The relation between the frog's slow diastolic (interpotentials) and potassium, calcium, adrenaline, noradrenaline, and tension.
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Animals↗
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Results for “DEFECTS, CONGENITAL/physiology”
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Serial cardiac output determinations in man.
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Cardiac Output↗
The significance of the pulmonary vascular bed in congenital heart disease. I. Normal lungs. II. Malformations of the heart in which there is pulmonary stenosis.
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Cardiovascular Abnormalities↗
The significance of the pulmonary vascular bed in congenital heart disease. III. Defects between the ventricles or great vessels in which both increased pressure and blood flow may act upon the lungs and in which there is a common ejectile force.
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Cardiovascular Abnormalities↗
Cardiac output measurement by the injection method without arterial sampling.
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Arteries↗
A study of the influence of tropical weather on output of volume, work, and power by the right and left ventricles of man at rest in bed.
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Climate↗
The mean manifest electrical axes of ventricular activation and repolarization processes (AQRS and AT) in congenital heart disease: frontal and horizontal planes.
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Electrocardiography↗
The circulatory effects of squatting.
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Blood Circulation↗
Estimation of stroke volume by means of the ballistocardiograph.
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Congenital Abnormalities↗
Cardiac dynamics and coronary blood flow consequent to acute hemorrhage.
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Cardiovascular Physiological Phenomena↗
The relation of the ballistocardiogram to cardiac function.
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Ballistocardiography↗
Central blood volume, cardiac output, and pulmonary vascular pattern in mitral stenosis.
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Blood Volume↗
Strength of cardiac conditioned responses with varying unconditioned stimulus durations.
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Conditioning, Classical↗
Plateau formation and sulphydryl groups in the plasma membrane.
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Cell Membrane↗
[Research on the hearts of experimental animals after complete ligation of the aorta and the pulmonary artery].
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Animals↗
[Physiopathological aspects of pulmonary circulation: the problem of chronic pulmonary hypertension].
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Cardiovascular Abnormalities↗
Some observations on cardiac automatism in certain animals.
Certain aspects of the acetylcholine hypothesis of cardiac automaticity have been tested in vitro with spontaneously beating cardiac tissue from rabbits, rats, dams, and hagfish. The beat of atria from rabbits and rats may be depressed or excited by acetylcholine, depending upon the state of the tissue. Proguanil and cocaine inhibition of the beat in the rat may be antagonized by acetylcholine so that reversal of the depression occurs. The action of acetylcholine on the hearts of clams was found to be strictly inhibitory. Proguanil and cocaine, in contrast to their action on mammalian atria, exert a stimulatory effect on the heart of the molluscs studied. In fact, cocaine stimulated these hearts when they were inhibited by acetylcholine. Studies on the non-innervated hagfish heart revealed that this tissue is completely insensitive to the action of acetylcholine. Extracts prepared from beating hearts of this species will accelerate hypodynamic hearts of the hagfish as well as of the mussel. An extract of the neurogenic lobster heart was without effect on the hagfish heart. Proguanil was likewise ineffective in concentrations which produced inhibition and excitation in rat and clam hearts respectively. It was concluded that acetylcholine does not play a role in the myogenic automatism of all species, and that another mechanism is responsible is suggested on the basis of results obtained in the hagfish hearts.
Acetylcholine↗
A study of inotropic mechanisms in the papillary muscle preparation.
The length-tension diagram, the force-velocity relation, the characteristics of the series elasticity, and the duration of the active state have been studied on the papillary muscle preparation of the cat heart, and on other examples of cardiac muscle. Positive inotropic changes such as the staircase phenomenon and post-extrasystolic potentiation occur without lengthening, but frequently with shortening, of the duration of the active state. They are accompanied by an increased velocity of contraction, and may be caused either by an intensification of the active state or by an alteration of the force-velocity characteristics of the contractile component. The changes in the force-velocity relation point to an adaptation of the velocity-efficiency relation in dependence on the frequency of contraction.
Animals↗