THE RENAL CIRCULATION 



I4 8 9 



GFR (C Cr ) so that FF increased an average of 24 per 

 cent. TiripAH was only slightly depressed. 



Ether; cyclopropane. Craig et al. (67) have shown that 

 light ether and cyclopropane anesthesia (stage III, 

 plane 1 ) in dogs produced no significant alteration in 

 PAH or creatinine clearance, but in deep anesthesia 

 (stage III, plane 3) depression of function occurred; 

 the PAH and creatinine clearances were reduced to 

 53 ± 8.9 per cent and 48 ± 7.7 per cent, respectively, 

 of the values observed during light anesthesia, despite 

 maintenance of blood pressure. The clearances re- 

 turned substantially to normal when the animal was 

 allowed to recover to stage III, plane 1 . The reduction 

 was attributed to afferent arteriolar constriction. 



Coller et al. (56) studied the action of ether and 

 cyclopropane on a series of humans, but their results 

 were complicated by accompanving surgery. How- 

 ever, four with ether showed no significant change 

 in renal blood flow (based on C ) or glomerular 

 filtration (Cm) ; one showed no change in blood flow- 

 but had a marked decrease in GFR; two showed de- 

 creases in both blood flow and glomerular filtration. 

 Under cyclopropane, two showed little or no decrease 

 in RBF, yet both showed significant decreases in 

 glomerular filtration. In two others, all renal function 

 was markedly reduced, but these cases were compli- 

 cated by accompanying shock. Burnett et al. (45) 

 reported that in eight patients during ether anes- 

 thesia maintained in stage III, plane 2, mannitol 

 clearance was reduced by 2 1 per cent, and C PAH by 

 39 per cent, with a resultant increase in FF of 25 per 

 cent. In seven patients receiving cyclopropane, these 

 changes were —31, — 52 and +35 per cent, respec- 

 tively. It is entirely probable that, according to the 

 work of Miles & DeVVardener (205), the reductions in 

 RBF resulting from ether and cyclopropane, when 

 they occur, are on a neurogenic reflex basis. Renal 

 vascular resistance increased in dogs inhaling cyclo- 

 propane, but in denervated kidneys there was no 

 effect. With ether, an actual fall in RVR occurred in 

 the denervated kidney, evidently a local dilatory 

 mechanism. This was confirmed when ether was in- 

 jected in the renal arterial flow measuring circuit 

 (rotameter); RVR again decreased, due to active 

 vasodilatation. 



AUTONOMY OF THE RENAL CIRCULATION 



History 



In the preceding sections devoted to extrinsic regu- 

 lation of renal blood flow (neurogenic and humoral), 



the underlying thread of circulatory autonomy was 

 revealed occasionally. Rein (252), in 1931 while 

 studying regional blood flow in dogs during changes 

 in systemic arterial pressure, was struck by the relative 

 constancy of the renal blood flow as compared to other 

 tissues. Unna (316), employing the Rein thermo- 

 strohmuhr, confirmed these observations and con- 

 cluded: "Es kann die Nierendurchsblutung unab- 

 hangig von arteriellen Druck reguliert werden." 

 Hartman et al. (1 35) and Opitz & Smyth (238) demon- 

 strated that this obtained under circumstances of 

 reflex alteration in blood pressure (carotid sinus nerve 

 stimulation, carotid clamping) and carbon dioxide 

 inhalation in kidneys that had been denervated, im- 

 plying an intrinsic mechanism. Enger et al. (85) found 

 evidence of autoregulation: partial clamping of the 

 renal artery brought renal flow down, but in a short 

 time there followed a partial restoration of flow. 

 Forster & Maes (91) studied the effects of elevation 

 of mean arterial pressure on the clearance of jfr-amino- 

 hippurate (PAH) and creatinine in rabbits whose 

 kidneys had been denervated and whose adrenal 

 glands had been demedullated. They too found that, 

 when blood pressure was elevated by neurogenic 

 mechanisms resulting from clamping of the carotid 

 arteries, these clearances were remarkably constant. 



Selkurt (271) plotted the response of blood flow in 

 dogs to progressive decrement of effective perfusion 

 pressure (A-V difference) by lowering arterial pressure 

 (aortic compression) in a "pressure-flow" relation- 

 ship. This was concave to the pressure axis in a range 

 of 14 to 117 mm Hg with flow relatively independent 

 of pressure at the higher range, but decreasing below 

 ca. 80 mm. Results were essentially the same in the 

 intact as in the denervated kidney. Hemorrhage ap- 

 peared to abolish the concavity of the pressure-flow 

 relationship. It was not manifested in the dead kidney. 

 The zero flow intercept on the pressure abscissa 

 averaged 14 mm Hg, a minimal yield pressure for 

 movement of blood through the vascular circuits. 

 Selkurt et al. (274) further analyzed the pressure-flow 

 relationship of PAH and creatinine clearance and 

 found that glomerular filtration rate manifested good 

 constancy in a range of 90 to 180 mm Hg. This im- 

 plied that one possible factor in "renal autonomy," 

 a change in vascular resistance due to changes in 

 blood viscosity incurred by filtration at the glomeruli, 

 could be ruled out. Calculations of regional vascular 

 resistance strongly suggested that the afferent ar- 

 terioles were an important point of control. 



Shipley & Study (282) confirmed and extended 

 these observations by examining the renal blood under 

 conditions of elevation of perfusion pressure by a 



