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Biomedical subjects

D L Azarnoff

Publications and source records attributed to D L Azarnoff.

At least 73 records · Page 4Linked to original sources
PubMed1975

Placental transfer and fetal urinary excretion of gentamicin during constant rate maternal infusion.

Placental transfer and fetal urinary excretion of gentamicin was studied in midtrimester goat and human previable fetuses during constant rate maternal infusion with the drug. Gentamicin was not detected in the serum of any of the goat fetuses, even when maternal serum concentrations ranged from 15.2 mug/ml to 20.9 mug/ml. However, gentamicin was present in the amniotic fluid of four animals. Gentamicin was also present in fetal urine collected from three animals. In contrast human fetal central venous serum concentrations of gentamicin were 21-37% of those in maternal serum after constant rate infusion of the mother. In addition, gentamicin was present in human fetal urine in concentrations 2-- 3 times those in fetal serum. The observed difference in fetal serum concentration of gentamicin between the two species represents a difference in placental permeability to gentamicin and/ or a difference in fetal renal clearance of the drug.

Amniotic Fluid↗
PubMed1975

1-methyl-4piperidyl-bis (P-chlorophenoxy) acetate: a new hypolipidemic peroxisome proliferator.

Administration of 1-methyl-4-piperidyl-bis(p-chlorophenoxy) acetate (SaH 42-348) at a dietary concentration of 0.15% for 3 weeks, increased the activity of catalase in both liver and kidney of male wild type (Cs-a strain) mice. A marked increase in the activity of short chain carnitine acyltransferase in the liver was also noted. By electron microscopy, a remarkable increase in the number of peroxisomes (microbodies) was noted in the liver cells. A mild to moderate increase in number of peroxisomes in proximal convoluted tubular epithelium of the kidney was also seen. These studies demonstrate that SaH 42-348 is a potent hepatic peroxisome proliferator.

Animals↗
PubMed1975

Separation and quantitative analysis of furosemide and 4-chloro-5-sulfamoylanthranilic adid (CSA) by high pressure liquid chromatography.

After extraction by ether from acidified plasma or urine and concentration into basic phosphate buffer, furosemide and 4-chloro-5-sulfamoylanthranilic acid (CSA) were separated on a high pressure liquid ion-exchange system and measured fluorometrically. Sensitivity is 0.2 mug/ml of ether compound in plasma and 0.1 mug/ml in urine with an 8% coefficient of variation. Interference by porphyrins in urine was eliminated by subtracting a second fluorometric measurement at a different wave-length from that used for furosemide. No quenching at this wave-length is seen with concentrations of furosemide up to 50 mug/ml. Standard curves of furosemide and CSA are linear from 0.2 mug/ml to 50 mug/ml.

Chromatography↗
PubMed1975

Plasma levels and excretion of estrogens in urine in chronic lever disease.

Plasma levels of nonconjugated estrone (E1), estradiol-17beta (E2), and estriol (E3) and excretion of these estrogens in urine in conjugated and nonconjugated forms were measured by radioimmunoassay in 17 healthy males and 33 males with alcoholic liver disease. Patients with liver disease had significantly elevated plasma levels of E1 (74.2 +/- 8.0 SE versus 26.0 +/- 1.7 pg per ml, P less than 0.001), E2 (29.3 +/- 2.2 versus 23.3 +/- 2.0 pg per ml, P = less than 0.05), and E3 (11.5 + 1.9 versus 6.5 +/- 0.7 pg per ml, P less than 0.01). Excretion of total E1, E2, and E3 in urine was significantly increased in patients with liver disease; the increase was primarily in the nonconjugated fraction. Among those patients with chronic liver disease, the presence of ascites was associated with significantly higher plasma levels of E1 and excretion of larger amounts of E1 and E2 in urine. On the other hand, no differences were observed in the small number of patients with gynecomastia. A direct correlation between the plasma level or excretion of E1 or E2 and several liver function abnormalities was observed. The relative hyperestrogenemia we report here may account for some of the clinical observations in chronic liver disease.

Adult↗
PubMed1975

Diphenylhydantoin potency and plasma protein binding.

Rats were given diphenylhydantoin (DPH) orally, and its potency in protecting against maximal electroshock seizures was determined. The effect of an intravenous dose of 100 mg of phenylbutazone per kg 1 hour before testing on the potency and on the total and unbound plasma concentration of DPH was then measured. Phenylbutazone treatment increased the potency of DPH in terms of dose and total drug concentration but did not affect the potency of unbound DPH. The anticonvulsant action of DPH depends upon the concentration of unbound drug in plasma and not upon total plasma concentration nor upon dose.

Administration, Oral↗
PubMed1975

Effect of portacaval shunt on the disposition of drugs with and without first-pass effect.

The pharmacokinetic parameters of lidocaine, antipyrine and salicylamide were studied in dogs before and after construction of a portacaval shunt. The systemic availability of antipyrine was not altered significantly by the surgical procedure whereas the availability of lidocaine and salicylamide, drugs with a marked first-pass effect, was increased from 14.8 +/- 2.8 to 81.3 +/- 5.2% and from 21.8 +/- 7.8 to 57.5 +/- 2.5%, respectively. Of the 78% first-pass extraction of salicylamide, 36% is due to hepatic extraction whereas the remaining 42% is accounted for by intestinal wall extraction. The presence of a portacaval shunt also reduced the plasma clearance of lidocaine and antipyrine, but not salicylamide. The apparent volume of distribution was decreased only with salicylamide. Surgical construction of a portacaval shunt in dogs in a good model to evaluate first-pass effect. Physicians should adjust downward the dose of drugs with a first-pass effect. Physicians should adjust downward the dose of drugs with a first-pass effect in patients with a surgical portacaval shunt or endogenous portal systemic shunts such as seen in cirrhosis of the liver.

Animals↗
PubMed1974

Nafenopin-induced hepatic microbody (peroxisome) proliferation and catalase synthesis in rats and mice. Absence of sex difference in response.

Nafenopin (2-methyl-2[p-(1,2,3,4-tetrahydro-1-naphthyl)phenoxy]-propionic acid; Su-13437), a potent hypolipidemic compound, was administered in varying concentrations in ground Purina Chow to male and female rats, wild type (Cs(a) strain) mice and acatalasemic (Cs(b) strain) mice to determine the hepatic microbody proliferative and catalase-inducing effects. In all groups of animals, administration of nafenopin at dietary levels of 0.125% and 0.25% produced a significant and sustained increase in the number of peroxisomes. The hepatic microbody proliferation in both male and female rats and wild type Cs(a) strain mice treated with nafenopin was of the same magnitude and was associated with a two-fold increase in catalase activity and in the concentration of catalase protein. The increase in microbody population in acatalasemic mice, although not accompanied by increase in catalase activity, was associated with a twofold increase in the amount of catalase protein. The absence of sex difference in microbody proliferative response in nafenopin-treated rats and wild type mice is of particular significance, since ethyl-alpha-p-chlorophenoxyisobutyrate (CPIB)-induced microbody proliferation and increase in catalase activity occurred only in males. Nafenopin can, therefore, be used as an inducer of microbody proliferation and of catalase synthesis in both sexes of rats and mice. The serum glycerol-glycerides were markedly lowered in all the animals given nafenopin, which paralleled the increase in liver catalase. All the above effects of nafenopin were fully reversed when the drug was withdrawn from the diet of male rats. During reversal, several microbody nucleoids were seen free in the hyaloplasm or in the dilated endoplasmic reticulum channels resulting from a rapid reduction in microbody matrix proteins after the withdrawal of nafenopin from the diet. Because of microbody proliferation and catalase induction with increasing number of hypolipidemic compounds, additional studies are necessary to determine the interrelationships of microbody proliferation, catalase induction, and hypolipidemia.

Animals↗