CARDIAC PERFORMANCE IN HEART–LUNG PREPARATIONS OF RATS WITH EXPERIMENTAL CARDIAC HYPERTROPHY

1966 ◽  
Vol 44 (1) ◽  
pp. 21-27 ◽  
Author(s):  
B. Korecky ◽  
M. Beznak ◽  
M. Korecka
Keyword(s):  
Cardiac Output ◽  
Left Ventricle ◽  
Arterial Pressure ◽  
Cardiac Hypertrophy ◽  
Cardiac Performance ◽  
Aortic Constriction ◽  
Chronic Anemia ◽  
Stepwise Increase ◽  
Thyroxine Treatment ◽  
Made In

Heart-lung preparations (h.l.p.) were made in normal rats and in rats with cardiac hypertrophy produced by aortic constriction, thyroxine treatment, or chronic anemia. In the h.l.p., arterial pressure was kept constant at 100 mm Hg, and maximum cardiac output (m.c.o.) was measured by stepwise increase in the inflow of blood until no further rise in cardiac output occurred. The m.c.o. of enlarged hearts was above normal, but not if it was expressed per gram of left ventricle weight. This latter value was not above normal in any of the enlarged hearts, contrary to earlier findings in whole animals. In fact, in one group of severely anemic rats it was significantly below normal.

scholarly journals CARDIOVASCULAR EFFECTS OF THYROXINE TREATMENT IN NORMAL RATS

1962 ◽  
Vol 40 (12) ◽  
pp. 1647-1654 ◽  
Author(s):  
Margaret Beznák ◽  
A. Marcsán ◽  
T. Fournier
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Cardiac Hypertrophy ◽  
Metabolic Rate ◽  
Normal Values ◽  
Cardiovascular Effects ◽  
Aortic Constriction ◽  
Thyroxine Treatment ◽  
The Right

Metabolic rate, blood pressure, weight and rate of the heart, cardiac output, and work were determined at weekly intervals in groups of normal rats receiving thyroxine. The measurements were made before and during the infusion of polyvinylpyrrolidone into the right side of the heart. The maximum values of cardiac output and work obtained during infusion were considered to be an approximate measure of the strength of the heart. Cardiac output and work in thyroxine-treated rats far exceeded the normal values before as well as during infusion. The greater strength was not merely the consequence of the greater size of the heart which developed in the course of thyroxine treatment. Hearts of similar size — coming from larger normal rats or from smaller normal rats with cardiac hypertrophy due to aortic constriction — did significantly less work than the hearts of thyroxine-treated rats.

scholarly journals CARDIOVASCULAR EFFECTS OF THYROXINE TREATMENT IN NORMAL RATS

1962 ◽  
Vol 40 (1) ◽  
pp. 1647-1654 ◽  
Author(s):  
Margaret Beznák ◽  
A. Marcsán ◽  
T. Fournier
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Cardiac Hypertrophy ◽  
Metabolic Rate ◽  
Normal Values ◽  
Cardiovascular Effects ◽  
Aortic Constriction ◽  
Thyroxine Treatment ◽  
The Right

Metabolic rate, blood pressure, weight and rate of the heart, cardiac output, and work were determined at weekly intervals in groups of normal rats receiving thyroxine. The measurements were made before and during the infusion of polyvinylpyrrolidone into the right side of the heart. The maximum values of cardiac output and work obtained during infusion were considered to be an approximate measure of the strength of the heart. Cardiac output and work in thyroxine-treated rats far exceeded the normal values before as well as during infusion. The greater strength was not merely the consequence of the greater size of the heart which developed in the course of thyroxine treatment. Hearts of similar size — coming from larger normal rats or from smaller normal rats with cardiac hypertrophy due to aortic constriction — did significantly less work than the hearts of thyroxine-treated rats.

scholarly journals TESTING THE INTERACTION OF HEART LEFT VENTRICLE AND CONTINUOUS-FLOW PUMP ON A MOCK CIRCULATION MODEL UNDER NORMAL AND PATHOLOGICAL CONDITIONS

2015 ◽  
Vol 17 (3) ◽  
pp. 43-49
Author(s):  
G. P. Itkin ◽  
A. A. Drobyshev ◽  
O. Yu. Dmitrieva ◽  
A. S. Buchnev ◽  
A. A. Sysoev
Keyword(s):  
Heart Failure ◽  
Cardiac Output ◽  
Left Ventricle ◽  
Arterial Pressure ◽  
Circulation Model ◽  
Systemic Circulation ◽  
Circulatory Support ◽  
Hemodynamic Parameters ◽  
Mock Circulation ◽  
Wide Range

Introduction. The preliminary study of new developed pumps for circulatory support on the hydrodynamic circulation model is an important step in the process of their designing. Hydrodynamic circulation models that can closely imitate cardio – vascular system are important to defi ne the range of effective functioning of the pumps under normal and heart disease conditions which is of great importance for defi ning the mode of these pumps in real clinical conditions.The aim of study is to create a new hydrodynamic circulation model of the systemic circulation to study the processes of interaction of heart left ventricle and continuous – fl ow pumps.Materials and methods. The main components of the mock circulation model (arterial and venous blocks) are designed as closed reservoirs with an air bag providing the necessary elasticity value of these reservoirs. The heart left ventricle was simulated with an artifi cial heart ventricle with a pneumatic drive Sinus-IS which allows to change its options in a wide range. As a test pump we used the fi rst native implantable axial pump VISH – 1. In the course of research we made the registration and recording of the basic hemodynamic parameters (pressure, fl ow) with a multichannel module Pumpax for the measurement of pressure parameters.Results. The designed circulation model allows to adequately reproduce the main hemodynamic parameters of the circulatory system in normal (arterial pressure – 110/77 mmHg, left atrium pressure – 7 mmHg and cardiac output – 4.2 l/min) and heart failure conditions (arterial pressure – 79/53 mmHg, left atrium pressure – 15 mmHg and cardiac output – 3.1 l/min). On the circulation model the interaction of heart left ventricle and continuous-fl ow pump in heart failure simulation was studied. The dynamics of the main circulation fi gures is shown under conditions of changing of the pump rotor speed. Meanwhile, the conditions of the closing of aortic valve are identifi ed which is important for theclinical use of this pump. Using a special separately fl exible camera on the pump inlet we modeled phenomena of negative pressure leading to unstable pump operation and reduction of pump fl ow.Conclusion. Characteristics of the developed hydrodynamic circulation model allow us to reproduce parameters of systemic circulation in a wide range and to use it in designing of new pumps for circulatory support.

scholarly journals Cardiopulmonary Interactions during Positive Pressure Ventilation

1996 ◽  
Vol 3 (6) ◽  
pp. 380-385
Author(s):  
John Granton
Keyword(s):  
Cardiac Output ◽  
Left Ventricle ◽  
Positive Pressure Ventilation ◽  
Contractile Function ◽  
Cardiac Performance ◽  
Positive Pressure ◽  
Loading Conditions ◽  
Cardiopulmonary Interactions ◽  
The Right ◽  
Cardiocirculatory Effects

Positive pressure ventilation (PPV) may lead to significant hemodynamic alterations. The cardiocirculatory effects of PPV occur through alterations in the loading conditions of the right and left ventricle and are mediated by changes in intrathoracic pressures and in lung volume. However, the net effect of PPV on cardiac output and hemodynamics is not always predictable. PPV may lead to either a decrease or an increase in cardiac performance. The cardiac consequences of PPV are also dependent on baseline loading conditions and contractile function of the heart.

scholarly journals Alteration of humoral and peripheral vascular responses during graded exercise in heart failure

2001 ◽  
Vol 90 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Robert L. Hammond ◽  
Robert A. Augustyniak ◽  
Noreen F. Rossi ◽  
Karen Lapanowski ◽  
Joseph C. Dunbar ◽  
...  
Keyword(s):  
Heart Failure ◽  
Blood Flow ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Plasma Renin ◽  
Cardiac Performance ◽  
Right Atrial ◽  
Plasma Norepinephrine ◽  
Vascular Conductance ◽  
Renal Vasoconstriction

We hypothesized that performance of exercise during heart failure (HF) would lead to hypoperfusion of active skeletal muscles, causing sympathoactivation at lower workloads and alteration of the normal hemodynamic and hormonal responses. We measured cardiac output, mean aortic and right atrial pressures, hindlimb and renal blood flow (RBF), arterial plasma norepinephrine (NE), plasma renin activity (PRA), and plasma arginine vasopressin (AVP) in seven dogs during graded treadmill exercises and at rest. In control experiments, sympathetic activation at the higher workloads resulted in increased cardiac performance that matched the increased muscle vascular conductance. There were also increases in NE, PRA, and AVP. Renal vascular conductance decreased during exercise, such that RBF remained at resting levels. After control experiments, HF was induced by rapid ventricular pacing, and the exercise protocols were repeated. At rest in HF, cardiac performance was significantly depressed and caused lower mean arterial pressure, despite increased HR. Neurohumoral activation was evidenced by renal and hindlimb vasoconstriction and by elevated NE, PRA, and AVP levels, but it did not increase at the mildest workload. Beyond mild exercise, sympathoactivation increased, accompanied by progressive renal vasoconstriction, a fall in RBF, and very large increases of NE, PRA, and AVP. As exercise intensity increased, peripheral vasoconstriction increased, causing arterial pressure to rise to near normal levels, despite depressed cardiac output. However, combined with redirection of RBF, this did not correct the perfusion deficit to the hindlimbs. We conclude that, in dogs with HF, the elevated sympathetic activity observed at rest is not exacerbated by mild exercise. However, with heavier workloads, sympathoactivation begins at lower workloads and becomes progressively exaggerated at higher workloads, thus altering distribution of blood flow.

EFFECT OF HYPOPHYSECTOMY AND HORMONE TREATMENT ON THE HEART–LUNG PREPARATION OF RATS

1966 ◽  
Vol 44 (1) ◽  
pp. 13-20 ◽  
Author(s):  
B. Korecky ◽  
M. Beznak ◽  
M. Korecka
Keyword(s):  
Growth Hormone ◽  
Body Weight ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Left Ventricle ◽  
Hormone Treatment ◽  
The Other ◽  
Hypophysectomized Rats ◽  
Lung Preparation ◽  
Made In

Heart–lung preparations (h.l.p.) were made in normal rats, hypophysectomized rats, and in hypophysectomized rats treated with either growth hormone or thyroxine or both. While mean arterial pressure was kept constant at 100 mm Hg, the flow into the heart was increased stepwise until cardiac output did not rise any further (maximum cardiac output (m.c.o.)). Hypophysectomy substantially decreased the m.c.o., even when expressed per kilogram body weight. Thyroxine treatment alone or with growth hormone completely restored the m.c.o. to normal. However, when the m.c.o. was calculated per gram of left ventricle weight, it did not reach the normal level in any of the hypophysectomized rats investigated. Growth hormone, on the other hand, raised the stroke volume (expressed per gram of left ventricle) of hypophysectomized rats without affecting the rate of the heart.

Increased cardiac output following occlusion of the descending thoracic aorta in dogs

1982 ◽  
Vol 243 (1) ◽  
pp. R152-R158 ◽  
Author(s):  
J. K. Stene ◽  
B. Burns ◽  
S. Permutt ◽  
P. Caldini ◽  
M. Shanoff
Keyword(s):  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Thoracic Aorta ◽  
Vascular System ◽  
Superior Vena ◽  
Vena Cava ◽  
Right Atrial ◽  
Mean Systemic Pressure ◽  
Extracorporeal Bypass

Occlusion of the thoracic aorta (AO) in dogs with a constant volume right ventricular extracorporeal bypass increased cardiac output (Q) by 43% and mean arterial pressure by 46%, while mean systemic pressure (MSP) was unchanged. We compared AO with occlusion of the brachiocephalic and left subclavian arteries (BSO) which decreased cardiac output by 5%, increased mean arterial pressure by 32%, and increased MSP by 11%. We feel these results confirm that AO elevates preload by transferring blood volume from the splanchnic veins to the vascular system drained by the superior vena cava. If the heart is competent to keep right arterial pressure at or near zero, this increase in preload will elevate Q above control levels. Comparing our data with results of other authors who have not controlled right atrial pressure, emphasizes the importance of a competent right ventricle in allowing venous return to determine Q.

MECHANISMS OF ADAPTATION OF THE LEFT VENTRICLE TO MUSCULAR EXERCISE

PEDIATRICS ◽  
1963 ◽  
Vol 32 (4) ◽  
pp. 660-670
Author(s):  
Jere H. Mitchell
Keyword(s):  
Cardiac Output ◽  
Left Ventricle ◽  
Stroke Volume ◽  
Pulse Rate ◽  
Individual Factors ◽  
Normal Male ◽  
Oxygen Intake ◽  
Mechanisms Of Adaptation ◽  
Male Subjects ◽  
Oxygen Difference

THE mechanisms of adaptation of the left ventricle to the demands of muscular exercise have intrigued cardiovascular physiologists for many years. Although highly complex, these adaptive mechanisms are more and more susceptible to analysis and quantification. In this presentation I will attempt to identify some of the individual factors which appear to be important in the response of the left ventricle to exercise, beginning with data obtained from experiments on conscious normal male subjects and proceeding to experiments performed on dog preparations in which individual factors were controlled and analyzed. The changes in oxygen intake, cardiac output, estimated arteriovenous oxygen difference, pulse rate and estimated mean stroke volume were determined in 15 normal male subjects during rest in the standing position and during treadmill exercise at the maximal oxygen intake level. Oxygen intake was obtained from the volume and composition of expired air, cardiac output by the dye dilution technique, and pulse rate from the electrocardiogram. Estimated arteriovenous oxygen difference was obtained by dividing the oxygen intake by the cardiac output (Fick principle) and estimated mean stroke volume by dividing the cardiac output by the heart rate. The data are shown in Figure 1. Oxygen intake increased from a mean value of 0.34 at rest to a maximal value of 3.22 L./min. The corresponding mean values for cardiac output were 5.4 and 23.4 L./min. and for arteriovenous oxygen difference were 6.5 and 14.3 ml./100 ml. Thus, as oxygen intake increased 9.5 times, the cardiac output increased 4.3 times and the arterio venous oxygen difference 2.2 times.

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