THE RENAL CIRCULATION 



I5°3 



table 14. Effect of Tilting on Renal Vascular Compensation in Man 



Position 



Cln 



ml min 



CpAH 



ml min 



RPF" 



ml min 



Medullary 6 

 Flow ml/min 



Pa c 



mm Hg 



True d FF 



Epah 



R K e 



■ RPF = Cpah/Epah- ''Medullary flow: RPF — Cpah- c Pa in Part B calculated from diastolic pressure + '3 pulse 

 pressure. d True FF == Ci„/RPF. 'Hemat. 40% (assumed); R K = (Pa - P V )/RBF, in mm Hg/ml/min. '[After 



VVerko et at. (334).] «[After Brodwall (36).] 



supporting the notion of differential blood flow to 

 cortex and medulla. 



VVerko et al. (334) found little increase in the renal 

 A-V oxygen difference during tilting, so that renal 

 oxygen consumption tended to decrease. The subject 

 in table 14 A showed a decrease from 25 ml per min 

 to 10 ml per min at a 45° tilt, but this was the greatest 

 change in the series. The data thus support the con- 

 cept of the flow-limited nature of the renal circula- 

 tion. 



Renal Hypoxia and Ischemia 



hypoxia. Analysis of the response of renal blood flow- 

 to hypoxic states has been complicated by the varied 

 techniques and experimental conditions employed, 

 and the varying degrees of hypoxia. Thus, the whole 

 organism may be expected to show a different re- 

 sponse than the isolated organ to hypoxia (278). 

 Ischemia presents not only the problem of reduced 

 oxygen supply, but also of accumulation of metabolites 

 in the organ. 



Caldwell et al. (47) gave to subjects oxygen intakes 

 as low as 9.3 per cent for periods of 5 to 17 min. No 

 consistent effects in C PA h and C Tn were observed; 

 blood pressure only occasionally showed a slight 

 tendency to increase. Berger et al. (15) experimentally 

 reduced arterial oxygen tension from ca. 97 mm Hg 

 to ca. 50 mm Hg in humans. C PA h increased by an 

 average of 13 per cent ( — 5.2 to +22.8) with no sig- 

 nificant change in C In or blood pressure. Acute ex- 

 posure of dogs to simulated altitudes of 18,000 feet 

 (79.4 mm Hg partial pressure of oxygen) and 24,000 

 feet (61 .6 mm Hg oxygen) caused an increase in renal 

 plasma flow at 18,000 feet, but this generally de- 



creased below ground level values at 24,cco fee 

 (193). The seal, when subjected to 10 per cent oxygen 

 or asphyxia, reacts with a significant decrease in RPF 

 and GFR (192), accompanied by marked slowing of 

 the heart and increases in blood pressure. It would 

 appear that mild hypoxic states unaccompanied by 

 systemic reflex vascular alterations manifest a slight 

 renal hyperemia, but more severe hypoxic states or 

 asphyxia trigger vasoconstrictor reflexes in which the 

 kidney participates. Other experimental approaches 

 confirm this. Bing & Knudsen (19) by direct observa- 

 tion of the mouse kidney noted blanching (cortical 

 ischemia) to occur in the range of 6.5 to 10.5 vol per 

 cent oxygen in the inspired air (average 7 vol %), 

 with arterial oxygen tension at 42 per cent of control. 

 It was concluded that a reflex was involved, with 

 centers sensitive to hypoxia in the spinal cord, for it 

 persisted after cord section at T4, but was lost with 

 renal denervation. It is likely that the medullary 

 centers activated by impulses from the chemoreceptors 

 in the carotid sinus and aortic arch would also par- 

 ticipate. 



acute renal ischemia. Numerous experiments have 

 been made in which the duration of ischemia has lasted 

 from several minutes to 3 and 4 hours. Short-term 

 occlusion results in rather transient hemodynamic 

 effects, while longer ischemia involves varying degrees 

 of tubular damage which must be taken into account 

 in interpreting clearance data. Short bouts (10-20 

 min) produce small but variable effects with rapid 

 recovery. No change in blood flow (246), or small de- 

 creases (76, 269), or even increases (87) have been 

 reported. Since brief ischemia has been reported to 

 cause reactive hyperemia (262, 293) and when clear- 



