288 Z. Fejfar 



In six rabbits with bilateral denervation the resting clear- 

 ances of inulin and PAH were practically the same as in the 

 rabbits without renal denervation (Brod and Sirota, 1949). 

 Cort and Kleinzeller (1956) therefore conclude that the dif- 

 ferences described are due to a direct nervous effect on 

 tubular cells rather than to a change in renal blood flow. 



It is difficult to compare results obtained from experiments 

 with tissue slices or in anaesthetized animals, with results 

 from human subjects, in which every disturbance of homeo- 

 stasis is immediately compensated for in several ways. 

 Neural and humoral regulation act simultaneously and it is 

 practically impossible to differentiate them. It seems, 

 nevertheless, that even in subjects with chronic heart failure, 

 retention of electrolytes and water is the result of haemo- 

 dynamic changes parallel with increased tubular reabsorption 

 of sodium and water. These changes may be initiated by a 

 reflex mechanism acting through adrenergic nerves. Increased 

 secretion of aldosterone and ADH is a secondary manifesta- 

 tion. This secondary aldosteronism may, however, prevail in 

 the long run, dominate the whole picture of chronic congestive 

 failure, and close the vicious circle. 



Further consequences of retention of salt and 

 vs^ater in heart failure. 



The retained sodium and water in congestive failure does 

 not enlarge the volume of extracellular fluid only. In patients 

 recovering from heart failure the reduction of body weight 

 was greater than the reduction in the amount of extracellular 

 fluid (Seymour et al., 1942), chloride output (Schroeder, 1950) 

 or sodium loss (Miller, 1950, 1951). This surplus water must 

 come from cells. In the development of congestive failure, 

 the water accumulates in both extracellular and intracellular 

 compartments. 



At the same time changes begin in the concentration of 

 extracellular and intracellular electrolytes. The loss of cellular 

 potassium in congestive failure was described in 1930 by 

 Harrison, Pilcher and Ewing. It has been ascertained by 



