Biomedical subjects

J S Biermann

Publications and source records attributed to J S Biermann.

21 records · Page 2Linked to original sources

PubMed1989

Metabolism of halothane in obese Fischer 344 rats.

Halothane is metabolized by an oxidative pathway to stable, nonvolatile end products, trifluoroacetic acid (TFAA) and bromide (Br-), and by reductive pathways to Br-and inorganic fluoride (F-). There is evidence that both oxidatively and reductively formed intermediates may produce hepatotoxicity, although the exact etiology of the fulminant hepatic necrosis seen in humans is unproven. Obese patients receiving volatile anesthetics exhibit higher serum anesthetic metabolite concentrations than do normal-weight patients, and thus might be at greater risk of hepatotoxicity because of higher concentrations of reactive intermediates from halothane metabolism. To eliminate the variables inherent in human clinical studies leading to confounding interpretation of data, this study determined the contributions of oxidative and reductive pathways to halothane metabolism in an animal model of human hypertrophic obesity, the most common form of human obesity. Eight pairs of obese (high-fat diet) and normal-weight (standard chow), male Fischer 344 rats were anesthetized with halothane for 4 h at an inspired concentration of 0.78%. Serum and urinary concentrations of TFAA, Br-, and F-were measured. Thirty-six hours following halothane anesthesia, mean serum TFAA concentrations peaked at 7.3 +/- 1.1 mM in obese rats and 4.7 +/- 0.7 mM in nonobese rats. TFAA urinary excretions during the 180-h period postanesthesia were 519 +/- 69 and 336 +/- 22 mumol, respectively. Peak serum Br- concentrations were 9.1 +/- 1.0 and 6.9 +/- 0.6 mM for obese and nonobese rats, respectively, and Br-urinary excretions were 127 +/- 30 and 79 +/- 14 mumol, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1986

Effect of diazepam treatment on hepatic microsomal anesthetic defluorinase activity.

Different dosing regimens with diazepam were evaluated in male Fischer 344 rats for their ability to enhance the metabolism of several inhalation anesthetics. In vitro metabolism was assessed by the rate of microsomal anesthetic defluorination as measured by the appearance of inorganic fluoride ion (i.e., defluorinase activity). Single daily doses of diazepam, 40 mg/kg, were delivered by gavage for either 7 or 14 days; more continuous dosing was achieved by administration of diazepam at 0.03% or 0.10% in food pellets. Hepatic microsomes isolated from treated rats showed significant dose-related elevations in methoxyflurane defluorinase activity, but not in enflurane or isoflurane defluorinase activities. The microsomal content of cytochromes P-450 and b5 and the NADPH-cytochrome-c-reductase activity was not significantly different among treated and untreated groups. Para-nitroanisole O-demethylase activity expressed per nmole cytochrome P-450 increased in the diazepam-treated groups. Extrapolation of these animal data to humans suggests that surgical patients treated chronically with diazepam are probably not at increased risk for inorganic fluoride-induced nephrotoxicity due to increased metabolism of the fluorinated inhalation anesthetics.

Anesthetics↗

PubMed1984

Comparison of the primary structures of clathrin light chains from bovine brain and adrenal gland by peptide mapping.

The structures of the polymorphic forms of clathrin light chains were analyzed by two peptide mapping procedures. Comparison of the products of partial digestion by V8 protease showed no common peptides between LCA and LCB from bovine brain. No similarities between clathrin light chains and tropomyosin chains from bovine brain and skeletal muscle were detected with this technique. The peptides produced by complete tryptic digestion of LCA and LCB from bovine brain and bovine adrenal gland were analyzed by reverse phase h.p.l.c. For both LCA and LCB the polypeptides from different tissues showed considerable homology. LCA from brain and adrenal gland shared 10 out of a total of 15 peptides. LCB from brain and adrenal gland shared 10 out of 14 peptides. In contrast, when LCA was compared with the LCB chain from the same tissue very few peptides were shared; 4/23 for brain and 3/21 for adrenal gland. These results strongly indicate that, within a tissue, LCB is not related to LCA by post-translational processing and that each chain is encoded by a separate gene. The data also demonstrate the close homology of the different forms of LCA and LCB expressed in different tissues within the same organism. Thus the polymorphic differences of clathrin light chains within a tissue are greater than those between tissues.

Adrenal Glands↗