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Biomedical subjects

D K Bogen

Publications and source records attributed to D K Bogen.

32 records · Page 2Linked to original sources
PubMed1989

Response of stretch receptors to static inflations and deflations in an isolated tracheal segment.

It has been proposed on the basis of differing responses to static lung inflations that there are two types of pulmonary stretch receptor which are organized in series or in parallel with airway smooth muscle. However, in prior studies, in which we examined the responses of a few receptors in a number of animals, we were unable to confirm this finding. In the present study we sought to definitively address this question by examining the response of a reasonable sample of receptors (greater than or equal to 5) from a single airway with a controlled mechanical environment. We examined the firing patterns of slowly adapting receptors in a tracheal segment, isolated in vivo, during inflations and deflations to different static levels of pressure between -20 and +30 cm H2O. The relationship between afferent firing and intra-tracheal pressure under static conditions was determined. We did not observe any evidence to support the existence of two distinct subtypes of receptors. During these studies we also looked for abrupt changes in the variability of afferent firing during the period of adaptation after the end of an inflation or deflation. Such changes have been described for other receptors with branched endings capable of generating spike potentials. These changes occur when the region generating the spike train seen in the parent fiber switches from one branch to another (pace-maker switching) and reflect the difference in the intrinsic variability of each branch. In the majority of fibers studied we saw no evidence of such switching and thus of the presence of multiple encoders in the receptor structure.

Air Pressure↗
PubMed1989

Measurement of end-systolic pressure-volume relations by intra-aortic balloon occlusion.

A new situ technique has been developed for measuring peak end-systolic elastance, Emax, that does not alter intrinsic or reflex-stimulated cardiac contractility. Afterload is varied by the inflation of an intra-aortic balloon catheter positioned in the ascending aorta. Balloon inflation is timed to interrupt ventricular ejection transiently at different times during the ejection phase, therefore, producing contraction at different ventricular volumes. Simultaneous measurement of left ventricular pressure and aortic flow during the occlusion sequence allows pressure versus ejected volume loops to be generated, from which the end-systolic pressure-volume relation is determined. End-systolic pressure-volume relation (ESPVR) was measured in six anesthetized Dorsett sheep with normal and enhanced contractile states. ESPVR was analyzed using both linear and nonlinear techniques. Although nonlinear components were seen in ESPVR, for the pressure-volume data range produced by the transient occlusions, linear approximations of ESPVR fit the end-systolic data points well. In the normal state, Emax, the slope of the linear ESPVR, was 1.01-5.08 mm Hg/ml in animals with body weights of 23-32 kg. After epinephrine infusion, Emax increased from 3.07 +/- 1.49 to 5.79 +/- 1.97 mm Hg/ml, which is consistent with previous investigations. Linear and nonlinear volume intercepts had a small increase with positive inotropic stimulation. Furthermore, serial measurements of Emax tracked cardiac function in depressed hearts with rapidly changing contractility.

Animals↗
PubMed1988

Changes in left ventricular systolic wall stress during biventricular circulatory assistance.

Extracorporeal membrane oxygenation (ECMO) reduces the systolic stress integral (SSI) in the normal left ventricle. We tested the hypothesis that the SSI does not decrease in poorly contracting, dilated, ejecting hearts during ECMO. In 14 sheep, four pairs of ultrasonic crystals measured changes in left ventricular (LV) wall thickness and three LV diameters. Volume calculations were validated by balloon distention of the ventricles after death (slope = 0.85; r = 0.85). SSI was measured during ECMO flows of 20 to 100 ml/kg/min in both normal and dilated, poorly contracting hearts produced by 30 minutes of warm ischemia. After warm ischemia, end-systolic elastance, an index of contractility, decreased from 8.3 +/- 0.6 mm Hg/ml to 2.9 +/- 0.4 mm Hg/ml (p = 0.001) and peak systolic pressure decreased from 47.4 +/- 0.7 mm Hg to 37.5 +/- 0.08 mm Hg (p = 0.01). In normal hearts, as ECMO flow increased, SSI decreased from 10.5 +/- 2.2 mm Hg.sec to 7.7 +/- 0.8 mm Hg.sec at 60 ml/kg/min (p = 0.001). However, in postischemic hearts, SSI progressively increased from 6.6 +/- 0.3 mm Hg.sec before ECMO to 12.4 +/- 1.8 mm Hg.sec at ECMO = 100 ml/kg/min. These studies indicate that the initial effect of ECMO on the poorly contracting, dilated heart increases LV wall stress and that the increase in stress is proportional to ECMO flow. The increase in stress is primarily due to an increase in afterload, which more than offsets decreases in systolic and diastolic volumes.

Animals↗
PubMed1987

Strain energy descriptions of biological swelling. I: Single fluid compartment models.

Strain energy functions are derived from biphasic soft tissue models in order to describe large-deformation, large-swelling, elastic behavior of nonlinear materials. The resulting analysis leads to calculations of stress-extension relations and tissue fluid pressure. Also explored are the elastic stability of the biphasic tissue models and the manner in which tissue pressure is altered by material deformation.

Animals↗
PubMed1987

Strain energy descriptions of biological swelling. II: Multiple fluid compartment models.

A series of multicompartmental, biphasic elastic tissue models is developed. In its most general form, the models consist of multiple tubular networks, each with an internal spring network. In addition, another spring network occupies the extratubular compartment. Strain energy functions are derived for the models, as well as expressions for the fluid pressures in each compartment arising from volume expansion or swelling. Calculations also show that the distribution of fluid among compartments is a significant determinant of tissue elasticity.

Animals↗
PubMed1987

Load-dependent relaxation with late systolic volume steps: servo-pump studies in the intact canine heart.

In isolated heart muscle preparations an abrupt increase in load during the latter portion of contraction (at a time when there is little if any potential to develop additional force) causes a premature and more rapid relaxation; this load-dependent relaxation characterizes relaxation in myocardium with normal sarcoplasmic reticulum. The purpose of our study was to assess whether or not the phenomenon of load-dependent relaxation is present in the intact heart and to describe the left ventricular response to abrupt load increments (volume steps) throughout the cardiac cycle. Using a microcomputer-controlled servo-pump attached to the apex of an intact canine heart, we studied the effects of 6 ml steps on left ventricular pressure transients during relaxation. Each volume step was carried out in a single beat with 20 stabilization beats separating the intervention beats; thus, at a heart rate of 120 beats/min, a sequence of 10 intervention beats could be carried out in less than 2 min. By performing the experiments on a single-beat basis (control vs intervention beat), we were able to minimize reflex and other physiologic feedback mechanisms that might alter the results. Studies were performed in five anesthetized dogs. In ejecting beats, an early step (immediately after aortic valve opening) caused an increase (3%) in the duration of systole (the time from the onset of pressure rise to the instant at which left ventricular pressure had declined to one-half its maximal value); in contrast, a late step (just before aortic value closure) caused a decrease (7%) in the duration of systole.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Measurement of peak systolic elastance in intact canine circulation with servo pump.

Peak systolic elastance (Emax) was measured in the intact canine circulation by means of a new experimental technique. In this technique the heart is isolated from the circulation during a single systole and subjected to controlled ventricular loads. An electropneumatic aortic occluder is used to isolate the ventricle, and a servo-controlled syringe pump is used to control the ventricular load. Because the experimental load is applied for a single heartbeat only, ventricular function can be measured without the interference of regulatory feedback mechanisms. In eight dogs, weighing 17-42 kg, the relationship between changes in endsystolic pressure and volume was determined from the single-beat application of purely compliant loads. The end-systolic relations were linear, and their slope, Emax, was inversely related to weight. The observed relation between Emax and body weight allows comparisons to be made between different preparations in which Emax has been determined. Values of Emax obtained from the single-beat preparation were found to be 27-74% above those reported in isolated heart preparations and nearly identical to those reported for in vivo or denervated in situ preparations.

Animals↗
PubMed1984

An analysis of myocardial infarction. The effect of regional changes in contractility.

In a preceding paper, we employed an initially spherical, modified membrane model of the infarcted ventricle to investigate the relation between ventricular function and both infarct size and infarct stiffness. In the present paper, we have applied the same model to a set of different questions, namely, the consequences of enhanced or depressed inotropic state within the noninfarcted myocardium. When infarcted ventricles containing up to 41% infarction are examined, stroke volume appears to be relatively insensitive to increases in inotropic state. However, stroke volume falls rapidly when inotropic state is depressed below 80% of normal. For the case of a ventricle with a large, weakly contracting segment which is not totally infarcted, stroke volume is impaired only when the contractility of the weak region is diminished below 50% of normal. Finally, the stress concentration around a region of infarction appears to be dependent more strongly on the inotropic state of the noninfarcted tissue than on the infarct size.

Animals↗
PubMed1980

An analysis of the mechanical disadvantage of myocardial infarction in the canine left ventricle.

An isotropic, initially spherical, membrane model of the infarcted ventricle satisfactorily predicts ventricular function in the infarcted heart when compared to clinical information and available ventricular models of higher complexity. Computations based on finite element solutions of this membrane model yield end-diastolic and end-systolic pressure-volume curves, from which ventricular function curves are calculated, for infarcts of varying size and material properties. These computations indicate a progressive degradation of cardiac performance with increasing infarct sizes such that normal cardiac outputs can be maintained with Frank-Starling compensation and increased heart rate for acute infarcts no larger than 41% of the ventricular surface. The relationship between infarct stiffness and cardiac function is found to be complex and dependent on both infarct size and end-diastolic pressure, although moderately stiff subacute infarcts are associated with better function than extensible acute infarcts. Also, calculations of extensions and stresses suggest considerable disruption of the border zone contraction pattern, as well as elevated border zone systolic stresses.

Animals↗
PubMed1979

Do cardiac aneurysms blow out?

The possibility is suggested that cardiac aneurysms are formed when an infarcted region of the ventricular wall becomes elastically unstable and "blows out". The consequence of such a blowout could be a large saccular aneurysm or even cardiac rupture. We use a nonlinear stress-strain relation capable of describing both the passive and active myocardial wall to examine this possibility in terms of large-deformation membrane theory. Ventricular infarcts made of a material having physical properties like rubber would be expected to blow out, but those made of passive myocardium would not.

Elasticity↗
PubMedDate not supplied

Restraining infarct expansion preserves left ventricular geometry and function after acute anteroapical infarction.

BACKGROUND: Expansion of an acute myocardial infarction predicts progressive left ventricular (LV) dilatation, functional deterioration, and early death. This study tests the hypothesis that restraining expansion of an acute infarction preserves LV geometry and resting function. METHODS AND RESULTS: In 23 sheep, snares were placed around the distal left anterior descending and second diagonal coronary arteries. In 12 sheep, infarct deformation was prevented by Marlex mesh placed over the anticipated myocardial infarct. Snared arteries were occluded 10 to 14 days later. Serial hemodynamic measurements and transdiaphragmatic quantitative echocardiograms were obtained up to 8 weeks after anteroapical infarction of 0.23 of LV mass. In sheep with mesh, circulatory hemodynamics, stroke work, and end-systolic elastance return to preinfarction values 1 week after infarction and do not change subsequently. Ventricular volumes and ejection fraction do not change after the first week postinfarction. Control animals develop large anteroapical ventricular aneurysms, increasing LV dilatation, and progressive deterioration in circulatory hemodynamics and ventricular function. At week 8, differences in LV end-diastolic pressure, cardiac output, end-diastolic and end-systolic volumes, ejection fraction, stroke work, and end-systolic elastance are significant (P<0.01) between groups. CONCLUSIONS: Preventing expansion of acute myocardial infarctions preserves LV geometry and function.

Analysis of Variance↗