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B Mühlbauer

Publications and source records attributed to B Mühlbauer.

44 records · Page 3Linked to original sources

Monoamine oxidase inhibition by the MAO-A inhibitors brofaromine and clorgyline in healthy volunteers.

The present study compared the extent and duration of MAO inhibition by the selective and reversible MAO-A inhibitor brofaromine with the selective and irreversible MAO-A inhibitor clorgyline using amine pressor tests and excretion of urinary amine metabolites (MHPG, tryptamine). The pharmacological characterization of clorgyline as an irreversible and brofaromine as a reversible MAO-A inhibitor in clinically effective doses was confirmed in humans.

Administration, Oral↗

Feeding-induced increase in urinary dopamine excretion is independent of renal innervation and sodium intake.

Food intake increases urinary dopamine excretion. To investigate the role of renal nerve activity in this renal response to feeding, we studied urinary dopamine excretion after chronic bilateral renal denervation (DNX, n = 8) in male Sprague-Dawley rats. Controls were sham operated (CON, n = 6). In a paired crossover design, animals were studied both in fed and fasted state. Time course measurements of renal tissue norepinephrine (NE) content in a third group of DNX rats showed a decrease by 90% not earlier than 18 h post-DNX, remaining to be reduced to this level until day 11. Renal NE content in DNX animals was measured at the end of the study to confirm complete denervation. In 24-h urine, collected from fed and fasted conscious CON and DNX rats in metabolic cages, concentrations of dopamine and sodium were measured during two different sodium intake regimens, i.e., tap water and 1 g/dl NaCl as drinking water. No influence of renal innervation on urinary dopamine could be observed in fed and fasted animals. The marked changes in urinary volume and sodium output due to the different sodium regimens were not paralleled by urinary dopamine excretion. However, urinary dopamine was increased 2.1- to 2.4-fold (P < 0.01) because of feeding in all groups, independent of sodium balance and renal innervation. We conclude that in conscious rats both basal urinary dopamine excretion and its marked increase in response to feeding are independent of sodium balance and of renal nerve activity.

Animals↗

Feeding but not salt loading is the dominant factor controlling urinary dopamine excretion in conscious rats.

We studied urinary dopamine excretion in three different groups of rats after the following treatment regimens: normal chow and tap water (controls, CON), normal chow and 1% NaCl as drinking water (high salt, HS), and chow with low sodium content plus tap water (low salt, LS). On days 5 and 7 of the respective dietary treatment, rats were placed in metabolic cages. Using a cross over design, chow was given (fed) or withheld (fasted). Urine was collected for 24 h and analyzed for sodium, creatinine, and dopamine. Urinary dopamine excretion did not change in proportion to large differences in sodium excretion in fasted animals. Sodium excretion was enhanced (45%) due to feeding only in the CON group but not in HS and LS rats. However, there was a striking increase in renal dopamine excretion in fed compared to fasted animals, irrespective of their sodium diet: 2.5-fold in CON, 2-fold in HS, and 1.8-fold in LS rats. Urinary creatinine excretion was significantly elevated during the feeding condition compared to fasted animals in all treatment groups. Our results demonstrate that urinary dopamine excretion is dominantly influenced by feeding but not by oral sodium intake in conscious rats. We conclude that 1) the dietary state of the animals should be controlled in experiments on renal dopamine production, 2) renally formed dopamine could be involved in the functional response of the kidney to oral food intake.

Animals↗

Effect of the selective MAO-A inhibitors brofaromine, clorgyline and moclobemide on human platelet MAO-B activity.

MAO-B activity was compared in healthy volunteers following oral treatment with clinically effective doses of the selective MAO-A inhibitors brofaromine (100 mg q.d. for 14 days), moclobemide (150 mg t.i.d. for 14 days) and clorgyline (5 mg t.i.d. for 10 days). Brofaromine and clorgyline did not alter platelet MAO activity. Following moclobemide treatment, MAO-B activity was reduced by 32% (p less than 0.05). It recovered during the 5 subsequent days after discontinuation of treatment. These results confirm earlier findings. The explanation for this finding may be that metabolites of moclobemide are active inhibitors of MAO-B.

Adult↗

Adenosine mediates tubuloglomerular feedback response: an element of metabolic control of kidney function.

Numerous studies have shown during the past 10 years that adenosine is present in the normoxic kidney and accumulates when ATP hydrolysis prevails over ATP synthesis. Local generation of adenosine by the macula densa cells and its release into the interstitium of the juxtaglomerular apparatus (JGA) is considered to be the link between the enhanced NaCl concentration in the tubular fluid and the subsequent responses including preglomerular vasoconstriction and reduction of renin release by the juxtaglomerular cells. Micropuncture and microperfusion experiments using specific adenosine agonists and antagonists support the concept that adenosine functions as a mediator in the signal transmission of the JGA.

Adenosine↗

[Systemic salmonella infections in chemotherapy in 2 children with acute lymphoblastic leukemia].

A 15 year old patient with acute lymphoblastic leukemia, previously diagnosed as being a salmonella carrier, developed S. typhimurium sepsis after allogeneic bone marrow transplantation, in spite of pretreatment with chloramphenicol. Clinical improvement and termination of salmonella excretion were achieved by treatment with multiple antibiotics. Another patient with acute lymphoblastic leukemia, a 3 year old boy not previously identified as a salmonella carrier, also developed sepsis and osteomyelitis, together with pathological fractures during chemotherapy. Chloramphenicol, administered after isolation of S. typhimurium from blood cultures, led to resolution of the bony defects, complete recovery, and cessation of salmonella excretion. Selective cultures for salmonellae seem indicated in patients with malignant diseases, prior to chemotherapy.

Adolescent↗

Urinary dopamine excretion in conscious rats: effect of carbidopa in different states of sodium balance.

Urinary dopamine excretion was studied in seven different groups of rats (n = 6-12) with the following treatment regimens: normal chow and tap water (controls, CON), single administration of furosemide 20 mg/kg i.p. on day 1 and subsequent feeding of low sodium chow (low salt, LS), normal chow and 1% NaCl as drinking water (high salt, HS), normal chow and 1% NaCl plus deoxycorticosterone acetate 1 mg/kg/day i.p. (high salt plus DOCA, HS+DOCA); carbidopa 20 mg/kg/day p.o. (CDP) was administered in animals on normal chow (CON+CDP), in high salt rats (HS+CDP), and in rats on high salt plus DOCA (HS+DOCA+CDP). On day 5, rats were placed in metabolic cages with free access to their respective drinking solution; chow was withheld. Urine was collected for 24 h and analyzed for sodium, creatinine, and dopamine. Urinary dopamine excretion rates did not change in proportion to large differences in sodium excretion in LS, HS, and HS+DOCA animals compared to CON. Only when urinary dopamine excretion of HS rats was compared to the LS group there was a moderate, but significant increase of 27%. In the groups treated with CDP renal dopamine excretion was decreased by approximately 60% in comparison to the groups with the respective treatment condition but without CDP. Urinary sodium output was unchanged by CDP in CON+CDP animals compared to CON. In HS+CDP and HS+DOCA+CDP groups renal sodium excretion was reduced by half compared to the HS and HS+DOCA groups, respectively. However, this effect was accompanied by a similar, approximately 55% reduction of oral volume and sodium intake.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗