Renal Blood Flow In Dogs Research Articles

Distribution of renal blood flow in dogs with congestive heart failure.

Studies were performed to determine whether the intrarenal distribution of cortical blood flow is altered in congestive heart failure. Utilizing the radioactive microsphere method, we studied eight dogs that developed congestive heart failure secondary to the construction of an aortocaval fistula. They had marked reduction in total renal blood flow not accompanied by intracortical redistribution of blood flow. All dogs had developed edema and/or ascites, and gained a mean of 3.4 kg; glomerular filtration rate, hematocrit, and urinary sodium excretion fell significantly. Renal vascular resistance increased; mean blood pressure and filtration fraction were unchanged. Furosemide was administered to a second group of nine fistula dogs. The drug produced a marked natriuresis associated with a decrease in outer cortical blood flow (zone 1) and an increase in midcortical zones 2 and 3; no change was observed in zone 4. We conclude: 1) chronic salt retention occurs in high-output heart failure in the absence of redistribution of renal cortical blood flow, and 2) the effect of furosemide on intrarenal hemodynamics of dogs with heart failure is similar to that seen in normal animals.

Autoregulation of renal blood flow in dogs at normal body temperature and at 27 degrees C.

1. Dogs cooled to 27 degrees C were compared with control dogs maintained at 38 degrees C. The mean arterial blood pressure, renal blood flow and glomerular filtration rate were lower in the hypothermic animals. 2. The relation between mean arterial blood pressure and renal blood flow was investigated. Auto-regulation of renal blood flow occurred in the kidneys of normothermic and hypothermic animals. Thus the reduction in renal blood flow during hypothermia is not due simply to the fall in mean arterial blood pressure. 3. Similarities between recordings of renal blood flow obtained at 38 degrees C and 27 degrees C suggest that its autoregulation occurs by the same mechanism at the two temperatures. 4. Autoregulation of renal blood flow occurred in hypothermic kidneys in the presence of a cold-induced vasoconstriction. The observed responses to cold and to alterations in mean arterial blood pressure may take place in different areas of the renal vasculature.

Intrarenal role of angiotensin II. Homeostatic regulation of renal blood flow in the dog.

The analogue, l-sarcosine-8-alanine-angiotensin II, a specific competitive antagonist of the vascular action of angiotensin II in the rat, blocked the decrease in renal blood flow after a single intrarenal injection of angiotensin II but not after an injection of norepinephrine in normal dogs, in a sodium-depleted dog, and in a dog with thoracic vena caval constriction. Infusion of the analogue at 0.2 µg/kg min -1 into the renal artery consistently increased renal blood flow and decreased renal resistance in both sodium-depleted dogs and dogs with vena caval constriction but did not alter these functions in normal dogs. In five sodium-depleted dogs, renal blood flow increased from an average control value of 196 ± 5 ml/min to 222 ± 11 and 246 ± 12 ml/min after 20 and 40 minutes of antagonist infusion (P < 0.01 and P < 0.005, respectively); renal resistance fell from 0.71 ± 0.03 mm Hg/ml min -1 to 0.62 ± 0.06 and 0.54 ± 0.03 mm Hg/ml min -1 (P < 0.005 for the 40-minute value). In five dogs with vena caval constriction, renal blood flow increased from 143 ± 16 ml/min to 178 ± 23 and 190 ± 19 ml/min after 20 and 40 minutes of analogue infusion (P < 0.02 and P < 0.005, respectively); renal resistance fell from 0.90 ± 0.14 mm Hg/ml min -1 to 0.73 ± 0.14 and 0.64 ± 0.10 mm Hg/ml min -1 (P < 0.01 and P > 0.02, respectively). Mean arterial blood pressure was not altered significantly by the analogue when it was infused at 0.2 µg/kg min -1 . Infusion of the analogue at 2.0µ/kg min -1 decreased arterial blood pressure and renal resistance and increased renal blood flow in five sodium-depleted dogs and in three dogs with vena caval constriction. These observations suggest an important intrarenal role for angiotensin II in the homeostatic regulation of renal blood flow in sodium-depleted dogs and in dogs with vena caval constriction.

Hemodynamic responses to glycols and to hemolysis.

Ethylene and propylene glycol both decrease renal blood flow in dogs while increasing flow through the superior mesenteric artery. The decrease in renal blood flow is not a passive response to dilatation of major vascular beds since it precedes the increment in superior mesenteric arterial flow and since it can be duplicated by direct injection of glycols into the renal artery. These rheological changes in response to glycols are at least partly due to hemolysis since intravenous injection of plasma from hemolyzed blood or of crystalline hemoglobin produces the same pattern of response, which is not blocked by phenoxybenzamine. However, the production of hemoglobinemia may not be the sole explanation for the vascular responses to the glycols, since a concentration of 2 %, which does not induce detectable hemolysis, still produces the characteristic increase in superior mesenteric artery blood flow.

Renal blood flow in dogs studied by means of a dye-dilution technique.

The renal blood flow in dogs was studied with a dye-dilution technique using indocyanine green. A new method of analyzing the dye-dilution curves was devised by which it was possible to estimate the magnitude of separate flow components of the curves. It could be shown that the curves comprise three different components, representing: (1) a rapidly circulating fraction containing most of the dye injected, (2) a more slowly circulating fraction, and (3) dye in recirculating blood. The influence of recirculating dye was studied. This fraction could be eliminated in the calculations of the blood flow values. To determinate the accuracy of the method, measurement of the renal venous outflow was made simultaneously. The blood pressure decreased during the outflow measurements. Though these always were made in the so-called “zone of autoregulation” it could be shown that renal blood flow diminished in parallel with the fall in blood pressure. Therefore, a modification of the outflow method was devised by which it was possible to obtain the correct value for the renal blood flow at every moment during the hemorrhage. There was very good correlation between the dye-dilution values and the venous outflow measurements, giving a ratio of 1.003 with a correlation coefficient, r = 0.95. The rapid component of the curves represented 88 ± 3% of the total blood flow, the slow component of the curves 12 ± 3%. These components apparently indicate kidney compartments with different intensities of blood flow, presumably the major part of the cortex, and the medulla, respectively.

Estimation of Renal Blood Flow in Dogs by Rate of Disappearance of Hippuran I-131 from the Vascular System

Estimation of Renal Blood Flow in Dogs by Rate of Disappearance of Hippuran I-131 from the Vascular System

Renal blood flow in dogs during diffusion respiration.

Two series of experiments were performed with appropriate controls on dogs in which respiratory arrest was produced and maintained by the injection of an overdose of thiopental or by administration of decamethonium, respectively. Renal blood flow was measured by a modification of the method of Selkurt ( Methods in Medical Research, vol. 1). A marked fall in renal blood flow coincident with apnea and anuria was found to occur consistently with diffusion respiration under thiopental. Both the renal ischemia and the anuria were preventable by renal denervation (pharmacological block). During diffusion respiration experiments in which decamethonium was used to cause and maintain apnea, a marked decline in renal blood flow or urine secretion did not occur during the first 15 minutes of apnea. It is concluded that the prompt onset of anuria in diffusion respiration under thiopental is due to a central synergism between thiopental and endogenous carbon dioxide. Further, it is reasoned that the delayed fall in renal blood flow and attendant anuria which occurred under decamethonium represent the central effects of increasing concentrations of carbon dioxide in the absence of thiopental. Submitted on November 5, 1958

Changes in renal blood flow in dogs during the inhalation of 30% carbon dioxide.

Mongrel dogs lightly anesthetized with thiopental sodium were used as experimental animals. After suitable controls were taken the changes in renal blood flow, urine volume, venous blood pH, blood pressure and heart rate, respiratory rate and volume and relative blood cell volume were measured at intervals during inhalation of 30% carbon dioxide in oxygen for 30 minutes. No anesthetic was administered during the period when CO2 was inhaled. No constant change in pH, hematocrit or heart rate was observed to result from the CO2 inhalation. Respiratory rate increased throughout the experiments. The inhalation of 30% carbon dioxide in oxygen produced a marked reduction in renal blood flow, concomitant with a marked oliguria. The renal ischemia under these conditions was prevented by pharmacological block of the left renal nerves (by injection of 5 ml of .5% tetracaine into the peripelvic area of the kidney). The pharmacologically denervated kidney continued to secrete urine in somewhat diminished quantities while the undenervated kidney developed severe oliguria or anuria. It is postulated that the renal ischemia observed in these experiments is a component of a generalized centrally induced vasoconstrictor response to the inhalation of a high concentration of carbon dioxide.

Effect of hemorrhage on estimated hepatic blood flow and renal blood flow in dogs.

ArticleEffect of Hemorrhage on Estimated Hepatic Blood Flow and Renal Blood Flow in DogsH. O. Heinemann, C. M. Smythe, and P. A. MarksH. O. HeinemannFrom the Department of Medicine, Columbia University College of Physicians and Surgeons, New York City, C. M. SmytheFrom the Department of Medicine, Columbia University College of Physicians and Surgeons, New York City, and P. A. MarksFrom the Department of Medicine, Columbia University College of Physicians and Surgeons, New York CityPublished Online:01 Sep 1953https://doi.org/10.1152/ajplegacy.1953.174.3.352MoreSectionsPDF (761 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByOrgan scaling in mammals: The liverComparative Biochemistry and Physiology Part A: Physiology, Vol. 71, No. 4The effect of haemorrhage on renal blood flow and intrarenal flow distributionInjury, Vol. 9, No. 2Hepatic Origin of Hyperammonemia Induced by Shock in Normal Rats26 September 2008 | Archives Internationales de Physiologie et de Biochimie, Vol. 85, No. 1The function of the hepatic artery21 June 2005The Effect of Hemorrhage on Hepatosplanchnic Hemodynamics, Liver Function and Hepatic MetabolismActa Physiologica Scandinavica, Vol. 89, No. 2Zur adrenerg gesteuerten Durchblutungsregulation im Mesenterialkreislauf der KatzeArchiv für Kreislaufforschung, Vol. 61, No. 2-4Splanchnic and General Hemodynamics After Acute Hemorrhage in the Anesthetized Dog27 September 2008 | Archives Internationales de Physiologie et de Biochimie, Vol. 75, No. 1Die Leberdurchblutung im h�morrhagischen Schock und ihre Beeinflussung durch eine isolierte SpendermilzPfl�gers Archiv f�r die Gesamte Physiologie des Menschen und der Tiere, Vol. 284, No. 3DYNAMICS OF THE CIRCULATION IN THE LIVERHEPATOPORTAL-LIENAL CIRCULATIONUrinary Elimination of Bromsulfalein in Man13 May 2010 | Scandinavian Journal of Clinical and Laboratory Investigation, Vol. 13, No. 1Effect of shock and of vasopressor drugs on the regional circulation of the brain, heart, kidney and liverThe American Journal of Medicine, Vol. 29, No. 2Schock und KollapsEffect of Hemorrhage on Hepatic Blood Flow Determined by Radioactive Colloidal Chromic Phosphate RemovalCirculation Research, Vol. 7, No. 2Verhalten des Splanchnicusgebietes und des Gesamtorganismus im tierexperimentellen hämorrhagischen SchockZeitschrift für Die Gesamte Experimentelle Medizin, Vol. 131, No. 1Der traumatische SchockSplanchnic Blood Flow after HemorrhageScience, Vol. 122, No. 3180RENAL CIRCULATION DURING ANAESTHESIA and SURGERY*22 February 2007 | Anaesthesia, Vol. 10, No. 1 More from this issue > Volume 174Issue 3September 1953Pages 352-356 Copyright & PermissionsCopyright © 1953 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1953.174.3.352PubMed13092255History Received 21 January 1953 Published online 1 September 1953 Published in print 1 September 1953 Metrics