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Biomedical subjects

J V Tyberg

Publications and source records attributed to J V Tyberg.

At least 19 recordsLinked to original sources
PubMed1992

Inosine--a natural modulator of contractility and myocardial blood flow in the ischemic heart?

The energetic role of inosine (INO) remains controversial. The aim of the present study was first to test whether endogenous INO consumption/production correlates with regional myocardial contractile performance and second to test whether locally increased levels of INO influence contractility and blood flow in severely ischemic myocardium. Fentanyl-anesthetized dogs with implanted sonomicrometry crystals and independently perfused left anterior descending coronary arteries were studied. Two relatively load-independent indexes of regional myocardial contractility derived from left ventricular pressure-segment length loops were used: the regional stroke work-end-diastolic segment length relationship (Wr/L(ed)) and the end-systolic pressure-segment length relationship (Plv/L(es)). Very good correlations between myocardial contractile performance (as measured by the slope of the regional Wr/L(ed) relationship) and endogenous INO consumption/production under both nonischemic and ischemic conditions were found. Ischemia severely depressed contractility, significantly shifting rightward the Wr/L(ed) and Plv/L(es) relationships. INO infused into the left anterior descending bypass, in a concentration of 600 to 800 mumol/L, partially restored contractile performance as evidenced by a significant leftward displacement of both relationships. Wr, measured at a common maximum L(ed), increased significantly by 61 +/- 5%. Border-zone collateral flow (microspheres) increased by 35 +/- 7% within the endocardial segments and by 34 +/- 9% in the epicardial segments, but no increase in flow in the ischemic region was measureable. With the current emphasis on recanalization with thrombolytic therapy and considering the apparent safety of INO, this naturally occurring nucleoside might prove to be a useful adjunctive agent in the treatment of acute myocardial ischemia.

Animals↗
PubMed1992

The importance of pericardial constraint in experimental pulmonary embolism and volume loading.

To clarify the magnitude of the contribution of pericardial constraint to the hemodynamic deterioration that is observed during acute pulmonary embolism, hemodynamics and chamber dimensions (sonomicrometry) were measured during pulmonary embolization and subsequent volume loading in six anesthetized and instrumented open-chest, open-pericardium dogs. Embolization markedly increased peak right ventricular systolic pressure (38 +/- 5 mm Hg before embolism to 64 +/- 12 mm Hg after repeated embolization, p less than 0.05). However, right ventricular stroke volume decreased by only an insignificant amount (17 +/- 7 ml to 15 +/- 6 ml, p = not significant). Indices of left ventricular end-diastolic volume (left ventricular area = anteroposterior x septum-to-left ventricle free wall diameters) and stroke work (stroke work = area of the left ventricular pressure-area loop) were also similar before and after repeated embolization. Volume loading after repeated embolization resulted in increased right ventricular stroke volume (15 +/- 6 ml to 20 +/- 4 ml, p = 0.06), left ventricular area (3320 +/- 600 mm2 to 3470 +/- 580 mm2, p less than 0.05) and stroke work (261 +/- 158 mm Hg to 425 +/- 170 mm Hg x mm2, p less than 0.05). These results are in marked contrast to those in a previously reported study in a closed-chest and closed-pericardium model in which there was a decrease in left ventricular preload and systolic function after similar embolization-induced right ventricular pressure loading. Moreover, there was a further decrease in these parameters as a result of volume loading after embolism in the closed pericardium experiments. In conclusion, pericardial constraint contributes to hemodynamic deterioration during both acute right ventricular pressure loading and subsequent volume loading. The hemodynamic response to both interventions in the intact animal is determined not only by the degree of right ventricular dysfunction but also by the degree of direct ventricular interaction.

Animals↗
PubMed1992

Venous modulation of ventricular preload.

The objective of this discussion has been to describe a simple conceptual model of the circulation that emphasizes the role of the venous capacitance vasculature and is based on simplified vascular pressure-volume relationships. First, it is hoped that this approach will avoid some of the misunderstandings and contradictions that have resulted from an approach to the veins that is based on pressure-flow relationships. As mentioned at the outset, the confusion between venous volume and flow has led to the anomalous but logical conclusion that decreased venous pooling corresponds to increased venous return (which must equal cardiac output in the steady state). Second, it is also hoped that the model will prove to be a useful starting point from which to better understand how the veins modulate cardiac output in the normal individual and how alterations in venous capacitance affect the hemodynamic profile of congestive heart failure.

Arteries↗
PubMed1992

Changes in the radius of curvature of the ventricular septum at end diastole during pulmonary arterial and aortic constrictions in the dog.

BACKGROUND: At end diastole, the position and shape of the ventricular septum depend on the transseptal pressure gradient. It is not clear, however, how the septal radius of curvature changes in response to the gradual change in transseptal pressure gradient during progressive pulmonary arterial constriction (PAC) and aortic constriction (AC). METHODS AND RESULTS: In 11 anesthetized open-chest dogs, the septal radius of curvature was measured from the short-axis two-dimensional echocardiogram, and the transseptal pressure gradient (left ventricular [LV] pressure minus right ventricular [RV] pressure) was calculated from ventricular pressures measured with micromanometers. Seven dogs were studied with both PAC and AC (group 1) and four dogs only with PAC, which was initiated before and after volume loading (group 2). The transseptal pressure gradient decreased during PAC. As the transseptal pressure gradient decreased, the septum shifted continuously leftward with decreases in the LV septum-free wall diameter and in LV cross-sectional area. The septal radius of curvature (Rs) increased until the septum became flat. The flat septum (i.e., Rs = infinity) occurred at a relatively constant value of transseptal pressure gradient (-4.6 +/- 1.4 mm Hg) independently of the absolute values of LV pressures when between 2 and 9 mm Hg, although necessarily a greater RV pressure was needed to make the septum flat when LV pressure was higher. After inversion, the septum again became curved, with a decrease in the absolute value of septal radius of curvature as the transseptal pressure gradient became increasingly negative. The septum was still concave to the LV cavity at zero transseptal pressure gradient, and its curvature decreased (i.e., its radius of curvature increased) with increases in ventricular pressures. During AC, the septal radius of curvature also increased, but with an increase in transseptal pressure gradient accompanied by increases in LV septum-free wall diameter and in LV area. In group 2 animals, at zero transseptal pressure gradient, the normalized septal radius of curvature was greater (p less than 0.005) at high LV pressure than at low LV pressure. The transseptal pressure gradient required to make the septum flat was not significantly different between low and high LV pressure, which confirmed the results of group 1. CONCLUSIONS: The results of the present study show that the shape and position of the ventricular septum are determined by the transseptal pressure gradient but that the shape of the septum is also affected by the ventricular pressures. The septum was not flat but rather still concave to the LV cavity at zero transseptal pressure gradient. Approximately 5 mm Hg of negative transseptal pressure gradient was required to displace the septum farther leftward and make it flat. The septal radius of curvature increased during both PAC (which decreased transseptal pressure gradient) and AC (which increased transseptal pressure gradient), indicating that the mechanisms involved in changing septal radius of curvature are different during PAC and AC.

Animals↗
PubMed1992

Changes in pericardial pressure during the perinatal period.

BACKGROUND: To determine how the tissues that surround the heart affect diastolic and systolic function during the perinatal period, we studied the pressure-diameter relation of the left ventricle in partially delivered fetal lambs. METHODS AND RESULTS: We anesthetized (1.5-2.0% halothane, balance O2) and ventilated six pregnant ewes (142-144 days of gestation) and then partially delivered each lamb by cesarean section. Each lamb was instrumented to record left ventricular anteroposterior diameters (endocardial ultrasonic transducers), pericardial pressure (liquid-containing balloon), and left ventricular pressure (transducer-tipped catheter). Left ventricular pressure-diameter relations were recorded under three conditions: initially, with a closed chest and closed pericardium (before ventilation); second, after interruption of the umbilical circulation and 1 hour of ventilation; and finally, when the lungs and the pericardium were retracted from the heart. Pericardial pressure (recorded at a common diameter, i.e., the maximal end-diastolic diameter recorded before ventilation) decreased by 48% after 1 hour of ventilation (p < 0.05). After ventilation, left ventricular anteroposterior diameters were 4-5% greater (p < 0.05) at each end-diastolic pressure compared (12.5, 15.0, 17.5, and 20 mm Hg). Thus, ventilation appeared to increase left ventricular diastolic compliance. Contractility also appeared to increase after ventilation when evaluated using ventricular stroke work as a function of end-diastolic pressure as preload. When we used a more appropriate measure of preload (i.e., transmural end-diastolic pressure), ventilation did not change left ventricular diastolic compliance or contractility. Thus, left ventricular systolic function increased because of an increase in preload. CONCLUSIONS: The tissues surrounding the fetal heart significantly augment pericardial pressure and limit left ventricular preload. The initiation of ventilation reduces pericardial pressure, increases left ventricular preload, and increases left ventricular systolic function. At birth, a decrease in pericardial pressure and the resulting increase in preload may help increase left ventricular output through the Frank-Starling mechanism.

Animals↗
PubMed1979

Reduction in ventricular endocardial and epicardial potentials during acute increments in left ventricular dimensions.

Unipolar potentials were recorded from the endocardium (Endo-Pot) and the epicardium (Epi-Pot) of the left and right ventricles of anesthetized open-chested dogs during acute changes in left ventricular dimension by blood transfusion. A pair of implanted ultrasonic crystals were used to detail changes in left ventricular (LV) anteroposterior diameter. When the diameter increased by an average of 11 per cent, LV Endo-Pot decreased by 28 per cent and LV Epi-Pot decreased by 15 per cent. Right ventricular Endo-Pot and Epi-Pot concurrently decreased by similar magnitude (-36 per cent). The relationship between potentials and LV diameter showed negative linearity over the ranges examined, and was not influenced by changes in hematocrit. No inverse relation between changes in Endo-Pot and Epi-Pot was observed. It is suggested that potentials when recorded directly from the endocardium or epicardium mainly reflect the electrical activity of the tissues in the immediate vicinity of the electrode. It is postulated that an increase in ventricular volume by producing stretching and thinning of ventricular walls, reduces the effective tissue mass represented in the electrode signal, thereby accounting for a reduction in both endo and epicardial potentials. Although the precise mechanisms of changes in ventricular potentials remains unclear, such changes, nevertheless, may indicate, in clinical circumstances, an acute shift in left ventricular volume.

Action Potentials↗
PubMed1979

Determination of frequency response from step response: application to fluid-filled catheters.

The performance of a fluid-filled catheter can be described by reporting its undamped natural frequency and damping ratio. These parameters can be measured by subjecting the catheter to sinusoidally varying pressures at a wide variety of frequencies to obtain the frequency response. They can also be computed from the response to a step change in pressure, which is often easier to produce. This paper derives the required equations and includes a graph which permits one to look up the undamped natural frequency after measuring the period and decay rate of the oscillation following a step change in pressure.

Cardiac Catheterization↗
PubMed1979

Resistance and volume changes caused by nitroprusside in the dog.

Changes in vascular volume caused by a pharmacologic agent are frequently inferred rather than directly measured. We investigated the effects of nitroprusside in 8 dogs divided into 2 groups: control and splenectomized. We anesthetized the dogs using pentobarbital, and surgically prepared a veno-right atrial bypass preparation whose controlled cardiac output and external reservoir allowed measurement of both changes in vascular resistance and changes in vascular volume. In both groups, blood pressure (mean +/- SD) decreased at each successive level of nitroprusside: 114 +/- 24 mmHg (base line), 101 +/- 19 mmHg (45 microgram/min), 90 +/- 16 mmHg (90 microgram/min), 81 +/- 17 mmHg (180 microgram/min), 68 +/- 18 mmHg (360 microgram/min). Nitroprusside caused a large and similar decrease in vascular resistance in both groups. In the control group, vascular volume increased above base line 5.5 +/- 2.7, 8.3 +/- 3.2, 11.6 +/- 2.9, and 14.7 +/- 3.5 ml/kg at each successive level of nitroprusside infusion, whereas in the splenectomized group vascular volume increased above base line 0.9 +/- 0.3, 2.5 +/- 1.0, 3.3 +/- 1.1, and 4.0 +/- 1.3 ml/kg at each successive level of nitroprusside infusion, but increased significantly less than the control group. We concluded that nitroprusside decreases vascular resistance and increases vascular volume and that the spleen is the major site of changes in vascular volume caused by nitroprusside.

Animals↗
PubMed1978

Pronounced dependence of ventricular endocardial QRS potentials on ventricular volume.

To evalulate the relation between ventricular endocardial potentials (QRS amplitude) and ventricular dimensions, left and right ventricular endocardial potentials were recorded with hook electrodes in anaesthetised open-chest dogs during transfusion and withdrawal of blood. Left ventricular end-diastolic diameter was measured by ultrasonic crystals, and end-diastolic volume was determined by thermodilution. In each dog, left ventricular endocardial potentials, whether recorded from anterior or posterolateral walls, decreased linearly as left ventricular end-diastolic diameter or volume increased, and vice versa. With an average increase in left ventricular end-diastolic diameter from 40.1 +/- 1.7 to 44.6 +/- 1.8 mm, left ventricular endocardial potentials decreased from 32.8 +/- 2.5 to 23.5 +/- 2.3 mV (P less than 0.001); and for an increase in left ventricular end-diastolic volume from 1.36 "/- 1.25 to 3.43 +/- 0.58 ml/kg left ventricular endocardial potentials decreased from 36.2 +/- 6.6 to 14.9 +/- 4.3 mV (P less than 0.001). Changes in right ventricular endocardial potentials paralleled the changes in left ventricular endocardial potentials. These findings indicate that acute changes in ventricular dimensions influence endocardial potentials considerably, and suggest a potential clinical application for detecting acute changes in ventricular volume.

Action Potentials↗
PubMed1978

Segment stroke work and metabolism depend on coronary blood flow in the pig.

We determined the mechanical and metabolic effects of graded myocardial ischemia in 23 open-chest, anesthetized pigs. By connecting the midportion of the left anterior descending artery (LAD) to the carotid artery via a constant volume, calibrated pump, we reduced the flow in the LAD to 0, 25, 50, and 75% of control rates for periods of 1 h. Flows of 100% and 150% were also examined. Using pairs of ultrasonic crystals to measure segment dimensions, we calculated segment shortening and thickening, and total and systolic stroke work in the ischemic and normally perfused segments. Blood gases, pH, and lactate and inosine balances were determined from the regional coronary venous blood. At coronary blood flows of 0, 25, 50, and 75% of normal resting flow, total segment work was 8 +/- 8, 25 +/- 4, 51 +/- 5, and 80 +/- 6% of control, respectively, while systolic segment work was -2 +/- 5, -10 +/- 5, 40 +/- 5, and 86 +/- 7% of control, respectively (means +/- SE). Thus, the decrease in total segment stroke work is proportional to the decrease in flow over the range 0-100%. However, no useful work (i.e., systolic work) is done until flow exceeds 25%. Segment shortening and thickening are significantly depressed with flows diminished by only 25%. Segmental inosine production correlates with lactate production and parallels decreased mechanical performance.

Animals↗
PubMed1978

Coronary sinus reflux. A source of error in the measurement of thermodilution coronary sinus flow.

In seven patients thermodilution coronary sinus flow (TD-CSF) was higher (164 +/- 21 ml/min) during ventricular pacing than during atrial pacing (119 +/- 21 ml/min, P less than 0.005) at identical heart rate, without an increase in the determinants of myocardial oxygen consumption. To assess the possibility of right atrial admixture in coronary sinus blood during ventricular pacing we compared electromagnetic coronary arterial blood flow (CBF) with TD-CSF in nine dogs during interventions that increased right atrial pressure. During ventricular pacing, rapid atrial pacing, pulmonary artery constriction and increased intrathoracic pressure, right atrial pressure increased and electromagnetic CBF was significantly less (41-166%) than TD-CSF. Marked reflux from the right atrium to the coronary sinus was also demonstrated by bolus injection of cold saline into the right atrium and continuous infusion of contrast material into coronary sinus. Caution needs to be exercised in interpreting TD-CSF in the presence of changing right atrial pressure.

Adult↗
PubMed1978

A mechanism for shifts in the diastolic, left ventricular, pressure-volume curve: the role of the pericardium.

Attempts to explain acute shifts in the pressure-volume relationship by changes in myocardial stiffness have been unsupported by animal experimentation and discouraged by calculations showing that making half the ventricle rigid would hardly account for the clinically observed upward shifts in the curve. Data collected in open-chest anesthetized dogs during volume loading with the pericardium open and closed indicate that when the pericardium is closed, left ventricular enddiastolic pressure is better predicted by right ventricular pressure than by left ventricular dimensions. These data support the hypothesis that acute, upward shift in the pressure-volume curve may be caused by an increase in pericardial pressure, in turn caused by an increase in the volume of the intrapericardial contents. This follows from the fact that measured left ventricular diastolic pressure is equal to the sum of the pressure differences accross the myocardium and the pericardium. Thus, increases in pericardial pressure raise measured ventricular diastolic pressure without change in ventricular volume: hence, an upward shift in the pressure-volume curve.

Animals↗