THE RENAL CIRCULATION 



I5°5 



pH decreased from ca. 7.45 to 7.10. Respiration rate 

 tripled, but blood pressure fell slightly. Renal blood 

 flow showed an average reduction to 24.3 per cent of 

 control (range 11-45%) at tne er, d °f tne 30-min 

 inhalation period. This was accompanied by oliguria 

 or anuria. Denervation of the kidney apparently pre- 

 vented the marked decrease in flow observed in the 

 intact kidney and urine production continued. The 

 authors concluded that the increased renal vascular 

 resistance was a reflex component of a more gen- 

 eralized vasoconstrictor response to high carbon 

 dioxide. Franklin et al. (93) by the visual "blanching" 

 technique in rabbits inspiring gas mixtures of in- 

 creased carbon dioxide content (up to 25 %) saw 

 blanching (cortical ischemia) when the blood carbon 

 dioxide content had increased to 140 per cent of con- 

 trol. The response was abolished by nerve section, 

 confirming the reflex nature of the phenomenon. 



Hvpercapnia is an important factor contributing to 

 the marked reduction in renal flow which results 

 during diffusion respiration (297). In this, with re- 

 spiratory arrest resulting from excess anesthetic action 

 or curare, oxygen is taken into the lungs by the con- 

 tinued removal of the gas from the alveoli by 

 hemoglobin uptake in the pulmonary circulation. 

 Breathing of pure oxygen for 1 hour prior to onset of 

 respiration arrest is essential ("denitrogenation"). 

 Blood content of carbon dioxide rises progressively, 

 since it is not removed by the quiescent lungs. After 

 30 min of apnea, blood flow had decreased to 28 per 

 cent of the control. Blood pressure had fallen an aver- 

 age of 23 mm Hg during this time and renal resistance 

 increased by 230 per cent. In a denervated series 

 (nerve block), these changes in renal blood flow and 

 resistance were restored to the decreasing control 

 trend. Again, a central origin of the renal ischemia 

 was predicated. Bohr et al. (27), although demon- 

 strating a lessened trend for C PAH to decrease in the 

 denervated kidney, nevertheless observed significant 

 decreases (PAH to 38 % of control with blood pressure 

 decrease from 1 16-95 mm Hg). Therefore, circulatory 

 pressor substances must be released in greater amounts 

 to contribute to the vasoconstriction. 



It seems reasonable to conclude that the reduction 

 in renal blood flow during hvpercapnia and acidosis 

 is centrally mediated. It is nevertheless surprising 

 that in none of these investigations was there recorded 

 an increase in blood pressure. From the reported 

 facts it would appear that the preponderant effect of 

 hvpercapnia and the accompanying acidemia was a 

 reflex increase in renal vascular resistance in the face 

 of an actual fall in arterial blood pressure, a con- 



comitance of events difficult to reconcile. It may be 

 that anesthesia alters the normal response. Also, it 

 must be kept in mind that the direct peripheral vascu- 

 lar action of carbon dioxide is dilatory (e.g. on vessels 

 of skeletal muscle), which action may become pre- 

 ponderant. This does not preclude the possibility that 

 other tissues, such as the kidney, respond only by con- 

 striction. 



Hemorrhagic Hypotension and Shock 



HEMORRHAGE AND HEMORRHAGIC SHOCK. Acute 



hemorrhage provokes responses in the renal circula- 

 tion which are typical of general compensatory mecha- 

 nisms set into play, viz. reflex vasoconstriction, and 

 shunting of blood to other tissues in order to com- 

 pensate for low blood flow. In the case of the kidney, 

 if blood loss is great enough, this means shutdown of 

 renal excretory function which, if prolonged, might 

 have serious consequences to the organism. Moreover, 

 a prolonged period of anoxic hypotension will impair 

 the function of the tubular epithelium, adding to the 

 problem of shock the probability of renal failure and 

 uremia. 



Following acute hemorrhage, the kidney's circu- 

 lating autonomy aids in reestablishing flow. Heine- 

 mann et al. (136) bled anesthetized dogs 1.3 to 3.9 

 per cent of body weight; blood pressure fell by 5 to 59 

 mm Hg to levels 91 to 51 per cent of mean control 

 values. Renal blood flow (based on C PA h) decreased 

 more than the blood pressure, signifying vasoconstric- 

 tion. In four representative experiments, RBF de- 

 clined from 16. 1 ( 1 5.6—16.6) to 4.5 (0.3-10.5) ml per 

 kg per min. In three animals, while hypovolemia and 

 hypotension were maintained, blood flow was re- 

 stored autonomously to 16.5 (11. 7-19. 5) ml per kg 

 per min in 25 to 70 min. Goodyer & Jaeger (107) 

 found similar responses to moderate hemorrhage in 

 anesthetized dogs, followed by restoration of flow. 

 Denervated kidneys showed a lesser decrease after 

 hemorrhage than the paired intact kidney, but both 

 showed compensatory restoration, indicating that the 

 autonomy is intrinsic. Dibenzyline selectively injected 

 into one renal artery reduced its responsiveness to 

 hemorrhage compared to the control side (129). 



Phillips et al. (247) found that rapid, massive hemor- 

 rhage in anesthetized dogs was accompanied by almost 

 complete cessation of RBF (C P ah/£pah)- If hemor- 

 rhage was not too great, arterial pressure rose as the 

 result of extrarenal vasoconstriction, and renal blood 

 flow was restored but at a figure less than before 

 hemorrhage. In the recovery phase, the kidney ap- 



