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Biomedical subjects

A Noordergraaf

Publications and source records attributed to A Noordergraaf.

At least 19 recordsLinked to original sources

Right ventricular-pulmonary arterial interactions.

The application of pulsatile models to hemodynamic data has made possible a more complete understanding of the relationship of pulmonary pressure and flow. To review the genesis of these concepts, the unique characteristics of the pulmonary artery and right ventricle are outlined as a basis for understanding why differences in their pulsatile properties from the systemic circuit must exist. The pulmonary impedance spectrum is introduced and the concept of optimal right ventricular-pulmonary artery coupling is explored based on a review of extensive experimental data. Finally, available studies of normal pulmonary impedance in man and abnormal impedance in human disease states are reviewed, with emphasis on disturbances in optimal ventricular-vascular coupling. The important implications of these concepts for understanding and treatment of cardiovascular disease are developed.

Coronary Disease

Cardiac adaptation of sarcomere dynamics to arterial load: a model of hypertrophy.

In the past, the dynamics of the left ventricle were studied by its response to altered venous and arterial load for a given heart. This led researchers to propose the concept of an arterioventricular match or optimal point of function. The model of this paper reverses that idea by fixing preload and afterload while computing cardiac function due to altered left ventricular size or shape, resulting from modification of the number of parallel and series sarcounits. A mathematical model of physiological hypertrophy is introduced. Series and parallel arrangements of sarcounits constitute a cylindrical model of the left ventricle. Filling occurs from a venous reservoir with constant pressure through a valve, while ejection takes place into a three-element model of the systemic arterial system through another valve. It is found that the dynamics of the myofibrils can be matched to those of the left ventricle by choosing a ventricular shape that results in a minimum in myocardial O2 consumption (MVO2) for any constant ventricular load. A unique solution for the size of the ventricle results if the rate of MVO2 is specified. The model is able to predict correctly hypertrophy due to hypoxia and due to pressure (concentric) and volume (eccentric) overloads.

Adaptation, Physiological

Thresholds for premature ventricular contractions in frog hearts exposed to lithotripter fields.

Piezoelectrically generated lithotripter shocks were shown to produce premature ventricular contractions of the frog heart. Anesthetized grass frogs, Rana pipiens, were studied following implantation of an aortic catheter and EKG leads. The most sensitive phase of the heart cycle for the generation of premature ventricular contractions with lithotripter shocks at 30 MPa peak pressure was found to be the T-P segment. During this phase of the heart cycle, the minimum peak-positive pressure shock wave necessary to produce a premature ventricular contraction in a frog heart was between 5 MPa and 10 MPa.

Animals

Similar pressure pulse propagation and reflection characteristics in aortas of mammals.

Similar pressure and flow waveforms recorded in mammalian aortas suggest that pulse transmission characteristics may also be similar. We examined the validity of this hypothesis, utilizing allometric equations of pertinent hemodynamic parameters and a model of the arterial system. Results show that both the reflection coefficient and the propagation constant times the aortic length are essentially invariant across the mammalian species investigated. Resolved forward and reflected propagating waves are also similar. These findings suggest that the arterial system in these mammals indeed functions in a similar manner.

Animals

Effect of interfacial tension on flow of fluorochemicals in the vasculature of the lung: a theoretical and experimental study.

Perfluorocarbons can be selectively imaged using magnetic resonance. When introduced in the vasculature they do not flow beyond a certain level. This level depends on the driving pressure. We consider here such flow stoppage in the case of the vascular bed of rat lung. A theoretical analysis based on the assumption that interfacial tension is primarily responsible for this phenomenon leads to a formula that predicts a "critical" radius of the vessels at where the flow stops. This radius depends on the driving pressure. The predicted result was verified experimentally using direct measurements on histological sections and was found to confirm the hypothesis.

Animals

Theoretical and experimental analysis of right ventricular bypass and univentricular circulatory support.

In this paper we examine the dynamic coupling between cardiac pump events and vascular arterial-venous factors that regulate the rate of blood flow around the circulation. A series of experiments were designed to test the feasibility of maintaining vascular and pulmonary function in the absence of the right heart and to characterize the physiologic and hemodynamic consequence of such an exclusion. Theoretical analysis of the cardiovascular system (excluding neuro-humoral factors) using both lumped time invariant and distributed compartmental mathematical equivalent representations, demonstrated that a change in cardiac output (Q) has an inverse-linear effect on venous and direct-linear effect on arterial pressure. A single blood-pump, in a form of a mechanical substitute or the biologic left-heart, alone can support the circulation. Cardiac output reserve is limited (50 percent of normal) because of the rapidly diminishing pulmonary venous-pressure as outflow is increased, irrespective of the pump's specific characteristics. Experiments in animals combined with mock-circulatory studies and computer modeling confirm that near normal flow can be sustained by increasing the stressed blood volume or reducing selectively the systemic venous compliance (i.e., inflatable pressure suit, venous constriction, intra-abdominal compression maneuvers, etc.). The right heart is not essential for normal pulmonary circulation but serves to maintain low systemic venous pressure and relatively high left-heart flow reserve. Purely mechanical properties of the vascular system determine the control and stability of the circulation.

Animals

Model-based analysis of transmural vessel impedance and myocardial circulation dynamics.

The basic structure of a model of the coronary circulation has been developed to explain the relationship between transmural perfusion dynamics and intramyocardial mechanics. The model is in the form of a topologically isomorphic network representation and incorporates experimentally measured time-varying perfusion and intramyocardial pressure sources as driving inputs to the model. The intramyocardial vessels are treated as nonlinear impedance elements possessing regional external pressure-dependent resistance and capacitance. Three circuit branches, perfusing the epicardial, subepicardial, and subendocardial muscle layers, are mathematically modeled and are used to predict time-dependent flow within the left ventricular myocardium. The phasic coronary blood flow characteristics predicted by the model exhibit waveform patterns that correlate qualitatively with those patterns measured experimentally. In addition, the pressure-dependent vascular capacitance induces a sustained (out of phase with arterial inflow) venous systolic flow. The model also exhibits retrograde systolic subendocardial flow and stop-flow pressure, which are dependent on coronary resistive and capacitive properties and on the perfusion pressure decay time constant. Furthermore, the results predict an abrupt decrease in subendocardial flow with perturbation of either arteriolar or capillary bed compliance. The model describes time-dependent intramyocardial properties that have been confusing and controversial in the understanding of coronary circulation dynamics. Several steps are identified that are expected to improve and refine the model significantly.

Animals

Estimation of total systemic arterial compliance in humans.

Systemic arterial compliance, a major component of aortic input impedance, was determined in 10 patients with congestive heart failure secondary to idiopathic dilated cardiomyopathy and 11 age-matched control subjects found free of detectable cardiovascular disease. Total arterial compliance was determined from high-fidelity ascending aortic pressure and velocity recordings using 1) the traditional monoexponential aortic diastolic pressure decay and 2) the direct solution of the equation, which describes the three-element windkessel model of the arterial system. Resting values for total arterial compliance (x10(-3) cm5/dyn) derived from method 1 were significantly correlated with compliance derived from method 2 (r = 0.89, P less than 0.01). However, method 1 values (control mean 1.15 +/- 0.27, heart failure mean 1.18 +/- 0.54) were consistently and significantly lower (P less than 0.001) than method 2 values (control mean 1.59 +/- 0.50, heart failure mean 1.38 +/- 0.60). Resting total arterial compliance in heart-failure patients was not significantly different from control subjects. Total arterial compliance did not significantly change with exercise in either group despite increases in arterial pressure. However, nitroprusside administration in the heart-failure group increased total arterial compliance both at rest and on exercise compared with the unmedicated state. These different methodological approaches to the estimation of total arterial compliance in humans resulted in significantly different absolute values for compliance, although both methods provided concordant results with respect to the response of arterial compliance to physiological and pharmacological interventions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult

The Korotkoff sound.

As the auscultatory method of blood pressure measurement relies fundamentally on the generation of the Korotkoff sound, identification of the responsible mechanisms has been of interest ever since the introduction of the method, around the turn of the century. In this article, a theory is proposed that identifies the cause of sound generation with the nonlinear properties of the pressure-flow relationship in, and of the volume compliance of the collapsible segment of brachial artery under the cuff. The rising portion of a normal incoming brachial pressure pulse is distorted due to these characteristics, and energy contained in the normal pulse is shifted to the audible range. The pressure transient produced is transmitted to the skin surface and stethoscope through deflection of the arterial wall. A mathematical model is formulated to represent the structures involved and to compute the Korotkoff sound. The model is able to predict quantitatively a range of features of the Korotkoff sound reported in the literature. Several earlier theories are summarized and evaluated.

Auscultation

Pulse reflection sites and effective length of the arterial system.

The concept of effective length (L) of the arterial system implies that it may be represented by a single viscoelastic tube terminated by an impedance, creating a single reflection site. Although the concept is straightforward, investigators for years have been unable to agree on the value of L. Proposed values range from a few millimeters to a few meters, confounding the identification of arterial reflection sites. This report shows analytically and illustrates with experimental data that the determination of the effective length leaves room for an infinite number of exact solutions for L and the corresponding terminal impedance if the input impedance of the tube is to match the measured input impedance of an arterial system. None of the possible values of L needs to bear any relationship to actual reflection sites.

Animals

Intramyocardial pressure: interaction of myocardial fluid pressure and fiber stress.

Previous measurements of intramyocardial pressure (IMP) have yielded systolic pressures that range from values lower than to far exceeding systolic left ventricular pressure (LVP). This study identifies a possible mechanism underlying these divergent observations by building on established morphology of the ventricular wall. It is hypothesized here that the generation of fiber stress as a manifestation of myocardial contraction increases fluid pressure in the myocytes and the interstitial spaces. This increase in fluid pressure in turn generates the pressure in the ventricular cavity. Thus there are two quantities of interest: intramyocardial fluid pressure (IFP) and intramyocardial fiber stress (IFS). To test the hypothesis, we conducted experiments on conditioned dogs, utilizing a side-mounted catheter-tip strain gauge transducer to sense IMP as the sum of IFP and some component of IFS. In addition, a recessed end-tip fiber-optic transducer with its sensing element shielded from local myocardial fibers was employed to sense IFP. Both IFP and IMP were measured at various depths in the left ventricular free wall. The effects of inotropic interventions by administration of epinephrine and propranolol, mechanical interventions via clamping of the aorta and ligation of the left anterior descending coronary artery, and neural interventions by stimulation of the ansa subclavian of the stellate ganglion and right vagus were recorded. A transmural gradient in the wall for both IMP and IFP was observed. Systolic values of IFP recorded in the endocardium match those of LVP, with peak IMP exceeding both. The results support the hypothesis and offer an interpretation of the long-standing controversy regarding the magnitude of IMP with respect to LVP.

Animals

Nonlinear structural and material properties and models: the pulmonary trunk.

General models are developed for static and dynamic geometric and material passive responses. The models are applied to data obtained from the main pulmonary arteries of calves and dogs. The structural model predicts distortions by simultaneous stretching and bending in a concise manner. Parameters are obtained by a five-element material model. This latter predicts static and dynamic, nonlinear, frequency-dependent, viscoelastic responses observed in biomaterials over the entire strain range irrespective of the nature of loading. Validity and baseline parameter values are investigated for the inactivated state, developed by poisoning the smooth muscle with potassium cyanide. Complexities, related to nonlinear (strain-dependent) and colloidal (thixotropic) properties of tissues, are analyzed. These properties enter into functional responses in a complex manner that can modify substantially concepts of material components and vary appreciably between physiologic circumstances and laboratory evaluations. We propose that, in general, evaluations of material responses must account for these properties.

Animals

Pressure pulse transmission into vascular beds.

Observations at the microcirculatory level have revealed that (a) the pressure pulse reaches the smallest vessel, and (b) the pulse wave velocity alters from a value in the order of meters/second in large arteries to a value in the order of centimeters/second in the microvessels. We investigate, herein, whether these experimental findings are consonant with linear pulse wave transmission theory in a branching system of vessels. Our computations, utilizing available data, show that this is indeed the case. For low frequency (1 Hz), cumulative attenuation is such that about one-third of the pulse, originating at the heart, reaches the capillary. A 10-Hz pulse, however, is virtually completely attenuated by the time the capillary is reached. Transmission time for a pulse, from heart to capillary, is also frequency dependent, with higher frequencies propagating more rapidly. Vasoconstriction, at the arteriolar level in the absence of reflection, can also strongly attenuate the pulse remnant at that site.

Blood Pressure

Directional disparity of pulse reflection in the dog.

Local reflection coefficients were experimentally determined in the dog for the first time at the aortoiliac junction using characteristic impedances derived from phase velocity, fluid density, and the vessels' cross-sectional areas. Reflection coefficients were determined for both the normal trifurcation and with the segment of aorta between external and internal iliacs occluded. For the normal case the coefficients were as follows: antegrade, 0.7; retrograde, -0.74. For the occlusion case the coefficients were as follows: antegrade, 0.33; retrograde, -0.67. These results provide experimental support for the concept that the vascular system, at least in this region, favors antegrade and suppresses retrograde pulse transmission. In addition, global reflection coefficients were determined in the femoral artery using a three-point pressure technique. Coefficient magnitudes varied from low (1.6 Hz) to high (9.6 Hz) frequencies, i.e., control, 0.42-0.22; vasoconstriction, 0.65-0.33; vasodilation, less than 0.1 for all frequencies. Discrepancies between results appearing in the literature are evaluated and shown to be associated with the method utilized as well as with system nonlinearities enhanced by tying branches.

Animals