved in an analytical way, even if we suppose an approximation for little oscillations. Now we are studying another two d-o-f mechanical system, with only one suspension point; we are also studying both the electrical equivalent circuits.

Humans↗
PubMed2001

Gene expression profiles of CLC chloride channels in animal models with different cardiovascular diseases.

Here for the first time we investigated the potential involvement of the CLC chloride channel family at the transcriptional level in different cardiovascular diseases. Northern blot and semiquantitative RT-PCR analyses were used to study the gene expression profiles of all CLC genes present in the heart and kidney; namely, CLC-2, CLC-3, CLC-4, CLC-5, CLC-6, CLC-7, CLC-K1, and CLC-K2. Rat models with distinctive cardiovascular diseases were studied: These included spontaneously hypertensive rats, nutritionally- and surgically-induced hypertensive rats with cardiac hypertrophy, as well as rats suffering from chronic heart failure due to myocardial infarction. The present data show that it was not possible to detect apparent differences in the CLC mRNA expression between the hearts and kidneys of diseased and control animals. Our data strongly suggest that altered transcript regulation of CLC chloride channels does not contribute to the cardiac and renal pathology in the examined cardiovascular diseases.

Animals↗
PubMedDate not supplied

Feedback control of mean aortic pressure in a dynamic model of the cardiovascular system.

Orbital measurements of the cardiac function of Space Shuttle crew members have shown an initial increase in cardiac stroke volume upon entry into weightlessness, followed by a gradual reduction in stroke volume to a level approximately 15% less than preflight values. In an effort to explain this response, it was hypothesized that gravity plays a role in cardiac filling. A mock circulatory system was designed to investigate this effect. Preliminary studies carried out with this system on the NASA KC-135 aircraft, which provides brief periods of weightlessness, showed a strong correlation between cardiac filling, stroke volume, and the presence or absence of gravity. The need for extended periods of high quality zero gravity was identified to verify this observation. To accomplish this, the aircraft version of the experiment was reduced in size and fully automated for eventual integration into a Get Away Special canister to conduct an orbital version of the experiment. This article describes the automated system, as well as the development and implementation of a control algorithm for the servoregulation of the mean aortic pressure in the orbital experiment. Three nonlinearities that influence the ability of the apparatus to regulate to a mean aortic pressure of 95 mm Hg were identified and minimized. In preparation for a Space Shuttle flight, the successful function of the servoregulatory scheme was demonstrated during ground tests and additional test flights aboard the KC-135. The control algorithm was successful in carrying out the experimental protocol, including regulation of mean aortic pressure. The algorithm could also be used for the automated operation of long-term tests of circulatory support systems, which may require a scheduled cycling of the pumping conditions on a daily basis.

Algorithms↗
PubMed2005

Genetic studies in rat models: insights into cardiovascular disease.

PURPOSE OF REVIEW: Limited to 2003-2004 publications, this review focuses on 'big picture' concepts learned from rat genetic studies of cardiovascular disease. RECENT DEVELOPMENTS: Analysis reveals insights into pathogenic paradigms, as well as experimental perspectives into rat-based systems of analyses of complex cardiovascular disease. Key concepts are forwarded. Multiple susceptibility genes underlie several quantitative trait loci for blood pressure suggesting a 'quantitative trait loci cluster' concept; hypertension end-organ disease quantitative trait loci are distinct from blood pressure quantitative trait loci indicating differential susceptibility paradigms for hypertension and each complication (stroke, renal disease, cardiac hypertrophy); distinct blood pressure quantitative trait loci are found in males and females indicating gender-specific susceptibility; and genetic subtypes comprise polygenic hypertension in rat models suggesting a genetic basis for clinical heterogeneity of human essential hypertension. Gender specific genetic susceptibility plays a key role in coronary artery disease susceptibility; multiple distinct quantitative trait loci underlie hyperlipidemia and type-2 diabetes, indicating multiple susceptibilities in risk factors for cardiovascular disease. Studies in transgenic inbred rat-strain models demonstrate value for serial, complex, cardiovascular pathophysiological analyses within a genetic context. SUMMARY: Cognizant of the limitations of animal model studies, observations from rat genetic studies provide insight into respective modeled human cardiovascular diseases and risk factor susceptibility, as well as systematically dissect the multifaceted complexities apparent in human complex cardiovascular disease. Given the recapitulation of many features of human cardiovascular disease, the value of rat model-based genetic studies for complex cardiovascular disease is unequivocal, thus mandating the expansion of resources for maximization of rat-based genetic studies.

Animals↗
PubMed2006

The relationship between homeostasis model assessment and cardiovascular risk factors in Iranian subjects with normal fasting glucose and normal glucose tolerance.

BACKGROUND: Insulin resistance is a complex problem which may not always correlate with all its cardiovascular risk factors in various populations. We investigated the relationship between homeostasis model assessment of insulin resistance (HOMA-IR) with cardiovascular risk factors in Iranian subjects with normal fasting glucose (NFG) and normal glucose tolerance (NGT). METHODS: Of the 605 subjects aged 25-79 y enrolled in this study, after the oral glucose tolerance test, 366 subjects aged 25-50 y and 135 aged >50 y were classified as NFG and NGT. Insulin resistance was estimated by the HOMA-IR. RESULTS: Women had higher values of body mass index (BMI), insulin and HOMA-IR than men in both age groups. The prevalence of insulin resistance, general and abdominal obesity, low HDL-C and physical inactivity was higher in women than men in the 2 age groups. Men had a higher prevalence of hypertension and hypertriglyceridemia in the group with age 25-50 y. The Pearson correlation controlled for age, BMI, waist circumference and physical activity showed that HOMA-IR had significant correlation with triglyceride and inversely associated with HDL-C in both sexes. In addition, the results of HOMA-IR quartiles demonstrated that the prevalence of hypertension, obesity, and low HDL-C was particular high in women with HOMA-IR >2.39. Multiple regression indicated that log HOMA-IR was independently predicted by BMI, triglyceride and HDL-C in men and BMI, HDL-C and waist-to-hip (WHR) ratio in women. CONCLUSIONS: HOMA-IR is associated with the features of metabolic syndrome with a sex difference in the degree and predictors of HOMA-IR and the frequency of cardiovascular risk factors.

Adult↗
PubMed1987

Assessment of animal models for investigating the cardiovascular adaptations to obesity.

Several animal models of obesity have been reviewed with respect to the cardiovascular adaptations to this disorder. While some cardiovascular data are available for each model reviewed, the spontaneously obese rat has been most extensively characterized. Biochemical adaptations of the myocardium to experimental obesity have been reported, but this area has not been investigated extensively. The combined effects of obesity and hypertension upon the heart have been observed recently in the aortic-coarcted, obese rat, which may serve in the future as a useful model for investigating the basis of heart failure that occurs when these disorders are observed concurrently in the clinical setting.

Adaptation, Physiological↗
PubMed1994

New models for predicting cardiovascular events.

Data from the Framingham Heart Study are used to derive equations for long-term predicted probabilities for death and a variety of cardiovascular endpoints. An accelerated failure method is employed, first the standard Weibull model and then a useful extension. The extension relaxes the assumption of proportional hazards implied by the standard Weibull model. Models differ markedly in form for the various endpoints, but in every case the varying scale model provided a significantly better fit. The resulting differences in predicted probability may be important in planning community health projects or clinical trials and in carrying out cost-benefit analyses.

Cardiovascular Diseases↗
PubMed2002

Model simulations of cardiovascular changes at the onset of moderate exercise in humans.

We have tested whether the cardiovascular changes at the onset of exercise could be simulated only by an increase in the baroreflex set point and locally induced vasodilatation in the exercising muscles. The mathematical model consists of a heart, a linear elastic arterial reservoir and two parallel resistive vascular beds. The arterial baroreflex loop is modelled by three separate time domain processing objects, each with its own gain, time constant and delay. These are intended to simulate the action of a sympathetic signal to the peripheral vascular bed, a parasympathetic signal to the heart and a sympathetic signal to the heart. We used this model with previously published experimental data to estimate the unknown parameters in the reflex control loop. In all 10 subjects and in the global averaged response, the short-term cardiovascular responses were adequately simulated by using individual sets of parameters in the model. An increase in the baroreflex set point and locally induced vasodilatation in the exercising muscles can explain almost all of the cardiovascular changes in the recorded variables (mean arterial pressure, RR interval and stroke volume) at the onset of exercise.

Arteries↗
PubMed1980

Mathematical model of the fetal cardiovascular system: the uncontrolled case.

A mathematical model was developed to study and to interpret the results of different experiments undertaken in the field of fetal cardiovascular physiology. This model consists of a total of six peripheral blood compartments and a detailed description of the heart. The unique characteristics of the fetal circulation, particularly the ductus arteriosus, the foramen ovale, and the placenta are incorporated into this model. No control mechanisms are incorporated. The model was validated by simulating several previously described experiments. First, the performance of the individual ventricles was measured. The results indicate that, in the normal physiological situation, the right ventricle is working near the upper limits of its function while the left ventricle works below its limits. Second, the circulatory system was stressed by increasing the blood volume and the results show a shift from right to left in the relative contributions of each ventricle to the total cardiac output. Finally, effects of clamping the several blood vessels of the umbilical cord were studied.

Animals↗
PubMed1995

Cardiovascular response to acute and chronic endotoxemia in an awake, volume-resuscitated, canine model.

The cardiovascular response to endotoxemia was evaluated in an awake, intravascular volume-resuscitated canine model. The animals were chronically instrumented for ultrasonic crystal dimension analysis and pressure measurements of the left ventricle (LV), aorta, right atrium (RA), and pulmonary artery (PA) and for cardiac output (CO) measurement. Lipopolysaccharide (Escherichia coli 011:B4) (LPS) was administered intravenously either as an acute, high dose bolus (5 mg/kg; n = 5), a high dose bolus after complete beta-blockade with propranolol (n = 3), or a chronic, low dose infusion (5 micrograms/kg/h; n = 7). Relative to baseline values, cardiac contractility was increased after acute high dose LPS bolus, however this effect was negated by beta-blockade. Chronic, low dose LPS infusion produced an increase in cardiac contractility at 1 h, a return to baseline by 4 h, and maximal contractile depression by 24 h. No change was seen in LV compliance after the high dose LPS bolus. The LV end diastolic volume was decreased by the high dose LPS bolus. This change was blocked by propranolol administration. Chronic LPS administration was accompanied by a decrease in LV compliance and an increase in LV end diastolic volume. Other cardiovascular indices (heart rate, CO, systemic vascular resistance) changed in a fashion similar to human sepsis. These findings confirm that endotoxemia in conscious canine subjects causes changes in cardiovascular function similar to that seen in human and animal models of sepsis. This study also allows us to explain some of the discrepancies between earlier studies of human sepsis and animal models in which the appropriate clinical conditions and an intact neuro-endocrine axis were not maintained.

Animals↗
PubMed2002

Short-term cardiovascular oscillations in man: measuring and modelling the physiologies.

Research into cardiovascular variabilities intersects both human physiology and quantitative modelling. This is because respiratory and Mayer wave (or 10 s) cardiovascular oscillations represent the integrated control of a system through both autonomic branches by systemic haemodynamic changes within a fluid-filled, physical system. However, our current precise measurement of short-term cardiovascular fluctuations does not necessarily mean we have an adequate understanding of them. Empirical observation suggests that both respiratory and Mayer wave fluctuations derive from mutable autonomic and haemodynamic inputs. Evidence strongly suggests that respiratory sinus arrhythmia both contributes to and buffers respiratory arterial pressure fluctuations. Moreover, even though virtual abolition of all R-R interval variability by cholinergic blockade suggests that parasympathetic stimulation is essential for expression of these variabilities, respiratory sinus arrhythmia does not always reflect a purely vagal phenomenon. The arterial baroreflex has been cited as the mechanism for both respiratory and Mayer wave frequency fluctuations. However, data suggest that both cardiac vagal and vascular sympathetic fluctuations at these frequencies are independent of baroreflex mechanisms and, in fact, contribute to pressure fluctuations. Results from cardiovascular modelling can suggest possible sources for these rhythms. For example, modelling originally suggested low frequency cardiovascular rhythms derived from intrinsic delays in baroreceptor control, and experimental evidence subsequently corroborated this possibility. However, the complex stochastic relations between and variabilities in these rhythms indicate no single mechanism is responsible. If future study of cardiovascular variabilities is to move beyond qualitative suggestions of determinants to quantitative elucidation of critical physical mechanisms, both experimental design and model construction will have to be more trenchant.

Blood Pressure↗
PubMed1998

Animal models of human cardiovascular disease, heart failure and hypertrophy.

The progress made in our understanding of the pathophysiology and treatment of congestive heart failure (CHF) would not have been possible without a number of animal models of heart failure and hypertrophy, each one having unique advantages as well as disadvantages. The species and interventions used to create CHF depends on the scientific question as well as on factors such as ethical and economical considerations, accessibility and reproducibility or the model. How closely the model should mimic the human syndrome of CHF depends on the scientific question under investigation. If the goal is to study pathophysiological processes like remodeling or the function of subcellular systems such as excitation contraction-coupling processes, contractile protein function or energetics, the model of heart failure should mimic the clinical setting as closely as possible. However, if defined causal connections are under investigation such as structure-function analyses or regulation of gene expression, exact reflection of the clinical setting by the animal model may be less important. In this review, animal models of heart failure are discussed with particular focus on similarities between the animal model and the failing human heart regarding myocardial function as well as molecular and subcellular mechanisms. In addition, new models of heart failure and hypertrophy, and finally some recent animal models of myocarditis are reviewed.

Animals↗
PubMed2006

The missing link between cardiovascular rhythm control and myocardial cell modeling.

Cardiac arrhythmia is currently investigated from two different points of view. One considers ECG bio-signal analysis and investigates heart rate variability, baroreflex control, heart rate turbulence, alternans phenomena, etc. The other involves building computer models of the heart based on ion channels, bio-domain models and forward calculations to finally reach ECG and body surface potential maps. Both approaches aim to support the cardiologist in better understanding of arrhythmia, improving diagnosis and reliable risk stratification, and optimizing therapy. This article summarizes recent results and aims to trigger new research to bridge the different views.

Biological Clocks↗