Water and Electrolytes in Congestive Failure 283 



A high central venous pressure and a secondary excretion of 

 humoral substances like aldosterone complicate the response. 



Werko and co-workers (1955), in a study of systemic and 

 renal haemodynamic changes in 146 subjects with different 

 cardiac disorders, came to a similar conclusion. Their results 

 suggest that "the adrenergic impulses could contribute to 

 the diminished renal blood flow in severe heart disease before 

 any signs of congestion are apparent". They think one of the 

 factors causing the release of adrenergic impulses may be a 

 decreased stroke volume. 



The origin of the afferent impulses of this functional 

 haemodynamic reflex is not known. There are, of course, 

 several pieces of evidence on the influence of nervous impulses 

 on diuresis. Viar and co-workers (1951) demonstrated an 

 increase in urine flow and excretion of sodium as the result of 

 a rising venous pressure in the head (following the compres- 

 sion of neck by a manometer cuff). Cort (1953), in agreement 

 with these results, found an increased diuresis with higher 

 elimination of sodium in subjects with the head lowered 

 (Trendelenburg position of 15°). The changes in renal blood 

 flow were not reported. Cathcart and Williams (1955) did not 

 confirm this. 



Gauer and co-workers (1954) described an increase in urine 

 flow in anaesthetized dogs during the negative pressure 

 breathing period. This was also found in healthy human 

 subjects (Sicker, Gauer and Henry, 1952, 1954). The rise in 

 diuresis was not accompanied by increased elimination of 

 electrolytes (Na+ or K+). This water diuresis was thought to 

 be caused by stimulation of volume or stretch receptors 

 localized in the cardiovascular system in the thorax (left 

 atrium or pulmonary veins). The values of renal plasma flow 

 were not measured in these experiments. We do not know, 

 therefore, if the changes reported were produced by a direct 

 influence on the renal tubules without any change in renal 

 haemodynamics . 



It is also difficult to use these findings to explain the electro- 

 lyte and water imbalance in heart failure. We have produced 



