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Biomedical subjects

T Kahn

Publications and source records attributed to T Kahn.

At least 145 records · Page 8Linked to original sources
PubMed1984

Extrarenal potassium transport and the beta 2-adrenergic system.

The distribution of a short-term potassium load was quantitated in three groups of acutely nephrectomized rats infused with KCl at 0.75, 1.50, and 2.25 mEq/kg/hr for 90 minutes. The rate of net potassium transfer from the extracellular fluid compartment to the intracellular fluid compartment was stable from 30 to 90 minutes and proportional to the rate of infusion, with no evidence of saturation of transport mechanisms. In the period 60 to 90 minutes, the calculated increments in intracellular potassium concentration over 10-minute intervals were similar to the respective increments in extracellular potassium concentration. The apparent volume of distribution of the infused potassium over this period was similar to total body water. At the termination of the infusions, the net potassium transfer rates rapidly fell to very low levels. Our studies support the view that the extrarenal modulation of short-term potassium load is dependent on changes in plasma potassium concentration that conform to a first-order linear kinetic model. The infusion of the selective beta 2-adrenergic blocker butoxamine without potassium administration to acutely nephrectomized rats resulted in a net efflux of potassium from the intracellular fluid compartment. The addition of butoxamine to three groups of rats receiving KCl at the previous rates resulted in a fixed decrement in net potassium transfer to the intracellular fluid compartment that was not significantly different from the net efflux of potassium seen with butoxamine alone. Despite beta blockade, the net transfer of potassium remained proportional to the infusion rate. Thus, in our studies, beta 2-adrenergic blockade had a relatively fixed influence on decreasing net potassium transfer, both under basal conditions and during short-term potassium administration.

Adrenergic beta-Antagonists↗
PubMed1983

Cortical and papillary absorptive defects in gentamicin nephrotoxicity.

Renal function was examined in rats given daily injections of gentamicin (100 to 150 mg/kg) for 10 to 14 days. Whole kidney inulin clearance fell and urine volume increased. Single nephron GFR of surface nephrons varied. Some nephrons had no filtration, some had low rates, and some had high rates. Abnormal renal tubular epithelial inulin permeability was demonstrated by microinjection. Micropuncture of individual nephrons early and later in their course demonstrated reduced fluid reabsorption along the proximal convoluted tubule of superficial nephrons. Rates of fluid delivery to the late proximal and distal tubule were elevated. The rate of fluid reabsorption in the superficial loop of Henle was increased. Maximal urine osmolality and papillary tissue content of urea was reduced. The polyuria, therefore, results from decreased fluid reabsorption by proximal tubules and, probably, by papillary collecting ducts. The decrease in proximal fluid reabsorption is probably secondary to impaired solute reabsorption. A decrease in collecting duct fluid absorption can be attributed to the observed decrease in papillary solute concentration.

Acute Kidney Injury↗
PubMed1983

Response to repeated frusemide administration on low chloride and low sodium intake in the rat.

In animals on a normal NaCl intake despite the repeated administration of a diuretic Cl and Na excretion return to baseline values after initial Cl and Na loss. In order to delineate whether this apparent resistance is consequent primarily on a decreased effect of the diuretic, or compensatory Cl and Na reabsorption when the diuretic is not acting, rats were injected with frusemide (1.5 mg twice a day intraperitoneally for 4 days) while on diets differing in Cl and Na content. On a normal NaCl diet Cl and Na excretion increased on day 1 and subsequently returned to baseline. On a low NaCl diet Cl and Na excretion remained above baseline on all 4 days, thereby demonstrating that frusemide continues to promote daily Cl and Na loss. On a low Cl-normal Na intake Na excretion returned to baseline after day 1, while Cl excretion remained above baseline on all 4 days. The increase in K and net acid excretion was highest in these studies. On a low Na-normal Cl intake Cl excretion returned to baseline after day 2, while Na excretion exceeded baseline on all 4 days. Daily K excretion increased least and net acid excretion decreased in these studies. Hourly data on all four diets indicate that frusemide always has an acute effect to promote both Cl and Na excretion. In the recovery period Cl or Na reabsorption is enhanced when the respective ion is available. The apparent resistance to daily frusemide administration on a normal NaCl intake is primarily consequent on enhanced reabsorption balancing the chloriuretic and natriuretic effects. Daily changes in K and net acid excretion are also determined, in part, by these opposing effects.

Aldosterone↗
PubMed1981

Morphologic and clinical correlates in renal amyloidosis.

Morphologic studies and clinical correlations were undertaken in 59 patients with renal amyloidosis. Spicularly arranged amyloid deposits in the glomerular capillary wall were found in all clinical groups but were more frequent and more extensive in primary amyloidosis and multiple myeloma. The severity of proteinuria correlated with the presence of spicules and podocyte destruction rather than with the amount of amyloid in the glomerulus. The spicules were associated with morphologic and clinical evidence of rapid amyloid deposition and a fulminant clinical course. The absence of spicules and the presence of extensive new basement membrane material may produce basement membrane thickening, lamination, and double capillary wall contours, which are associated with mild proteinuria and, rarely, resolution of amyloidosis. Nodular or mixed nodular-diffuse patterns of glomerular amyloid deposits were more frequent in patients with secondary amyloidosis and a longer clinical course. Renal failure generally corresponded to severe glomerular amyloidosis and tubular atrophy. However, a relatively precipitous, usually irreversible decrease in renal function frequently occurred in patients with renal amyloidosis and did not always have a morphologic explanation. The duration of life from the time of biopsy no death in patients with primary amyloidosis (nine months) was markedly shorter than in those with secondary amyloidosis (more than 50 months).

Amyloid↗
PubMed1981

Glucocorticoid-induced alterations in the sodium potassium pump of the human erythrocyte.

To evaluate the effects of glucocorticoids on the Na-K pump in human subjects, were evaluated the intracellular sodium and potassium, 42K influx across and the [3H]ouabain binding to cell membranes of intact human erythrocytes from a group of subjects taking glucocorticoids and a group of normal subjects. Intracellular sodium concentration was lower (7.2 +/- 0.4 vs. 10.9 +/- 0.2 mmol/liter cell water) and intracellular potassium concentration higher (149.8 +/- 1.5 vs. 137.2 +/- 1.2 mmol/liter cell water) in erythrocytes from steroid-treated patients. In spite of a significantly decrease intracellular sodium which normally diminishes ouabain-sensitive 42K influx, the ouabain-sensitive K influx was unchanged in erythrocytes from the steroid-treated group. Maximum [3H]ouabain binding was markedly higher in the steroid-treated group (835 +/- 44 vs. 449 +/- 11 sites/cell). There was close linear correlation between [3H]ouabain binding and inhibition of K pump, suggesting the specificity of ouabain binding to Na-K pump sites on the cell membrane. Association kinetics for ouabain were similar in the two groups despite the marked difference in the amount of [3H]ouabain binding. External potassium concentration required for half-maximum ouabain-sensitive K influx was identical in the two groups. Thus, the additional Na-K pump sites in the steroid-treated group were qualitatively similar to those in normals. These results suggest that administration of glucocorticoids leads to an increase in the number of Na-K pump sites. The increase in the number of Na-K pump sites may explain the low levels of intracellular sodium and higher cell potassium observed in steroid-treated subjects.

Adult↗
PubMed1981

Glucose-induced hyperkalemia in diabetic subjects.

Four insulin-deprived patients with diabetes mellitus and normal baseline potassium and aldosterone levels became hyperkalemic when given 100 g of glucose orally. The increases in plasma potassium concentrations averaged 1.3 mEq/L (range, 0.7 to 1.8 mEq/L) and were accompanied by increases in plasma aldosterone level. Four other insulin-deprived diabetics had normal plasma potassium and aldosterone responses when given 50 mEq of potassium chloride orally. These findings suggest that glucose-induced hyperkalemia is not infrequent in diabetics and that it is not usually associated with hypoaldosteronism. The acute suppression of aldosterone biosynthesis with aminoglutethimide did not lead to increased plasma potassium levels following oral potassium loads. This suggests that the acute responses of aldosterone to potassium loads may not be important in preventing postprandial hyperkalemia.

Adult↗
PubMed1980

Course of gentamicin nephrotoxicity.

Metabolic balance and morphologic studies were performed on rats receiving gentamicin 100 mg/kg/day for a period of 8--10 days and during the recovery period. Daily urine flow rate increased with the administration of gentamiccin and remained elevated up to 20 days following the discontinuation of gentamicin, although BUN and plasma creatinine were virtually normal 10 days after the discontinuation of gentamicin. During the development of renal failure means daily electrolyte excretion remained normal. During the recovery period, however, sodium and potassium excretion exceeded control values while chloride and net acid excretion remained normal. Proteinuria developed during the administration of gentamicin and returned to normal 6--10 days after the discontinuation of gentamicin. Ten days of netilmicin administration (150 mg/kg/day) resulted in only mild tubular degeneration and no azotemia.

Animals↗
PubMed1980

A comparative study of steroid therapy in acute experimental spinal cord injury.

Steroids are commonly used in the treatment of acute spinal cord injury patients although a review of the literature fails to define a consistent regimen for administration with regard to optimal preparation or dosage or schedule. This study was designed to evaluate the effect of exogenous steroids on the outcome of experimental spinal cord injury and the effect of experimental spinal cord injury on endogenous cortisol production. Thirty female rhesus monkeys received a 660 gm cm lesion to the T10 spinal cord. They were randomly placed into one of six groups of five animals each. Two groups were controls used to assess the endogenous cortisol response to spinal cord injury. These animals received no steroids. The other four groups received one of two commonly used steroid preparations. All animals were evaluated serially for neurological status using motor testing and for general physical status. Serial cortisol determinations were obtained for an eight-week post injury period. The steroid groups showed some benefit from treatment when compared to the untreated controls. There were no significant differences in physical condition between treated and control groups. Of special interest was the response of endogenous cortisol production to spinal cord injury. Early cortisol elevation following injury peaked by eight hours and then precipitously dropped to baseline levels before 24 hours following injury.

Animals↗