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Biomedical subjects

H Fujimura

Publications and source records attributed to H Fujimura.

At least 163 records · Page 9Linked to original sources
PubMed1985

Effects of butorphanol and its metabolites on the levels of monoamines and their metabolites in the rat brain.

The effects of butorphanol and its main metabolites, norbutorphanol and hydroxybutorphanol, on the contents of monoamines and their metabolites in various regions of the rat brain were compared with those of morphine and pentazocine using the HPLC-ECD method. The administrations of morphine and pentazocine increased dopamine turnover in the striatum and hypothalamus in a drug dose-dependent manner. The stimulative effects of butorphanol on the dopamine system were weaker than those of morphine and pentazocine, and there were no dose-dependencies in these effects of butorphanol. Butorphanol, morphine and pentazocine increased 5-HT turnover, but there was no drug dose-dependent effect in the case of butorphanol. These differences for the effects of butorphanol from those of morphine and pentazocine seemed to result from the antagonist-agonist property of butorphanol and from a different manner of interaction with the opioid receptor. The effects of butorphanol on the levels of the norepinephrine system were weak. It was considered that the effects of butorphanol on monoamine turnover were produced by the action of butorphanol itself, because norbutorphanol and hydroxybutorphanol showed little change on the level of monoamines and their metabolites.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1985

Cephem antibiotics and alcohol metabolism.

Mechanisms of the disulfiram-like reaction of cephem antibiotics were studied. Changes in ethanol (EtOH) and acetaldehyde (AcH) levels in the blood with EtOH loading following daily intravenous administration of cephem antibiotics were determined in rats and the following were found: The daily intravenous injection of cefazolin, cefotiam (CTM), cefsulodin, cefoxitin or ceftizoxime in no way varied the changes in the EtOH and AcH levels in the blood with EtOH loading. The daily intravenous injection of cefmetazole, cefoperazone, cefamandole, latamoxef, cefmenoxime or cefotetan caused the AcH level in the blood to be elevated significantly until at least 8 hours after the EtOH loading, but was inert on the EtOH level on the blood. The daily administration of 1-methyl-2-tetrazoline-5-thione (TZ), a compound having a partial structure similar to those of the cephem antibiotics elevating the AcH level in the blood on EtOH loading, was inert on the EtOH level in the blood but elevated the AcH level in the blood. The daily administration of 1-(2-dimethylaminoethyl)-2-tetrazoline-5-thione (MTZ), a compound having a partial structure similar to that of CTM, was inert either on the EtOH or AcH level in the blood. The cephem antibiotics elevating the AcH level in the blood all had a (1-methyl-1H-tetrazol-5-yl) thiomethyl group in the 3 position of the aminocephalosporanic acid nucleus. It was though that the disulfiram-like reaction caused by the cephem antibiotics was derived from the elevation of AcH level in the blood.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaldehyde↗
PubMed1985

[Antitumor effect of OK-432 (3)--mechanisms of tumor growth inhibition by OK-432 induced activated macrophages].

Spleen cells and peritoneal exudate cells obtained from BALB/c mice which had received an i.p. injection of 0.1 mg of OK-432 4 days previous to sacrifice, were examined by Winn's neutralization assay for their antitumor activity against Meth-A sarcoma cells in BALB/c mice. Both of the cell preparations clearly inhibited the growth of admixed Meth-A cells, but when these same cell populations were treated on a Sephadex G-10 column, the effector activity seen in Winn's assay disappeared. The effector cells responsible for tumor inhibition were therefore considered to be cytotoxic macrophages. However, the inhibitory effect of these cytotoxic macrophages in Winn's assay was not evident in either X ray (300 rad)-irradiated BALB/c mice or in nu/nu BALB/c mice. These results indicate that the antitumor activity of cytotoxic macrophages is associated with a sequential immune mechanism in which T cells may play an important role.

Animals↗
PubMed1984

The effect of clidanac, a potent anti-inflammatory drug, on mitochondrial respiration: a consideration on the uncoupling activity of optical enantiomers.

The uncoupling activities of clidanac and its dechlorinated derivative on oxidative phosphorylation were examined using isolated rat liver mitochondria. Clidanac was found to uncouple the oxidative phosphorylation and no difference was detected in the uncoupling potency of the two enantiomorphs. Dechlorclidanac was significantly less effective in the uncoupling activity than clidanac.

Animals↗
PubMed1984

[The effects of various drugs on the binding site of bilirubin in serum albumin].

In the presence of various drugs, the concentration of free bilirubin which was released from the first binding site of bilirubin in serum albumin was evaluated, using a sensitive method based on static fluorescence quenching of dansyl serum albumin. Bilirubin bound to human serum albumin more strongly than to bovine serum albumin. Non-steroidal anti-inflammatory drugs, fenamates and allylphenyl propionic acids, affected the bilirubin-serum albumin interaction. Flufenamic acid and ketoprofen released bilirubin from human serum albumin. The bilirubin bound to the serum albumin was not influenced by the presence of indomethacin, but clidanac strongly dissociated bilirubin from the bilirubin-serum albumin complex. Sulfa-drugs, antibiotics, steroidal agents, warfarine, tolubutamide and phenytoin showed no significant effects on the bilirubin-serum albumin interaction. The fluorescence quenching method may be useful to evaluate the interaction of drug-bilirubin-serum albumin.

Animals↗
PubMed1984

[Interaction of suprofen and serum albumin].

The serum albumin-interaction of suprofen (SPF), a novel anti-inflammatory drug, was compared with those of indomethacin (IM) and ketoprofen (KTP). The binding constants of these drugs were determined with difference absorption spectra based on the binding to bovine serum albumin (BSA). The constants for SPF and IM were nearly equal, and the value for KTP was smaller than those of the other drugs. The magnitude of the inhibitory effect on heat denaturation of BSA reflected the difference in these binding constants. In the presence of these drugs, the tryptophan fluorescence in BSA was quenched (IM, SPF and KTP, in this order). The metachromagy based on the binding of an azodye, HABA, to BSA was potentiated by IM or SPF. Phenylbutazone suppressed the absorption of the metachromagy. SPF displaced only the binding of the fluorescent Site II probe, dansylproline, to human serum albumin (HSA), and both the bindings of dansylproline and dansylamide (Site I probe) to HSA were inhibited by KTP or IM. KTP released bilirubin from BSA and HSA, but SPF and IM did not show any effects on the bilirubin-serum albumin binding. These results all support that there is considerable interaction between SPF and serum albumin and that the mode of the interaction differs from those of KTP and phenylbutazone.

Animals↗
PubMed1984

[Active oxygen and anti-inflammatory drug: measurement by luminol dependent chemiluminescence].

The active oxygen produced from stimulated phagocytic cells emits luminol-dependent chemiluminescence (CL) upon reaction with luminol. So the active oxygen was measured by using the CL and the results of this were compared with those by the LDH-NADH method. Moreover, effects of nonsteroidal anti-inflammatory drugs (NSAID) on the generation of active oxygen were studied by both methods. Rat peritoneal and pleural exudated cells (PEEC and PLEC) emitted strong CL on incubation with zymosan, but that from rat whole blood cells was very weak. The effects of superoxide dismutase, catalase, NaN3 and L-ascorbic acid on the generation of active oxygen from rat phagocytic cells were different between CL and LDH-NADH methods. These discrepancies seem to be due to the different kinds of active oxygen that can be measured by both methods. Except for BW-755C, most of the NSAID had only a slight inhibitory effect on the generation of active oxygen measured by both methods, and the ex vivo effect was the same as that observed in vitro. It may be considered that NSAID decrease the phagocytic function of cells by non-specifically stabilizing the biological membrane and inhibit slightly the generation of active oxygen from phagocytes. On the other hand, the CL method could be performed not only in PEEC and PLEC, but also in whole blood cells. From these results, it was suggested that CL measurement can be used as a simple and valuable method for the detection of all types of active oxygen including superoxide anion radical and its metabolites and for testing cellular functions and drug actions on them.

Animals↗