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Biomedical subjects

R Hamburger

Publications and source records attributed to R Hamburger.

At least 37 records · Page 2Linked to original sources
PubMed1977

On the mechanism of lithium-induced renal tubular acidosis.

The effect of lithium chloride administration on urinary acidification was studied in dogs. Lithium-treated dogs developed hyperchloremic metabolic acidosis with alkaline urine. Bicarbonate loading resulted in a normal increase in urinary Pco2 in normal dogs but failed to produce the same response in lithium-treated dogs. The bicarbonate titration curve of lithium-treated dogs revealed a small leak of bicarbonate at low plasma levels of bicarbonate; at high plasma levels bicarbonate reabsorption was significantly higher in lithium-treated dogs. This pattern of bicarbonate reabsorption is identical to that described in classic distal renal tubular acidosis. Sodium sulfate administration resulted in a normal urinary acidification ilithium-treated dogs. It is possible that lithium administration induces distal renal tubular acidosis by allowing excessive back-diffusion of acid. This excessive back-diffusion of acid would result in a low urinary Pco2 during bicarbonate loading. Sodium sulfate administration, by increasing the negative intratubular potential, would restrict back-diffusion of hydrogen ion and thereby result in a normal acidification in lithium-treated dogs. We previously demonstrated that postureteral obstruction of the kidney fails to increase urinary Pco2 during bicarbonate loading and to lower urinary pH with sodium sulfate. It is possible that a low urinary Pco2 during HCO3 loading can occur as a consequence of either diminished hydrogen ion secretion (postobstructed kidney) or excessive back-diffusion of acid (lithium administration). Further studies are indicated to determine whether both mechanisms may be found in patients with distal renal tubular acidosis.

Absorption↗
PubMed1976

Distal Tubule [Na+] and juxtaglomerular apparatus Renin activity in uranyl nitrate induced acute renal failure in the rat. An evaluation of the role of tubuloglomerular feedback.

It has been previously demonstrated that single neophron filtration rate, whole kidney glomerular filtration rate and total renal blood flow decreased by 30-35% 6 h after uranyl nitrate induced acute renal failure in the rat. In order to evaluate a role of the renin-angiotensin system in the initiating phase (0-6 h) of this model of acute renal failure determinations of plasma renin activity, superficial (S) and deep (D) juxtaglomerular apparatus (JGA) renin activity and distal nephron [Na+] were obtained. Plasma renin activity increased from the control value of 1.5 +/- 0.3 (S.E.M.) to 2.9 +/- 0.4 ng/ml/h (P less than 0.005) at 6 h. Mean renin activity in S- and D-JGA's of control rats was 6.99 +/- 0.41 and 2.67 +/- 0.21 ng/JGA/h, respectively. After uranyl nitrate, renin activity in S-JGA's increased to 13.62 +/- 0.80 ng/JGA/h (P less than 0.001) at 2 h and remained elevated, 12.56 +/- 0.90 and 12.75 +/- 0.87 ng/JGA/h at 4 and 6 h. D-JGA renin activity increased (P less than 0.05) to 7.04 +/- 0.53, 6.23 +/- 0.31 and 3.44 +/- 0.33 ng/JGA/h at 2, 4 and 6 h after uranyl nitrate. Distal tubule [Na+], 27 samples in 6 rats, increased from a mean control value of 53.7 +/- 1.2 mEq/l to 116.9 +/- 2.5 mEq/l, 24 samples in 6 rats (P less than 0.001). Prompt increases in JGA renin activity were observed in the initiating phase of acute renal failure, suggesting a role for the renin-angiotensin system in the pathophysiology of this nephrotoxic model. The association of increased JGA renin activity and increased distal [Na+] is consistent with a role for the tubuloglomerular feedback mechanism in the initiating phase of uranyl nitrate induced acute renal failure in the rat.

Acute Kidney Injury↗
PubMed1975

[Natural occurrence of progesterone in commercial milk products (author's transl)].

By means of radioimmunoassay the concentrations of progesterone in commercial milk products were determined. The values range from 1.4 ng/ml (skin milk) to 300 ng/g (butter). The results show a close correlation between progesterone and fat contents in milk products. It is discussed that - due to recent progress in analytical methods - hormones in their natural occurrence in food are now measurable in micro-quantities which were not yet considered to be of biological importance; these findings should provoke a revision of terms like "free of hormones" in the sense of "zero tolerances".

Animals↗
PubMed1975

Surface tension and cloud point changes of polyoxyethylenic non-ionic surfactants during autoxidation.

Changes in the surface tension-concentration curves of the non-ionic surfactant cetomacrogol, a polyoxyethylenic (POE) hexadecyl ether containing about 24 ethylene oxide (EO) groups, have been examined during autoxidation of aqueous solutions. The curves exhibit decreases in cmc values and changes in the slopes below and above the cmc which lead to the loss of the sharp break characteristic of micelle-formation. There is also a progressive decrease in the cloud point during autoxidation. Surface tensions and cloud points of a series of known POE hexadecyl ethers containing from 10 to 60 EO units have been measured and related to the number of EO units present. From these data, it is apparent that autoxidation of cetomacrogol is accompanied by degradation of POE chain rather than the hydrocarbon chain, the number of EO units lost up to the time at which the solution becomes turbid being about 14. The significance of such measurements is discussed in relation to the detection of decomposition and pending rapid decomposition in synthesized and commercial surfactants.

Catalysis↗
PubMedDate not supplied

Bumetanide-induced diuresis and natriuresis: effect of prostaglandin synthetase inhibition.

The effects on the renal actions of bumetanide of two inhibitors of prostaglandin synthetase, acetylsalicylic acid (ASA) and indomethacin, were studied in eight normal adults. Indomethacin alone resulted in a significant decrease in FENa compared to the control period. Bumetanide alone resulted in increases in urine volume, FENa, and plasma renin activity. Both ASA and indomethacin blunted the increases in urine volume and sodium excretion, although the inhibition by indomethacin was greater than that of ASA. In addition, indomethacin completely inhibited the bumetanide-induced increase in plasma renin activity. No consistent relationship between these effects and urinary prostaglandin E2 or F excretion was noted. These studies indicate that prostaglandin synthetase inhibitors may interfere with the effects of bumetanide.

Adult↗