THE VASOCONSTRICTOR ACTIVITY ACQUIRED BY DEFIBRINATED BLOOD DURING PERFUSION OF THE ISOLATED KIDNEY OF THE DOG
Authors: O'Connor W. J. , Verney E. B. , Vogt Marthe 
Published: December 2014

1. When a kidney of the dog was perfused with defibrinated blood by one heart‐lung preparation and a loop of jejunum by another, the transposition of the kidney to the heart‐lung‐gut circuit was followed by a fall in perfusion flow through the gut. Similar but smaller responses were observed when, in like experiments, a forelimb or a segment of large intestine was used in place of the loop of jejunum.2. The kidney appeared to be specifically responsible for the phenomenon since it was absent in control experiments in which the spleen or the limbs of the dog were substituted for the kidney.3. The kidney liberated the vasoconstrictor substance over long periods of perfusion (e. g. 3 to 5 hours) and the gut‐vessels responded to it after periods of perfusion of similar duration.4. A single exposure of the gut‐vessels to the effluent blood from the kidney produced in them a refractoriness to subsequent exposures, and this persisted in spite of prolonged irrigation of the vessels with blood entirely free from the constrictor substance.5. When the initial exposure was maintained, the constriction of the gut‐vessels was followed by relaxation. This relaxation was shown to be due to the development of refractoriness to the substance liberated by the kidney.6. The more quickly the intestinal vessels constricted on exposure to the effluent blood from the kidney, the more rapidly did the refractory state develop.7. The liberation of the vasoconstrictor substance by the kidney and the refractoriness of the gut‐vessels were observed in the presence of atropine in the perfusate in a concentration of 0·1 to 0·2 mg./ 100 c. c. blood.8. The liberation of the substance and the refractoriness of the vessels also occurred when pump‐lung or pump‐oxygenator preparations were substituted for heart‐lungs in the perfusion system.9. The phenomenon of vasoconstriction in the gut when its vessels were exposed to the effluent blood from the kidney did not occur when, instead of defibrinated blood, the perfusate was blood rendered incoagulable by heparin. Nor under these conditions did it occur when the arterial supply to the kidney was severely obstructed. The addition of heparin to defibrinated blood did not, however, interfere with its occurrence nor with the subsequent development of a refractory state in the gut‐vessels.10. Degenerative section of the autonomic nerves around the superior mesenteric artery did not appreciably affect the responses of the jejunal vessels to the effluent blood from the kidney.11. The renal substance was not rapidly inactivated or destroyed in the blood of the heart‐lung preparation.12. Histamine has been excluded from being the substance responsible for the observed constriction of the gut‐vessels.13. The results are discussed with a view to their possible bearing on experimental hypertension of renal origin.It is a pleasure to thank Professor de Burgh Daly for his help in connexion with the technique of negative pressure ventilation used in some of our experiments. We would also express our indebtedness to the Government Grant Committee of the Royal Society for defraying part of the expenses incurred in this work.