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Biomedical subjects

H Osswald

Publications and source records attributed to H Osswald.

At least 109 records · Page 6Linked to original sources
PubMed1982

Role of adenosine in signal transmission of tubuloglomerular feedback.

The present study has developed a new hypothesis for the regulation of renal hemodynamics based on the theory of a metabolic control of local blood flow. Adenosine has been proposed as the mediator of tubuloglomerular feedback. We have reported on the renal effects of adenosine, the renal tissue levels of adenosine in relation to those of ATP, and the effects of adenosine synergistic substances (dipyridamole, erythrohydroxynonyladenine) and adenosine antagonistic substances (theophylline, adenosine deaminase) on the tubuloglomerular feedback response of the nephron. A hypothetic model has been presented that incorporates adenosine as a mediator in the signal transmission of the tubuloglomerular feedback mechanism.

Adenine↗
PubMed1981

Polyamine responses in a solid transplanted tumor (S180) in liver and in urine during endotoxin-induced tumor injury in the mouse.

Polyamine (PA) and ATP concentrations have been measured in the S180 sarcoma damaged by endotoxin (1) 4 hours after administration, coinciding with the onset of hemorrhage, (2) at 8 hours, and (3) at 24 hours, preceeding overt necrosis. The putrescine (PU) content increased promptly, the spermidine (SPD) level dropped by 30% between 8 and 24 hours, while the spermine (SPM) concentration remained unchanged. The ATP level fell, reaching 1% of the control value at 24 hours. The parallel between increases in tumor PU content and urinary PU excretion appears to be largely fortuitous; no similar correlations existed in the cases of SPD and SPM. The development of tumor stasis and the alterations seen in PA metabolism of tumor-free controls suggest that the changes in liver PA concentrations and in urinary excretion primarily reflect responses of nonmalignant cells. Both these findings in animals without tumors and existing data from other experimental systems are consistent with the thesis that PA response patterns to a particular procedure are qualitatively similar regardless of the presence or absence of a malignant growth, and are characteristic of the procedure employed.

Adenosine Triphosphate↗
PubMed1981

Adenosine induced fall in glomerular capillary pressure. Effect of ureteral obstruction and aortic constriction in the Munich-Wistar rat kidney.

The effect of acute ureteral obstruction (UO) and reduction of renal artery pressure (AC) on the adenosine-induced renal vasoconstriction was studied in the Munich-Wistar rat. Infusion of adenosine, 0.05 mumol/min . kg body weight, into the thoracic aorta, was associated with a fall of directly measured glomerular capillary pressure (Pgc) from 45.2 + 1.8 to 32.5 + 1.7 mm Hg, P less than 0.001. Elevation of ureter pressure to 39 + 2 mm Hg abolished the fall of Pgc following adenosine infusion, 51.3 + 1.7 vs. 50.0 + 1.3 mm Hg, NS. Reduction of renal artery pressure to 70 mm Hg by an aortic clamp above the renal arteries also prevented the fall of Pgc due to adenosine, 36.8 + 0.9 vs. 36.4 + 1.8 mm Hg, NS. Administration of indometacin (10 mg/kg i.v.) restored the ability of adenosine to reduce Pgc in UO from 41.5 + 1.1 to 25.9 + 2.6 mm Hg (P less than 0.001) and in AC from 34.0 + 3.4 to 28.2 + 75.7 mm Hg (P less than 0.02). Since previous studied have demonstrated that in UO and AC renal prostaglandin synthesis is enhanced the effects of indometacin suggest that prostaglandins could be antagonistic to the action of adenosine on the kidney. The data show that the renal vasculature becomes insensitive to the vasoconstrictive action of adenosine during elevated ureter pressure and reduced renal artery pressure.

Adenosine↗
PubMed1980

Overadditive chemotherapeutic synergism of prospidine and inosine when given sequentially to the Sarcoma 180 implanted intramuscularly.

The chemotherapeutic effectiveness of prospidine monotherapy on the Sarcoma 180 implanted i.m. was compared with several prospidine/inosine combinations. The chemotherapeutic action of the combination was enhanced overadditively when inosine was given 6 h after prospidine. This particular combination caused not only a significant curative action and tumor inhibition as compared with prospidine monotherapy, but also decreased the toxic effects.

Animals↗
PubMed1979

Potentiation of the chemotherapeutic action of 5-fluorouracil by combination with cytidine or guanosine on HRS-sarcoma.

The chemotherapeutic action of 5-fluorouracil monotherapy on HRS-Sarcoma in mice was compared with those of 5-fluorouracil nucleoside combinations (thymidine, cytidine or guanosine). The curative action of 5-fluorouracil was potentiated without increasing its toxicity, when cytidine or guanosine were applied at definite intervals before or after 5-fluorouracil.

Animals↗
PubMed1979

Suramin enhancement of the chemotherapeutic actions of cyclophosphamide or adriamycin of intramuscularly-implanted Ehrlich carcinoma.

The chemotherapeutic action of cyclophosphamide or adriamycin monotherapy on hyperdiploid Ehrlich carcinoma was compared with that of sequential combinations of suramin and cyclophosphamide and suramin and adriamycin. The chemotherapeutic action of the suramin-cyclophosphamide combination or of the adriamycin-surmin combination was significantly enhanced when the combination partners were applied at definite intervals.

Animals↗
PubMed1979

Effects of acetazolamide and changes of acid-base balance on the content of cyclic nucleotides in the rat kidney.

Changes in tissue levels of cyclic adenosine 3':5'-monophosphate (cAMP) and cyclic guanosine 3':5'-monophosphate (cGMP) in the rat kidney in response to acid-base changes and administration of acetazolamide were measured. cAMP was determined according to the method described by Gilman and cGMP by radioimmunoassay. 1 mg/kg acetazolamide increased bicarbonate excretion 100-fold over the control values to 2.52 +/- 0.5 mEq/min (mean +/- SEM; n = 6), but did not influence cGMP and cAMP tissue content. 10 and 100 mg/kg acetazolamide increased cGMP tissue levels to 0.277 +/- 0.048 and 0.482 +/- 0.07 pmol/mg dry weight in comparison to 0.192 +/- 0.04 in the controls, whereas no changes in cAMP levels occurred. Chronic as well as acute metabolic alkalosis induced an increase of cGMP levels (0.26 +/- 0.03 and 0.29 +/- 0.06 pmol/mg), whereas chronic metabolic and acute respiratory acidosis lowered cGMP levels to 0.14 +/- 0.02 and 0.13 +/- 0.02 pmol/mg. cAMP tissue levels were not affected by changes in acid-base balance. The data could suggest that cGMP participates in the regulation of acid-base balance and renal effects of acetazolamide.

Acetazolamide↗
PubMed1979

Renal elimination kinetics and plasma half-life of oxalate in man.

The renal handling of oxalate was studied by the injection of 14C-oxalate together with inulin as a glomerular marker into the renal artery in 6 patients. From the recovered amounts of the injected substances in the urine, time-concentration curves were constructed. Oxalate was excreted into urine 2.31 +/- 0.05 (SE) fold when compared to inulin. The maximal concentration of oxalate occurred at the same time as inulin, and there was no urinary precession of oxalate in comparison to inulin. From this part of the study we conclude that oxalate in addition to its filtered amount can probably enter the early part of nephron. In a second type of study, plasma levels of oxalate and inulin were observed over a period of 180 min, following intravenous injections in 7 volunteers. The decline of oxalate plasma concentrations followed first-order kinetics. Calculation of the rate constants of elimination assuming the 'one compartment open' model resulted in an oxalate to inulin ratio of 1.21 +/- 0.05. The oxalate half-life of elimination was 92 +/- 8 min, whereas that of inulin amounted to 112 +/- 9 min. The higher value of the calculated volume of distribution of oxalate compared to that of inulin indicates that oxalate enters a larger space than the extracellular fluid volume. The urinary recovery of intravenously injected oxalate was 97.2 +/- 1.4%, indicating that oxalate is excreted exclusively by the kidney. The observed differences of oxalate excretion, obtained with these two methods, could be attributed to the higher amount of ionized oxalate in the disequilibrium technique (rapid injections), entering the urine in a higher rate. Such a mechanism could explain the hyperoxaluria in calcium oxalate stone-forming patients.

Half-Life↗
PubMed1979

Mesangial function in ureteral obstruction in the rat. Blockade of the efferent limb.

The kinetics for mesangial uptake and transport of radiolabeled aggregated human immunoglobulin (Ig)G (AHIgG(125)I) deviated markedly from normal in male Sprague-Dawley rats with ureteral obstruction. Four experimental groups, each containing 25 rats, were used: (a) bilateral ureteral ligation (BUL) with release of one ureter 24 h later; (b) unilateral ureteral ligation with release 24 h later [UUL(R)]; (c) unilateral ureteral ligation without release (unreleased) [UUL(U)]; (d) uremia-control, which consisted of rats with ligated left ureter and a severed right ureter. A similar number of sham-operated rats served as control for each group. AHIgG(125)I (45 mg/100 g body wt) was given intravenously 1 h after release of the ureteral obstruction (25 h after ureteral obstruction or sham surgery). Groups of five control and five experimental animals were sacrificed at 2, 4, 8, 16, and 24 h after injection. At all time intervals, concentrations of AHIgG(125)I in isolated glomeruli from control animals were similar to values obtained from nonobstructed kidneys of UUL(U) and UUL(R) rats: a linear decrease in concentration over a period of 24 h was observed when the logarithm of glomerular AHIgG(125)I concentration was plotted against time. Aberrations in the kinetics were apparent in obstructed kidneys but not in liver, spleen, or blood concentrations of AHIgG(125)I: (a) At 2 h in all obstructed kidneys, glomerular concentration of AHIgG(125)I was markedly reduced. (b) In BUL (released or unreleased), glomerular concentrations of AHIgG(125)I from 4 to 16 h were congruent with 10-fold those in UUL(U) or UUL(R) kidneys. (c) The significant decline in glomerular concentration between 4 and 16 h in control and nonobstructed kidneys was not observed in UUL(R), UUL(U), or BUL (released or unreleased) kidneys; in all obstructed kidneys, a plateau in glomerular concentrations of AHIgG(125)I was observed between 4 and 16 h. (d) After 16 h at a time when the blood level of AHIgG(125)I had decreased to 3% of initial values, there was progressive fall in glomerular AHIgG(125)I. Similar results were obtained in the uremia-control group in rats, which indicated that uremia per se had no measurable effect on mesangial kinetics. These studies demonstrate that ureteral occlusion induces alterations in mesangial uptake (afferent limb) and egress (efferent limb) of macromolecules. Particularly evident is the "blockade" of the efferent limb which is demonstrable at high blood levels of AHIgG(125)I. These alterations in the transit of macromolecules through the mesangium may be mediated in part by the hemodynamic changes that accompany ureteral obstruction.

Animals↗
PubMed1979

Pharmacokinetic studies of oxalate in man.

The observation of the plasma concentrations after rapid intravenous administration of inulin and 14C-oxalate to six normal and one hyperoxaluric subjects allowed estimations of the half-life of elimination of oxalate (mean 91.7 min), volume of distribution of oxalate (mean = 32.5 liters), calculation of the miscible oxalate pool (mean 3.7 mg), of the plasma oxalate concentration (mean = 11.1 microgram per 100 ml), of the oxalate clearance (252 ml per min), and the determination of the oxalate turnover rate (0.027 mg per min). The 14C-oxalate/inulin clearance ratio was 2.44 implying an additional excretion mechanism apart from glomerular filtration. Inasmuch as 97.2 per cent of the administered tracer were recovered unchanged in urine, nonrenal loss of oxalate is not an appreciable factor. The data of one hyperoxaluric patient are compared with those of the healthy subjects.

Amino Acid Metabolism, Inborn Errors↗
PubMed1978

Renal handling of oxalate. A micropuncture study in the rat.

Clearance and micropuncture experiments were performed in rats to study the renal handling of oxalate. The 14C-oxalate to 3H-inulin clearance ratio (Cox/Cin) was 1.36 +/- 0.04 and was lowered by probenecid (200 mg/kg) to 1.11 +/- 0.03 (+/- S.E., n = 6, P less than 0.005). An attempt was made to localize the assumed secretion of oxalate in three different micropuncture protocols. In free flow micropuncture experiments single nephron clearance of oxalate was not different when obtained from proximal or distal tubular puncture sites. The fractional delivery of oxalate averaged 0.84 +/- 0.03 regardless of the puncture site from mid-proximal to late distal. This finding indicates a net outflux of oxalate in an early proximal loop since oxalate is freely ultrafilterable. In microperfusion experiments the mean recovery of oxalate ranged from 79--90%. The outflux of oxalate correlated linearly with the tubular load (r = 0.95). The results suggest that no net secretion occurs in superficial nephron segments accessible for micropuncture. Since whole kidney clearances of oxalate always exceeded glomerular filtration rate, it is concluded that net addition of oxalate into the tubular fluid can occur at sites beyond the superficial late distal tubules or is due to higher delivery of oxalate by deep cortical nephrons.

Animals↗