摘要:

Observations on the circulatory functions of 4 giraffes are recorded. Both the right and the left heart were catheterized under local anesthesia with a miniature manometer.Cardiac output was determined by employing both indicator dilution method and the Fick principle. Other parameters, such as the circulation time, blood volume, velocity, right and left ventricular pressure ascent as well as the changes in blood pressure occurring with changes in the Posture of the head were recorded. The difficulties of the experiments created certain limitations in their interpretation. The arterial blood pressure is high by human standards and adequate to maintain cerebral perfusion without other means of support. The arterial pressure pulse contour suggests a relatively lax vascular bed with considerable reserve distensibility. Values for cardiac output and blood volume were roughly comparable to those recorded in domestic cattle of the same approximate weight.

ISSN:0009-7330    

出版商:OVID    

年代:1960

数据来源: OVID

摘要:

The major vessel occlusion method applied to the supine, anesthetized dog with an open chest has proven useful in elucidating the role of the venous system in the complex phenomenon of venous return. This method momentarily isolates a large part of the venous system from the arterial system and from the action of the heart and the respiratory and muscle pumps. Simultaneous occlusion of the thoracic inferior vena cava and the descending aorta (MVO) divides the dog's circulation into a cephalad zone and a caudad zone. Experimentally induced changes in the status of the cephalad circulation during MVO can affect the caudad zone only through neuronal pathways. Therefore, MVO makes it possible to investigate the responses of the venous system to vascular reflex activity as well as direct and indirect actions of drugs. During the “resting” state, blood returns to the heart because of the existence of a venous pressure gradient of 3 to 4 mm. Hg, operant between the reactive venous reservoir and the central venous conduit (“intra-venous” gradient). Augmentation of sympathetic tone produces an increase in venous return, of venous origin, due to an increase in the effective “intra-venous” pressure gradient from 3 to 4 mm. Hg to 5 to 10 mm. Hg. The ability of the venous system to increase venous return independently, has been shown to be a significant factor in thearterialhypertensive response to carotid occlusion. The venous system can serve as a buffer against the effects of sudden, momentary changes in arterial flow by maintaining, reducing, or augmenting venous return.

ISSN:0009-7330    

出版商:OVID    

年代:1960

数据来源: OVID

摘要:

The effect of increasing the activity of the ventricle on its contractility was investigated. Several beats after the ventricle increases the amount of tension it develops per unit of time, it exhibits an increased contractility as shown by the increase in work and the more rapid development of pressure from a given end-diastolic pressure or fiber length. This has been termed homeometric autoregulation in contradistinction to the Frank-Starling or heterometric type of autoregulation. It was found that changes in coronary flow are not essential to the exhibition of this phenomenon. Possible mechanisms and the physiologic significance of the findings are discussed.

ISSN:0009-7330    

出版商:OVID    

年代:1960

数据来源: OVID

摘要:

A method is described for the continuous recording of changes in the length of a segment of left ventricular myocardium, and its advantages and limitations are discussed. The curve depicting the relation between ventricular diastolic pressure and simultaneous changes in the length of a myocardial segment is presented. For a given increment in pressure, the myocardial segment length increases more at low ventricular diastolic pressure than at high pressure. Atrial systole causes a substantial increase in myocardial segment length when the ventricle is on the sensitive part of its pressure-length curve.

ISSN:0009-7330    

出版商:OVID    

年代:1960

数据来源: OVID

摘要:

During the continuous and simultaneous recording of left ventricular diastolic pressures and changes in the length of a segment of left ventricular myocardium it was demonstrated that neither cardiac sympathetic nor vagal efferent nerve stimulation produces a change in ventricular myocardial extensibility. It was further shown that, at the heart rates studied, autonomic nerve stimulation does not modify the end-diastolic pressurelength curve. These data indicate that, during cardiac sympathetic stimulation, the augmented ventricular stroke work from any given end-diastolic Pressure is accomplished without a change in end-diastolic fiber length.Evidence was obtained, however, which suggests that the abbreviation of diastole at high imposed heart rates or large stroke volumes may leave an inadequate time for ventricular relaxation to take place and for inertial and viscous factors to be dissipated. Under these circumstances, sympathetic stimulation, by shortening systole and thereby lengthening diastole, permits the ventricle to remain on its “normal” pressure-length curve. This component of cardiac sympathetic efferent activity is peculiarly appropriate to the tachycardia that occurs with increased sympathetic outflow to the heart.

ISSN:0009-7330    

出版商:OVID    

年代:1960

数据来源: OVID

摘要:

At constant heart rates, efferent stimulation of the vagus nerve and of the left stellate ganglion revealed the following: 1. Vagal stimulation exerts a profound depressant effect on the strength of the atrial contraction and can thereby influence ventricular filling and ventricular stroke work; it elevates mean atrial pressure at any given level of ventricular stroke work. This occurs under experimental conditions wherein the vagal stimulation used does not produce an alteration in the performance characteristics of the ventricle. The effects of vagal stimulation are blocked by atropine. 2. Stellate ganglion stimulation or norepinephrine infusion augments the strength of atrial contraction and thus the atrial contribution to ventricular filling. The augmented atrial contraction takes place in a shorter period of time. 3. Stellate ganglion stimulation or norepinephrine infusion increases the external stroke work and power produced by the ventricle from any given mean atrial pressure and from any given end-diastolic pressure or fiber length.4. There is a family of curves representing the relation between end-diastolic fiber length and stroke work, as well as a family of curves representing the relation between mean atrial or end-diastolic pressure and stroke work.5. When taken together with the well-known sympathetic and parasympathetic effects on heart rate, the above data are believed to comprise a reasonably comprehensive description of the means available to the central nervous system for directly inducing acute changes in the activity of the heart.

ISSN:0009-7330    

出版商:OVID    

年代:1960

数据来源: OVID

摘要:

A lowering of pressure in the carotid sinus reflexly increases the force of atrial systole by (a) increasing sympathetic activity to the heart (carotido-sympatho-atrial reflex) and(b) decreasing efferent vagal activity to the heart (carotido-vago-atrial reflex); an elevation of carotid pressure has the reverse effect. The carotid sinus can thereby vary ventricular end-diastolic pressure and fiber length. A change of pressure in the carotid sinus reflexly modifies the ventricle's contractility such that from a given end-diastolic pressure or fiber length, with a low carotid pressure the ventricle's contraction will be substantially augmented and from a high carotid pressure it will be diminished. The role of the carotid sinus in circulatory regulation has been likened to a voltage regulating element in an electronic system; i.e., it causes an appropriate variation of input into the system so as to maintain a constant voltage when the current requirements of the system it is supplying are changed.

ISSN:0009-7330    

出版商:OVID    

年代:1960

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1960

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1960

数据来源: OVID

ISSN:0009-7330    

出版商:OVID    

年代:1960

数据来源: OVID