The Acid-Base Metabolism

Astrup, Poul; Jørgensen, K.; Andersen, O. Siggaard; Engel, K.

doi:10.1016/s0140-6736(60)90930-2

Cited by 553 publications

(127 citation statements)

References 8 publications

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“…The slices were incubated for various periods of time in an atmosphere of 95% O 2 -5% CO 2 . During aerobic incubation, the concentration of oxygen in the flask was never less than 70%; during anaerobic incubation, the mean concentration of oxygen was 3.0 ± 0.3% (SE) as determined by the Astrup technique [1].…”

Section: Tissue and Incubation Techniquesmentioning

confidence: 95%

In Vitro Metabolism of Palmitic Acid in Human Fetal Tissue

Yoshioka

Roux

1972

Pediatr Res

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Section: Tissue and Incubation Techniquesmentioning

confidence: 95%

In Vitro Metabolism of Palmitic Acid in Human Fetal Tissue

Yoshioka

Roux

1972

Pediatr Res

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“…Standard bicarbonate is the bicarbonate concentration of fully oxygenated blood at 38O Celsius, when the PCO, has been adjusted to 40 mmHg (Astrup et al 1960). By adjusting the PCO, to 40mmHg, alterations in bicarbonate in blood secondary to changes in PCO, disappear and the standard bicarbonate therefore exclusively describes metabolic acid-base changes.…”

Section: Discussionmentioning

confidence: 99%

Relationships Between Oxygen and Carbon Dioxide Tensions and Acid-Base Balance in Arterial Blood and in Medullary Blood from Long Bones in Dogs

Eriksen

Tøndevold

Jansen

et al. 1979

Acta Orthopaedica Scandinavica

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“…The net acid excretion was performed within 1-3 days on urine frozen previously [5]. Blood acid-base status was determined by the equilibration method of Astrup et al [1], 125 I-iothalamate clearance by the method of Cohen et al [6], blood and urine electrolyte determinations by routine chemistry methods, and urine amino acid analysis performed on a Beckman AutoAnalyzer [17]. Figure 1 depicts the minimal blood total CO 2 at various times after ingestion of ammonium chloride.…”

Section: Laboratory Methodsmentioning

confidence: 99%

“…The purpose of this study was (1) to compare the renal tubular and glomerular function in four populations: normal adults with two kidneys, unilaterally nephrectomized adult allograft donors who served as control subjects, recipients of live-related donor allografts, and recipients of cadaveric donor allografts; (2) to investigate renal function in the above recipients at various times after transplantation. Table I.…”

Section: Introductionmentioning

confidence: 99%

The Adaptation of Hydrogen Ion Excretion Associated with Nephron Reduction in Post-transplant Patients

et al. 1973

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ExtractThe compensatory growth of the single and transplanted kidney is demonstrated by the improvement of glomerular filtration rate (GFR) of the single kidney to achieve 50-90% of the normal value. The compensatory renal tubular acid excretion is also studied. It is clearly demonstrated that in response to a standard ammonium chloride load (75 mEq/m 2 ) systemic acidosis (tCO 2 < 16 mEq/liter) occurs uniformly at 300^4-00 min but maximal renal acid excretion (98 ± 12 and 76 ± 17 yuEq/min/ 1.73 m 2 ) occurs in the normal and single kidney subjects, respectively, at 300-400 min, whereas, for the transplant subjects, maximal acidifications of 72 ± 34 and 74 ± 26 juEq/min/1.73 m 2 are achieved at 800 and 1,400 min for live-related and cadaveric allografts, respectively. The slower and suboptimal renal response accounts for the persistence of metabolic acidosis in the transplant population.The studies document that the important limiting factor is the reduction in glomerular filtration rate in the transplant subjects. When the low net acid excretion in the two transplant groups are factored by GFR, they become comparable with the control (donor) group as well as the normal group (P > 0.95), i.e., each remaining nephron is excreting acid normally (or supernormally) and is supportive of the "intact nephron" hypothesis.The data show a marked difference in urinary pH during acidosis between the two transplant groups: 50% of the cadaveric allografts have an inability to lower urine pH below 5.4 compared with 10% only of the live-related allografts which show such a defect. This would imply that cadaver allografts are more susceptible to an acute acid load. SpeculationThe ischemia sustained at the time of transplantation results in acute tubular damage and proportionate lowering of the glomerular filtration rate which account for the impaired acidification capacity in the kidney allografts. It is also possible that circulatory damage to the glomeruli may occur in the transplantation process. It is even possible that intrarenal circulation may be altered by either transplantation or nephrectomy; although, admittedly, this last possibility seems quite unlikely. It is open to speculation what effect the age difference between the donors and the recipients may have on their different responses to acute metabolic acidosis. 712Adaptation of hydrogen ion excretion 713

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The Acid-Base Metabolism

Cited by 553 publications

References 8 publications

In Vitro Metabolism of Palmitic Acid in Human Fetal Tissue

In Vitro Metabolism of Palmitic Acid in Human Fetal Tissue

Relationships Between Oxygen and Carbon Dioxide Tensions and Acid-Base Balance in Arterial Blood and in Medullary Blood from Long Bones in Dogs

The Adaptation of Hydrogen Ion Excretion Associated with Nephron Reduction in Post-transplant Patients

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