Water and Electrolytes in Congestive Failure 281 



not start to fall until more than an hour after intravenous 

 injection of 40 [ig. aldosterone. 



It would appear to us, therefore, that neither of these 

 humoral substances is the primary cause of the retention of 

 salt and water in heart failure. 



The results of haemodynamic changes in human subjects 

 following intravenous injection of Dibenamine called our 

 attention to the importance of reflex (neurohumoral) regula- 

 tion in the genesis of haemodynamic changes in congestive 

 failure. 



Blockade of adrenergic impulses by Dibenamine in patients 

 with heart failure caused a diminution of a high peripheral 

 vascular resistance and central venous pressure. Cardiac 

 output increased. Renal blood flow rose in a great majority 

 of investigated subjects, suggesting that this was independent 

 of the increase in CO. These changes were not produced by 

 blocking the adrenergic impulses in the heart or by an in- 

 creased secretion of adrenaline (Fejfar and Brod, 1950c, 

 1951, 1954; Brod, Fejfar and Fejfarova, 1951, 1954) (Fig. 5). 

 The increase in renal blood flow in seven out of nine patients 

 in congestive failure was accompanied by a rise in urine flow 

 and an increased elimination of sodium or chloride. 



We were able to conclude from our results that, with the 

 onset of congestive failure, reflex (neurohumoral) vasocon- 

 striction develops in both arterial and venous circulation. 

 The function of this selective vasoconstriction may be to 

 secure a sufficient supply of oxygenated blood to working 

 tissues such as the heart and other muscles. 



A haemodynamic pattern resembling chronic heart failure 

 (i.e. unequal distribution of blood supply to various organs, 

 increased utilization of oxygen in tissues, and an insufficient 

 CO) may also be found in clinical circumstances with a 

 diminished return of venous blood to the heart (e.g. mitral 

 stenosis, constrictive pericarditis), or when the amount of 

 circulating blood and oxygen decreases, as well as in acute 

 heart failure or peripheral circulatory failure (see Fejfar, 

 1958). A similar haemodynamic picture can be seen in severe 



