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Biomedical subjects

B M Bayer

Publications and source records attributed to B M Bayer.

41 records · Page 3Linked to original sources
PubMed1980

Influence of indomethacin and other anti-inflammatory drugs on mobilization and production of neutrophils: studies with carrageenan-induced inflammation in rats.

The intrapleural injection of carrageenan in the rat, after a delay of 90 min, resulted in the accumulation of 100 to 300 million neutrophils in the pleural cavity, a 6-fold increase in the numbers of circulating neutrophils and the mobilization of large numbers of neutrophils from bone marrow. Thymidine labeling of bone marrow cells showed that neutrophils underwent a period of maturation (2--3 days) before release into the circulation and accumulation in the pleural cavity. Nonsteroidal anti-inflammatory drugs reduced, in a dose-dependent manner, the accumulation of white cells and fluid. Indomethacin, the most potent of the drugs tested, was equally effective whether given 30 min before or 90 min after carrageenan. This drug had no significant effect on the production or number of white cells in bone marrow, spleen or thymus. In contrast, methotrexate suppressed the inflammatory reaction only after prolonged treatment had produced almost complete depletion of cells in bone marrow and dexamethasone could be given in doses that largely depleted thymus and spleen of their white cells but which had little effect on neutrophil accumulation. It is concluded that neutrophils were mobilized from stores of mature cells in bone marrow and that indomethacin suppressed mobilization of these cells without impairing normal white cell homeostasis.

Animals↗
PubMed1979

Arrest of cultured cells in the G1 phase of the cell cycle by indomethacin.

Indomethacin reversibly inhibited growth of rat hepatoma cells (HTC) and human diploid fibroblasts in the G1 phase of the cell cycle. Cytophotometric measurements showed that greater than 90% of cells incubated for 48 hr with indomethacin had a DNA content that corresponded to the G1 state. Synchronous growth of both the HTC and fibroblast cultures occurred after removal of drug as indicated by the sequence of changes in [3H]thymidine incorporation into DNA, cellular DNA content, mitotic index and cell number. Autoradiographs of HTC cell cultures incubated with [3H]thymidine indicated that all (98%) of the cells engaged in DNA synthesis following the removal of indomethacin. Since viability of the cells was not impaired, even by prolonged exposure to indomethacin, this drug provides a means of synchronizing growth. Suppression of cell proliferation could contribute to the therapeutic and/or toxic effects of indomethacin in vivo.

Animals↗
PubMed1979

The pharmacodynamics of 4-(p-chlorophenylthio)butanol (W-2719) in humans.

4-(p-Chlorophenylthio)butanol (W-2719) is absorbed, metabolized and excreted when administered orally to human volunteers. The butyrate (W-2718) and the acetate (W-2683) metabolites were found in plasma with W-2683 being the major biotransformation product and detectable seven days after administration with an apparent half-life of 33.2 h. p-Chlorothiophenol appeared to be the major biotransformation product in urine and was detectable through day 6. As in plasma, the other major biotransformation product was W-2683, which was again detectable through day 7 and had a t 1/2 in urine of 40.8 h. The minor metabolite found in urine was W-2718. No W-2719 was found in either plasma or urine after oral administration.

Adult↗
PubMedDate not supplied

Distinction between the in vitro and in vivo inhibitory effects of morphine on lymphocyte proliferation based on agonist sensitivity and naltrexone reversibility.

We have previously reported that administration of a single dose of morphine (25 mg/kg) to rats results in a naltrexone-sensitive suppression of mitogen-stimulated lymphocyte proliferation. To further delineate the site of action of this inhibitory effect, the in vitro and in vivo effects of morphine on mitogen-stimulated lymphocyte proliferation were examined. In vitro, concentrations of morphine exceeding 0.1 mM exhibited a dose-dependent inhibition of Concanavalin A-induced proliferation of both whole blood and splenic lymphocytes. This inhibitory effect of morphine on lymphocyte proliferation was not attenuated by co-incubation with the opioid antagonist naltrexone (0.25 mM). These data indicate that the in vitro inhibitory effects of morphine occur at only high concentrations and are not opioid receptor mediated. In vivo, a dose-dependent inhibition of blood lymphocyte proliferation was also observed 2 h following the subcutaneous injection of morphine. In contrast to these effects, proliferation of splenic lymphocyte cultures was not significantly inhibited by morphine at doses of up to 40 mg/kg. However, following morphine administration, a greater than 90% inhibition of proliferation was obtained in cultures containing either whole blood or Ficoll-separated lymphocytes, indicating that plasma was not a contributory factor in the differential sensitivity of blood and splenic lymphocyte responses to morphine. Moreover, in these experiments, significant inhibition of lymphocyte proliferation occurred at plasma concentrations that were two orders of magnitude less than those required to produce inhibition in vitro. The in vivo inhibition of lymphocyte proliferation by morphine (10 mg/kg) was completely antagonized by pretreatment with naltrexone (5 mg/kg).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗