Renal ammoniagenesis following glutamine loading in intact dogs during acute metabolic acid–base perturbations

1987 ◽  
Vol 72 (1) ◽  
pp. 61-69 ◽  
Author(s):  
Jorge Areas ◽  
Sevag Balian ◽  
Dianna Slemmer ◽  
Mario Belledonne ◽  
Harry G. Preuss
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Metabolic Acidosis ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Respiratory Acidosis ◽  
Glutamine Metabolism ◽  
Acid Base ◽  
Acute Metabolic Acidosis ◽  
Qualitative Changes

1. Adaptation of renal ammoniagenesis during acute metabolic acidosis in intact dogs may be nonexistent or, at least, markedly less than in chronic acidosis. This contrasts to adaptation in acute respiratory acidosis, where levels similar to those attained in chronic acidosis occur within hours. 2. Accordingly, the inability to discern marked changes in acute metabolic acidosis compared with acute respiratory acidosis has been attributed to decreased glomerular filtration rate and renal blood flow seen frequently in the former. 3. In our studies, we found early changes in ammoniagenesis and glutamine metabolism during acute metabolic acidosis, but not of the magnitude seen in chronic acidosis, even considering the changes in renal blood flow (RBF) and glomerular filtration rate (GFR). Exogenous glutamine loading allowed us to discover that the qualitative changes in glutamine metabolism during acute metabolic acidosis differed from control but fell short of those seen in chronic metabolic a acidosis. 4. We also examined glutamine metabolism when renal ammoniagenic adaptation was acutely inhibited in chronically acidotic dogs. Infusing NaHCO3 into chronically acidotic dogs decreased renal ammonia production significantly (247 μmol min−1 100 ml−1 GFR vs 148 μmol min−1 100 ml−1 GFR: P < 0.001) and glutamine extraction (111.8 μmol min−1 100 ml−1 GFR vs 90.9 μmol min−1 100 ml−1 GFR: P < 0.02). 5. The qualitative changes in renal glutamine metabolism in both studies suggest that alterations in deamination of glutamate formed from glutamine are responsible, at least in part, for adaptation to acute acid–base perturbations. 6. Compared with respiratory acidosis, adaptation to metabolic acidosis is progressive and prolonged.

The Acute Effects of Respiratory and Metabolic Acidosis on Renal Function in the Dog

1976 ◽  
Vol 50 (3) ◽  
pp. 165-169 ◽  
Author(s):  
M. O. Farber ◽  
J. J. Szwed ◽  
A. R. Dowell ◽  
R. A. Strawbridge
Keyword(s):  
Cardiac Output ◽  
Glomerular Filtration Rate ◽  
Metabolic Acidosis ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Urine Volume ◽  
Respiratory Acidosis ◽  
Effective Renal Plasma Flow

1. Effective renal plasma flow, glomerular filtration rate and cardiac output were measured in osmotically loaded dogs before and during comparable acute respiratory and metabolic acidosis. 2. Urine output increased in control dogs and in animals with metabolic acidosis, but declined with respiratory acidosis. Effective renal plasma flow and glomerular filtration rate declined with respiratory and metabolic acidosis. 3. When respiratory acidosis was buffered with sodium bicarbonate, urine volume increased and glomerular filtration rate and effective renal plasma flow were unchanged; with trihydroxymethylaminomethane, urine volume increased but glomerular filtration rate and effective renal plasma flow fell. 4. When metabolic acidosis was buffered with sodium bicarbonate, urine volume increased; with trihydroxymethylaminomethane, urine volume increased but glomerular filtration rate fell. Cardiac output declined only during metabolic acidosis, both buffered and unbuffered. 5. These studies demonstrate that, even with osmotic loading: (1) respiratory acidosis causes a decrease in glomerular filtration rate, effective renal plasma flow and urine volume; (2) metabolic acidosis depresses glomerular filtration rate and effective renal plasma flow but does not change urine volume even though cardiac output falls; (3) sodium bicarbonate is more effective than trihydroxymethylaminomethane in preserving renal function during respiratory and metabolic acidosis.

Reversible Renal Nerve Denervation in the Cat: Effects on Haemodynamic and Excretory Functions of the Ipsilateral and Contralateral Kidneys

1982 ◽  
Vol 63 (s8) ◽  
pp. 215s-217s ◽  
Author(s):  
R. Golin ◽  
A. Stella ◽  
A. Zanchetti
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Renal Nerves ◽  
Renal Nerve ◽  
Contralateral Kidney ◽  
Cooling Period ◽  
Renal Changes ◽  
Water And Sodium Excretion

1. In anaesthetized cats, reversible nenal nerve denervation (cooling of the renal nerves on one side at 4°C for 16 min) was performed and its effects on haemodynamic and excretory functions of the ipsilateral and the contralateral kidneys were studied. 2. Renal nerve cooling did not cause any change in arterial pressure. Slight increase in blood flow, no change in glomerular filtration rate and a large increase in water and sodium excretion occurred in the ipsilateral kidney; simultaneously, no change in blood flow, a slight and transient decrease in glomerular filtration rate, and a significant decrease in diuresis and natriuresis were observed in the contralateral kidney. 3. Ipsilateral and contralateral renal changes were equally evident in the early (minutes 0 to 8) and late phases (minutes 8 to 16) of the cooling period. 4. When renal nerve cooling was repeated after surgical denervation of the contralateral kidney all contralateral effects were abolished.

Renal glomerular filtration rate and hepatic blood flow during voluntary diving in Weddell seals

1983 ◽  
Vol 245 (5) ◽  
pp. R743-R748 ◽  
Author(s):  
R. W. Davis ◽  
M. A. Castellini ◽  
G. L. Kooyman ◽  
R. Maue
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Hepatic Blood Flow ◽  
Filtration Rate ◽  
Hepatic Function ◽  
Inulin Clearance ◽  
Weddell Seals ◽  
Icg Clearance ◽  
The Mean

Renal and hepatic function were studied during voluntary dives in Weddell seals by measuring the clearance rate of inulin and indocyanine green (ICG). Inulin is cleared exclusively by the kidneys and measures renal glomerular filtration rate (GFR). ICG is cleared by the liver and is blood flow dependent at concentrations used. Studies were conducted from a portable hut with a trapdoor placed over an isolated hole in the sea ice near McMurdo Station, Antarctica. An intravertebral extradural catheter was inserted percutaneously under light anesthesia in subadult seals weighing 130-200 kg. When released into the ice hole, the seals made voluntary dives, but always had to return to breathe. Serial blood samples were taken after single injections of inulin and ICG and analyzed within 24 h. The mean half time (t 1/2) for inulin clearance while resting at the surface was 27.3 +/- 13.0 min (n = 43) and the mean t 1/2 for ICG clearance was 18.3 +/- 7.3 min (n = 23). The mean resting GFR was 3.6 ml X min-1 X kg-1 (range 3.2-3.9, n = 3). Inulin and ICG clearance rates did not change from resting levels during dives shorter than the seal's aerobic dive limit (ADL). Inulin clearance decreased over 90% during dives longer than the ADL, but there was no significant reduction in ICG clearance during dives lasting up to 23 min. It appears that normal renal GFR and hepatic blood flow continue during natural aerobic dives. During dives that exceed the ADL, GFR is reduced but hepatic blood flow may be maintained.

Genetic co-segregation of renal haemodynamics and blood pressure in the spontaneously hypertensive rat

1988 ◽  
Vol 74 (1) ◽  
pp. 63-69 ◽  
Author(s):  
S. B. Harrap ◽  
A. E. Doyle
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Spontaneously Hypertensive Rat ◽  
Plasma Renin ◽  
Spontaneously Hypertensive

1. To determine the relevance of renal circulatory abnormalities found in the immature spontaneously hypertensive rat (SHR) to the genetic hypertensive process, glomerular filtration rate and renal blood flow were measured in conscious F2 rats, derived from crossbreeding SHR and normotensive Wistar–Kyoto rats (WKY), at 4, 11 and 16 weeks of age by determining the renal clearances of 51Cr-ethylenediaminetetra-acetate and 125I-hippuran respectively. Plasma renin activity was measured at 11 and 16 weeks of age. 2. Mean arterial pressure, glomerular filtration rate and renal blood flow increased between 4 and 11 weeks of age. Between 11 and 16 weeks the mean glomerular filtration rate and renal blood flow did not alter, although the mean arterial pressure rose significantly. At 11 weeks of age, during the developmental phase of hypertension, a significant negative correlation between mean arterial pressure and both glomerular filtration rate and renal blood flow was noted. However, by 16 weeks when the manifestations of genetic hypertension were more fully expressed, no correlation between mean arterial pressure and renal blood flow or glomerular filtration rate was observed. Plasma renin activity was negatively correlated with both glomerular filtration rate and renal blood flow, but the relationship was stronger at 11 than at 16 weeks of age. 3. These results suggest that the reduction in renal blood flow and glomerular filtration rate, found in immature SHR, is genetically linked to the hypertension and may be of primary pathogenetic importance. It is proposed that the increased renal vascular resistance in these young animals stimulates the rise of systemic arterial pressure which returns renal blood flow and glomerular filtration rate to normal.

Renal Blood Flow, Glomerular Filtration Rate, and Renal Oxygenation in Early Clinical Septic Shock*

2018 ◽  
Vol 46 (6) ◽  
pp. e560-e566 ◽  
Author(s):  
Jenny Skytte Larsson ◽  
Vitus Krumbholz ◽  
Anders Enskog ◽  
Gudrun Bragadottir ◽  
Bengt Redfors ◽  
...  
Keyword(s):  
Septic Shock ◽  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate

USE OF HEMODIALYSIS IN THE TREATMENT OF QUINIDINE POISONING

PEDIATRICS ◽  
1973 ◽  
Vol 52 (1) ◽  
pp. 95-99
Author(s):  
Ekkehard W. Reimold ◽  
Walter J. Reynolds ◽  
David E. Fixler ◽  
LaVerne McElroy
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Treatment Period ◽  
Filtration Rate ◽  
Renal Excretion ◽  
Artificial Kidney ◽  
Flow Rates ◽  
Urine Acidification ◽  
Forced Diuresis

Hemodialysis was used in addition to forced diuresis in the treatment of quinidine poisoning of a 3-year-old girl. The estimated retained dose of quinidine was 1,600 mg. During a 36-hour treatment period the patient excreted through the kidneys 768.1 mg quinidine (21.3 mg/hr). Hemodialysis almost doubled the quinidine elimination by removing 145 mg in eight hours (18.1 mg/hr): renal excretion, 55%; hemodialysis, 45%. The quinidine elimination with dialysis is high when high blood flow rates through the artificial kidney can be maintained. Adequate glomerular filtration rate and urine acidification are necessary for high renal excretion of quinidine.

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