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Biomedical subjects

B Lamberts

Publications and source records attributed to B Lamberts.

At least 19 recordsLinked to original sources
PubMed1990

Induction of drug metabolism enzymes by dihalogenated biphenyls.

The effects of pretreatment with symmetrically dihalogenated biphenyls (DXBs, X-F, Cl(C), Br(B) and I) on rat liver drug metabolism enzymes were investigated. 4,4'-DFB, -DCB, and -DBB as well as 2,2'-DFB appeared to be inducers of microsomal cytochrome P-450-linked monoxygenases (N-demethylases of aminopyrine and ethylmorphine). However, no structure-induction relationship was found. 4,4'-DXBs also induced a cytochrome P-448-linked mono-oxygenase (ethoxyresorufin O-deethylase), and their order of induction potential seemed to parallel the increase of the size of the halogen substituent. Therefore, 4,4'-DXB's may be categorized as mixed-type inducers, the cytochrome P-450 component being the more pronounced. Data on the cytochrome P-448 induction by dihalogenated biphenyls with only para substituents may be considered as a refinement of the previously described structure-activity relationship in this respect. All of the DXBs except 3,3'-DCB and 4,4'-DIB, enhanced, like phenobarbital, the activity of UDP-glucuronyltransferase toward 4-hydroxybiphenyl. Only 4,4'-DFB was able to induce the activity of glutathione S-transferase toward 1,2-epoxy-3-(p-nitrophenoxy)propane. Studies after 4,4'-DBB-treatment revealed, like phenobarbital, a preferential induction of ethylmorphine N-demethylase on rough endoplasmic reticulum-derived microsomes, whereas UDP-glucuronyltransferase activity toward 4-hydroxybiphenyl was induced to a larger extent on smooth endoplasmic reticulum microsomes, suggesting a dissimilar enzyme induction in microsomal subfractions.

Animals↗
PubMed1982

Plasma catecholamine concentration in hypertensive subjects with chronic renal failure before and during treatment with the beta-receptor blocking drug metipranolol.

In seven male hypertensive patients with chronic renal failure (serum creatinine level 6.9 +/- 4.1 mg%) plasma catecholamine levels were in the same range as in five normotensive healthy volunteers. Treatment with the beta-receptor blocker metipranolol (2 x 20 mg/day orally for 2 weeks) significantly elevated plasma catecholamine levels in the hypertensive patients with chronic renal failure, but not in the healthy volunteers. Blood pressure and heart rate were reduced in both groups.

Adrenergic beta-Antagonists↗
PubMed1978

[Drug side-effects in patients treated by their general practitioner (author's transl)].

Drug side-effects were registered in 50 of 2688 patients on the day of admission to hospital. These were severe in 52%, moderate in 18% and mild in 30%. Three deaths were clearly related to drug side-effects. Side-effects of cytostatic treatment were not included. Cardiac glycosides and anticoagulants were the drugs with the highest incidence of side-effects (50%).

Ambulatory Care↗
PubMed1978

Therapy with essential amino acids and their nitrogen-free analogues in severe renal failure.

The effects of therapy with essential amino acids and their nitrogen-free hydroxy and keto precursers on nitrogen and amino acid metabolism of patients with chronic renal failure were examined. Data obtained under treatment with essential amino acids and alpha-keto acid analogues showed higher levels of plasma amino acids, C3-complement, and transferrin than with a low-protein diet alone. Nitrogen balance became positive and plasma urea levels fell. With keto acid analogue therapy, these effects could be obtained with a reduced nitrogen intake. Supplementation of a low protein diet with alpha-hydroxy acid analogues was associated with more positive nitrogen balance and a rise in plasma histidine and methionine. However, plasma levels of three other essential amino acids fell.

Amino Acids↗
PubMed1977

[Pathogenesis of the toxic and allergic nephrotic syndrome. Metabolic studies on kidney-cortex slices and on glomeruli].

The in vitro metabolism of isolated rat glomeruli in Daunomycin-nephrosis (DMS) and neophrotoxic nephritis (ANS) was determined in order to investigate questions about the nephrotic syndrome. Glomeruli of rats with Daunomycin-nephrosis influenced metabolic steps as follows: 1. Oxydative decarboxydation of pyruvate and probably also of alpha-ketoglutarate is decreased. This disturbance might be located in the formation of acetyl-and/or succinyl-CoA. 2. Incubation with pyruvate and alpha-ketoglutarat resulted in reduced oxygen uptake, and resynthesis of ATP. 3. Incorporation of thimidin into glomerular DNS is inhibited in the beginning stage of Daunomycin-nephrosis; while incorporation of amino acids into glomerular protein is not, beta-oxydation of fatty acids is at least until entrance into the TCA cycle undisturbed. In contrast, glomeruli of rats with nephrotoxic nephritis utilised more oxygen and the stationary concentration of ATP within the glomeruli was elevated. The pathway of the nephrotic syndrome is not exactly known. Metabolic and morphologic studies with glomeruli of the immunologically and the toxically induced nephrotic syndrome showed different biochemical and histological disorders for the same clinical symptoms. As the beginning of nephrotic syndrome very different lesions in the glomerulus have to be expected, which result in a greater permeability of basal membranes.

Animals↗
PubMed1976

Effect of urine metabolites from healthy and uremic subjects on gluconeogenesis in slices of rat kidney cortex and liver.

A high molecular weight fraction was obtained by extended dialysis of urine of healthy and uremic subjects. After addition to the incubation medium, this fraction inhibited gluconeogenesis by rat kidney cortex slices. From the six subfractions extracted by gel chromatography (Sephadex G 100) fraction IV caused a decrease of glucose formation. The activity of PEP-carboxykinase but not of pyruvate carboxylase was reduced, indicating a decreased formation of phosphoenol pyruvate. The total high molecular weight fraction stimulated glucose release by liver slices from fed but not from starved rats. In the absence of amino acids, urea formation was not stimulated. The activity of pyruvate carboxylase was reduced in both groups, PEP-carboxykinase activity was, however, only reduced in the starved group. The addition of uremic serum caused increased glucose release. Inhibition of PEP-carboxykinase activity by quinolinic acid (15 mM) resulted in inhibition of glucose formation by 35% in the uremic group and 54% in the control group in livers of 24 hr starved rats. Thus in uremia there may be incorporation of serine carbon skeletons into glucose via hydroxypyruvate, not via pyruvate. Chromatography on calibrated columns indicated that about 40% of the urinary fractions had molecular weights in the upper range of the "middle molecules" category. The positive correlation between toxicity and the total amount of high molecular weight substances excreted do not confirm the hypothesis of augmented retention of "toxins" in uremic patients. It must be appreciated that these results refer only to the undialyzable fraction of urine which contains only 0.5% by weight of the total urine solids.

Animals↗
PubMed1975

[Stimulation of renin secretion in vitro by a factor in serum of rats (author's transl)].

The stimulating effect of rat serum on renin release from kidney slices of this species was demonstrated. This "renin-releasing-factor" is not dialysable. It can be activated at 56 degree C. The factor is found in the gamma-Globulin and the albumin fraction of serum. Its role is discussed in a possible system of humoral regulation of RAS in the manner of a feed back mechanism including a releasing system.

Animals↗
PubMed1975

Podocytes of rat kidneys with nephrotoxic serum nephritis. A combined transmission and scanning electron microscopic study.

Rats with a nephrotoxic serum nephritis reveal changes of proteinuria and content of serum proteins as well as serum cholesterol in the direction of a nephrotic syndrome as is seen after Daunomycin. Nevertheless, the morphological findings with TEM and especially with SEM are quite different. A striking feature of the nephritis is the rather good preservation of cell processes through all the time of experiment in spite of the elevated proteinuria. Moreover, podocytes with furrowed or ribbed surfaces originate and are most numerous when the signs of inflammation are most pronounced. These furrowed podocytes are interpreted as representing a special reactive, perhaps mobilized form. With SEM it is evident that the glomeruli are altered focally and segmentally in the nephrotoxic serum nephritis.

Animals↗