RENAL HEMODYNAMIC FACTORS IN CONGESTIVE HEART FAILURE *

Although we have long known that renal blood flow is decreased in relatively mild cardiac incompetence, it is only recently that we have begun to appreciate that blood flow distribution in the kidney is altered in congestive failure (Bargar et al., 1966) and that the redistribution may have considerable functional significance. I shall describe here some of these changes in intrarenal distribution of blood flow produced by circulatory stress, and discus the possible implications with particular regard to sodium and water balance in congestive heart failure. We were stimulated to pursue these studies on distribution of blood flow in the kidney by ohance observations made in dogs with experimental, right4ded congestive heart failure produced by superimposing pulmonary artery stenosis on tricuspid insufficiency (Barger et al., 1950). We had noted that our dogs with valvular incompetence, like other patients with cardiac disease, were unable to excrete an intravenous load of saline as rapidly as did the normal (Barger et al., 1955). However, from these observations we were not able to asses the relative importance of intrarenal versus extrarenal factors in the salt and water retention of heart disease, and wondered whether sodium excretion would increase unilaterally if a salt load were given directly into the renal artery of an unanesthetized dog with congestive failure. In an attempt to answer this question, Rudolph & Rokaw (1956) developed a technique for chronic catheterization of the renal artery. To insure proper placement of the tip of the catheter proximal to the first bifurcation of the renal artery, a bolus of indigo carmine was injected through the catheter at operation, and the sudden appearance of the blue dye noted uniformly filling the subcapsular peritubular capillaries in the normal animal. In the catheterization of the renal artery of the dog with congestive failure we were puzzled by the very patchy filling of the subcapsular region, or nearly complete absence of dye at the surface at a time when transillumination of the renal artery assured us that the jet stream from the catheter creater sufficient turbulence for good mixing. This filling defect of the outer cortical region was the first suggestion we had that blood flow had been redistributed away from the surface of the kidney in congestive heart failure. With the development of the technique for chronic catheterization of the rend artery and splitting the urinary bladder (Desautels, 1957), we were able to answer the quevtion raised above and to determine whether the redistribution of blood flow in the dog in failure had functional significance (Barger, 1956). Thus, as shown in FIGURE 1, when hypertonic saline was infused into the left renal artery of the nolmal unanevthetized dog, sodium excretion from the infused side (solid line) rose markedly with little change in sodium excretion from the conltrol kidney (dotted line). At a later date, in the same animal now in frank congestive heart failure but with a normal glomerular filtration rate, the intrarenal infusion of the same amount of hypertonic saline produced no rise in sodium excretion. Thus,