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Biomedical subjects

D Loew

Publications and source records attributed to D Loew.

At least 91 records · Page 5Linked to original sources
PubMed1977

Inhibition of furosemide-induced natriuresis by acetylsalicylic acid in dogs.

The effect of intravenously administered acetylsalicylic acid (ASA) has been investigated in two sets of experiments in conscious dogs. In the first part of the study ASA 70-90 mg/kg was infused for 40 min. Urine flow, free water clearance, renal blood flow and urinary excretion of sodium did not change significantly as compared to placebo treated animals. This is in contrast to the effects of comparable ASA doses in the pentobarbital anaesthetized dog. In the second part of the study the effects of pre-treatment with the same ASA doses of 5 ml 0.6% NaCl (placebo) on some renal effects of furosemide 1 mg/kg (intravenously) were investigated. In the placebo group acute furosemide treatment increased CIN in five out of six dogs and CPAH in all six dogs, these increases being most prominent the first 10 min after drug administration. After pre-treatment with ASA the initial increases in CIN and CPAH were almost abolished. CIN was reduced by 23.8% and CPAH by 30.6% during the first six clearance periods (0-6- min) after diuretic treatment in the ASA group as compared to the placebo group. Although urinary sodium excretion also increased in ASA pre-treated dogs, the effect of furosemide was greater in all dogs in the placebo group (P less than 0.05), and the effect of furosemide on fractional tubular reabsorption of sodium was significantly attenuated after pre-treatment with ASA.

Animals↗
PubMed1976

Dose-dependent influence of acetylsalicyclic acid on platelet functions and plasmatic coagulation factors.

Lysine salt of acetylsalicylic acid (ASA) was given to ten patients by intravenous infusion. Blood samples taken at intervals during the infusion permitted the examination of the influence of the dose of ASA on platelet functions. Aggregation was significantly reduced when 50 mg ASA had entered circulation, while a diminution of PF3 and PF4 availability could only be demonstrated when the dose had reached 500 and 200 mg, respectively. In order to exclude a longer latency time for the diminution of PF3 and pf4 availability, a second series of ten patients received intravenous injections of 100 and 300 mg ASA, respectively. From these patients, blood was taken 1 h after the injection. The decrease of PF3 and PF4 availability in these cases was comparable to the results of the first group. In a third series of patients, a daily intravenous dose of 2,000 mg ASA was given. In these cases, a moderate decrease of factors II, VII, IX and X was observed. Since the appearance of a PIVKA effect could also be demonstrated, vitamin K antagonism was assumed when a high dose of AS

Adult↗
PubMed1975

[Use of sodium chloride in the German Federal Republic (author's transl)].

In order to obtain data on the amount of sodium chloride used in the German Federal Republic, 106 persons of different social groups, with healthy kidneys, were investigated, measuring the sodium chloride contents in their 24-hour urine. The sodium chloride intake follows from the sodium chloride secretion because the regulation of the sodium household is effected through the renal excretion, and with healthy people the daily intake of sodium chloride down to a limit value of 200 mVal per day is eliminated without delay. The values measured are between 4.7 and 32.7 g, the mean figure corresponded to 13.1 g.

Adult↗
PubMed1975

Influence of intravenously administered acetylsalicylic acid on platelet functions. A pharmacodynamic and pharmacokinetic study.

The influence of intravenously administered acetylsalicylic acid (ASA) on the kinetics of platelet function was examined in 10 patients. Simultaneously, assays of salicylate in plasma were performed. A significant inhibition of platelet aggregation as well as PF 3 and PF 4 availabilities could be demonstrated 2 min after injection. A decrease of platelet adhesion was significant after 15 min. The inhibition of platelet functions was still present after 24 h and was partially demonstrable after 72 h. The concentration of salicylate in plasma 2 min after injection of ASA was only about two thirds of the level calculated from mere distribution in circulation. After 1 h, half of the initial salicylate had disappeared from plasma. No salicylate could be found after 24 hours. ASA also depressed platelet functions when added to platelet-rich plasma in vitro in a concentration of 100 mug/ml. Inhibition of platelet aggregation and of PF 4 availability were dependent on the time of incubation. Their onset was much slower in vitro than in vivo. No inhibition of the PF 3 availability could be found in vitro. The inhibition of platelet functions by ASA is demonstrable almost immediately after injection while the duration of this inhibition is considerably longer than the elimination time of salicylate from plasma. This allows the conclusion that a direct intravascular reaction between ASA and platelets occurs and that the inhibition of platelet functions is irreversible.

Aspirin↗
PubMed1975

[Quantitative determination of the main metabolites of acetylsalicylic acid/2nd communication: the concentrations of salicylic acid and its metabolites in patients with renal insufficiency (author's transl)].

Quantitative Determination of the Main Metabolites of Acetylsalicylic Acid / 2nd Communication: The concentrations of salicylic acid and its metabolies in patients with renal insufficiency 9 patients suffering from renal insufficiencies of varing degrees and treated regularly by hemodialysis were given 1.5 g Colfarit (microcapsulated acetyl salicylic acid) as a single dose. The concentrations of salicylic acid (SA), salicyluric acid (SU), further salicylic acid conjugates (SAC) and salicyluric acid conjugates (SUC) were determined in the blood plasma. Likewise urea and creatinine were determined. SA concentration decreased continually and, at the end of the trial (72 h after application), had vanished almost completely from the plasma of most patients. SU increased at first and decreased afterwards. With the exception of the dailysis time SAC and SUC increased during the trial. After 3 days the SUC level was more than 50% of total salicylate (SSS) in most patients. SSS (the sum of SA + SU + SAC + SUC) did not change very much before dialysis, but showed a rather high decrease during the first hours of dialysis. tafter dialysis the SSS levels rose again, apparently as a consequence of a redistribution and of the synthesis of conjugates with decreased tissue affinity. It could be shown that SSS in the blood plasma does not parallel SSS in the whole body. The interindividual variation of SA metabolism as well as the variation of the biological blank values was rather high. The results are discussed with regard to salicylate pharmacokinetics in renal insufficiency and to normal salicylate metabolism.

Adult↗