Biomedical subjects
M Fulop
Publications and source records attributed to M Fulop.
Impaired renal function exaggerates hyperbilirubinemia in bile duct-ligated dogs.
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Increased ureteral back pressure enhances renal tubular sodium reabsorption.
Moderate increases of ureteral back pressure usually cause decreases of glomerular filtration rate and even greater decreases of sodium excretion. It has been assumed previously that increased ureteral back pressure does not enhance renal tubular sodium reabsorption directly and that the decreases of sodium excretion are caused by the decreases of glomerular filtration rate. In the experiments reported here, the effect of increased ureteral back pressure on urinary sodium excretion was studied in dogs in which changes of filtration rate were minimized by infusing saline while ureteral back-pressure was increased. When ureteral back pressure was increased on one side by 10-23 cm of water, the inulin clearance of the experimental kidney decreased by only 3-12% in 21 experiments, did not change significantly (+/-2%) in eight experiments, and increased by 3-8% in seven experiments. The sodium excretion of the experimental kidney decreased in all experiments regardless of whether its inulin clearance increased, decreased, or was unchanged from control values. When the inulin clearance of the experimental kidney increased or remained unchanged during increased ureteral back pressure, its reabsorption of sodium increased more than could be accounted for by the increase of filtered sodium. When the inulin clearance of the experimental kidney decreased during increased ureteral back pressure, its reabsorption of sodium decreased less than could be accounted for by the decrease of filtered sodium.Therefore, the effect of increased ureteral back pressure to decrease urinary sodium excretion is caused in part by increased tubular reabsorption of sodium.
The effect of acute ureteral pressure elevation on the excretion of urea and sodium in dogs.
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The phosphaturic effect of sodium bicarbonate and acetazolamide in dogs.
Urinary inorganic phosphate excretion was studied before and during the administration of sodium bicarbonate and acetazolamide in dogs that were not given infusions of phosphate. The excretion fraction of filtered phosphate increased after sodium bicarbonate or acetazolamide was given. This phosphaturia was attributed to decreased tubular reabsorption of phosphate consequent to alkalinization of either tubular urine or cells.
Defective urinary acidification in Wilson's disease.
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Bilirubinemia and renal failure.
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Diuretic action of glycerol in dogs.
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The effect of bile salts on the binding of bilirubin by plasma proteins.
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Possible diphenylhydantoin-induced arrhythmia in hypothyroidism.
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Flow diagrams for the diagnosis of acid-base disorders.
This article discusses flow diagrams and tables intended to provide a systematic approach to the rapid laboratory differential diagnosis of acid-base disorders in the emergency department.
The ventilatory response in uncomplicated diabetic ketoacidosis.
The ventilatory response to uncomplicated sub-acute metabolic acidosis was studied by measuring arterial blood CO2 tension (PaCO2) and pH in 27 episodes of diabetic ketoacidosis without coexisting lactic acidosis. From those data, regression equations and 95% confidence bands were calculated for the relations between PaCO2 and pH. These relations were very similar to those previously described by others in patients with chronic uremic acidosis.