Role of the Veins in Venous Return

Abstract

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 the arterial hypertensive 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.

The Effects of Acute Hypoxia on the Systemic Venous and Arterial Systems and on Myocardial Contractile Force

“…The potential importance of any changes in venous tone are apparent when it is considered that this segment of the circulation contains the major portion of the systemic blood volume (7). Small changes in the diameter of the veins might be expected to produce large changes in the volume of the venous bed and in the magnitude of the venous return to the heart; any such changes could, in turn, modify the cardiac output and, therefore, the arterial pressure (8)(9)(10)(11). In the present investigation the activity of the chemoreceptors, the adrenal glands, and the spleen was also studied, since these organs have been implicated in the circulatory responses to hypoxia (12)(13)(14)(15)(16)(17)(18).…”

Effect of Histamine and Other Endogenous Amines on the Peripheral Hemodynamics in Rabbits Under the Controlled Cardiac Output

“…Intravenously administered adrenaline or noradrenaline which firstly acts on the right ventricle and pulmonary vascular bed produced a slight decrease in the left auricular outflow (9), which favours the above view that the increase in the left auricular outflow caused by adrenaline or noradrenaline mostly resulted from the increase in venous return. Role of the veins in venous return was emphasized by Bartelstone (13).…”

The significance of adenosine cyclic 3′,5′‐monophosphate for the contraction of smooth muscle

“…in dog8. The method of Bartelstone (1960) To study the action of noradrenaline in the caudal vascular bed during M.V.O., the dose of noradrenaline, contained in a volume of saline less than the volume of the polythene cannula, was placed in the 1 ml. syringe.…”