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The mechanism by which venous pressure is elevated in human heart disease, and the exact relation between venous pressure and the plethora of late cardiac failure are still uncertain.Starling, primarily from his results with the heart-lung preparation (1), suggested the following se- quence: Cardiac failure --elevated venous pressure -> accumulation of blood in the large veins -- compensatory arteriolar constriction -> anoxia of bone.marrow --increase in blood volume.This hypothesis with its tacit assumption that "back pressure" occurs in the intact animal, as it does more clearly in the heart-lung preparation, has been challenged recently by Starr, Jeffers and Meade (2), and by Warren and Stead (3) who relate venous pressure to cardiac failure essentially as follows: "Impaired cardiac function" -> decreased renal excretion of sodium and water (mechanism un- known) -4 increased blood volume -> elevated venous pressure.Starr et al, (2) observed that acute damage of the right ventricle failed to elevate significantly the venous pressures of dogs, but these studies were limited to the resting state.Warren and Stead (3) found in cardiac patients, also during rest, that administering water and sodium chlor- ide increased blood volume before venous pressure rose significantly.They concluded that the earl- iest manifestation of cardiac insufficiency is a re- tention of fluid, the cause of which is not clear, associated with an increase of blood volume.This plethora or hypervolemia is said then to be re- sponsible for the elevated venous pressure which 'Research Fellow in Physiology, Commonwealth Fund.
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Landis et al. (1946) studied this question.
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