Biomedical subjects
Publications and source records attributed to M Terasawa.
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The production of spleen- and thymus-rosette forming cells (RFC) in BALB/c mice 4 days after immunization with 5 X 10(8) sheep red blood cells (SRBC) was inhibited by traxanox at doses of 10-30 mg/kg, p.o. This agent (100 mg/kg, p.o.) suppressed the 19S hemagglutinin titer and elevated the 7S hemagglutinin titer. The transfer of spleen-RFC of thymus-RFC into syngeneic recipient mice 4 days after immunization with SRBC increased the production of spleen hemolytic plaque forming cells (HPFC). This increase was abolished by the transfer of spleen-RFC obtained from mice treated with traxanox (30 mg/kg, p.o.), but not by the transfer of spleen-RFC treated with anti-Lyt 2.2 antiserum and complement. The viability of the spleen-RFC in mice treated with traxanox was decreased by treatment with anti-Lyt 2.2 antiserum and complement. Traxanox (3-30 mg/kg, p.o) significantly increased the inhibition of HPFC, spleen-RFC and thymus-RFC production by Concanavalin A at a dose of 50 micrograms/mouse. This agent (3-30 mg/kg, p.o) inhibited the production of HPFC, spleen-RFC and thymus-RFC in mice 4 days after the secondary immunization. These results suggest that traxanox may inhibit antibody production via the induction of Lyt 2.2 positive cells (suppressor T cells).
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A 30-year-old female had an acute myocardial infarction complicated by congestive heart failure. Angiography demonstrated an aneurysm in the area of the left aortic sinus. The aneurysm compressed and displaced the main trunk of the left coronary artery and the proximal portion of the left anterior descending artery. This aneurysm was considered to be the cause of the infarction. Aortic valve replacement and removal of the aneurysm were performed. Postoperative studies revealed good function of the replaced valve, good antegrade filling of the left coronary artery, and improved left ventricular function.
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Both C57BL/6 and BALB/c mice were immunized intravenously with lipopolysaccharide (LPS, 10 micrograms/mouse) on day 0, and hemolytic plaque forming cells (HPFC) in the spleen were assayed on day 4. Traxanox given orally at a dose of 30 mg/kg augmented the HPFC production to LPS in both mice. This agent (3-30 mg/kg) restored significantly the suppressed HPFC production to LPS in the BALB/c mice pretreated with carrageenan (0.03 mg/mouse), but did not restore it in the BALB/c mice pretreated with cyclophosphamide (25 mg/kg). The transfer of spleen adherent cells of the mice immunized with LPS and treated with traxanox to the syngeneic mice resulted in a significant increase in the HPFC production to LPS. The HPFC production to trinitrophenylated polyvinylpyrrolidone, a T cell-independent antigen was not affected by the treatment with traxanox or carrageenan. These results suggest that traxanox has a capacity to augment the immune response by affecting macrophage function.
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The effect of traxanox on SRS-A release was examined in vivo and compared with that of disodium cromoglycate (DSCG). Intravenous antigen challenge produced an intense anaphylactic bronchoconstriction that showed a peak time of 5 min in egg albumin-sensitized guinea pigs pretreated with three agents, mepyramine (2.5 mg/kg, i.v.), indomethacin (1 mg/kg, i.v.) and propranolol (0.05 mg/kg, i.v.). This bronchoconstriction was almost completely inhibited by additional pretreatment with an SRS-A antagonist, FPL 55712 (2.5 mg/kg, i.v.). A lipoxygenase inhibitor, BW755C (10 mg/kg, i.v.), also significantly inhibited this reaction. These results indicate that this anaphylactic bronchoconstriction is due to the release of endogenous SRS-A. In this model, traxanox (5 and 10 mg/kg, i.v.) showed a dose-related inhibition, but DSCG (10 mg/kg, i.v.) did not. FPL 55712 (1 mg/kg, i.v.) administered at the peak time of the bronchoconstriction caused a relaxation. Traxanox, on the other hand, failed to relax this reaction. In IgE-mediated rat passive peritoneal anaphylaxis (PPA), traxanox (0.01--10 micrograms/rat, i.p.) inhibited the release of SRS-A and histamine dose-dependently. This inhibitory effect was about 10--20 times as potent as that of DSCG. In addition, both traxanox (0.1 microgram/rat, i.p.) and DSCG (1 microgram/rat, i.p.) showed a synergistic effect in combination with isoproterenol (0.01 microgram/rat, i.p.) and an additive effect with theophylline (100 micrograms/rat, i.p.) in inhibiting the release of SRS-A in rat PPA. These results suggest that traxanox inhibits the release of SRS-A in vivo, so that it may be clinically effective in treating patients with allergic bronchial asthma.
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Organic acids in the hearts of patients with idiopathic cardiomyopathy, obtained by biopsy, were studied using gas chromatography--mass spectrometry. The profiling of organic acids was compared among eight cases of hypertrophic cardiomyopathy, three cases of congestive cardiomyopathy, and nine cases of other heart diseases, which were regarded as controls. It was found that almost all organic acids, especially deoxyaldonic acids of 2-deoxytetronic acid, 2,3-dideoxypentonic acid, 3-deoxy-2-C-(hydroxymethyl)tetronic acid, 3-deoxyerythropentonic acid and 3-deoxy-2-C-(hydroxymethyl)erythropentonic acid, were accumulated in large amounts in the heart in congestive cardiomyopathy, while these acids were decreased in hypertrophic cardiomyopathy. It was therefore suggested that deoxyaldonic acid metabolism in the heart in congestive cardiomyopathy is quite different from that in hypertrophic cardiomyopathy.
In order to characterize temporal pattern sensitivity in the cat ganglion cells, a new analysis technique by semi-Markov models which was developed in the previous papers (Tsukada et al., 1975-1977) was applied to input-output relations of the receptive-field. Three types of statistical spot stimuli positioned in the center region of receptive fields were used. Each type of stimulus has an identical histogram in the inter-stimulus intervals and therefore the same mean and variance, but different correlations between adjacent inter-stimulus intervals (Type 1, positive; Type 2, negative; and Type 3, independent processes). From the output spike trains of cat retinal ganglion cells to each stimulus, mean, variance, and histogram were computed. As the result of investigating these data, we could draw the following conclusion from the resultant output interval histograms. The receptive-field-center responses of cat ganglion cells can be classified into two groups (Types L and N) according to the difference of responsiveness to the three types of statistical spot stimuli. A Type L response has the same histogram in interspike intervals for all three stimuli, and is not sensitive to the temporal pattern, while a Type N response has three different forms depending on each type of stimulus showing high sensitivity to the temporal pattern. These results were also simulated by the Markov chain model and discussed with relation to neural coding and classification of ganglion cell types.
Traxanox sodium, a benzopyranopyridine derivative showing a potent oral antiallergic activity in the rat, was compared with disodium cromoglycate (DSCG) for ability to block the release of histamine from the rat mast cell in vitro. Traxanox sodium showed dose-, antigen- and time-dependent inhibiton of the IgE-mediated release of histamine. The 50% inhibitory concentration was 0.04 microM for traxanox sodium, 1 microM for DSCG and 660 microM for theophylline. All these drugs blocked the release of histamine potentiated by preincubation of the mast cell with 10 micro M adenosine at lower concentrations than those which could inhibit the IgE-mediated histamine release. In addition, traxanox sodium at concentration of 1-100 microM inhibited the histamine release caused by 0.25 microgram/ml compound 48/80 in the presence and absence of calcium, and the drug at 100 micro M slightly inhibited the release caused by 0.2 microgram/ml ionophore A23187. These results suggest that traxanox sodium is a more potent inhibitor than DSCG on the histamine release from the mast cells of the rat, and a part of its antiallergic action is due to a selective inhibition of the immunological release of allergic mediators from the mast cell.
The 48-hour passive cutaneous anaphylaxis (PCA) and passive anaphylactic bronchoconstriction in rats induced by an IgE-like antibody against DNP-Ascaris were inhibited by intravenous treatment with traxanox sodium in a dose dependent manner. In both experiments, traxanox sodium was more potent than disodium cromoglycate (DSCG), especially as an inhibitor of bronchial anaphylaxis. In the PCA test of rats using a double sensitization technique according to the Orr's method, traxanox sodium was demonstrated not to inhibit antigen-antibody combination, but to inhibit the release of chemical mediators at a stage following antigen-antibody combination. Traxanox sodium inhibited the complement dependent immune hemolysis, but not the hypotonic hemolysis in vitro. However it failed to inhibit the Forssman anaphylaxis in the guinea pig in vivo. Traxanox sodium (50-250 mg/kg p.o.) showed an inhibitory effect on the direct passive Arthus reaction (DPAR) of the rats. Furthermore, it delayed the onset of the hyperacute form of experimental allergic encephalomyelitis (EAE) and reduced mortality in the rats. DSCG was less effective on DPAR and EAE. In conclusion, traxanox sodium is considered to have a wider spectrum of anti-allergic activity than DSCG since it has a suppressive effect not only on the type I allergic reaction, but also on the type III and IV allergic reactions.
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Y-12, 141 (0.1 approximately 0.3 mg/kg) given i.v. 1 min before the antigen challenge inhibited both the 48-hour passive cutaneous anaphylaxis (PCA) and active anaphylactic bronchoconstriction of rats mediated by IgE-like antibody. The anti-PCA activity of Y-12, 141 (0.3 mg/kg i.v.) given 1 min before the antigen challenge decreased significantly by predosing with Y-12, 141 (1 approximately 3 mg/kg i.v.) 60 min before the antigen challenge. The induction of tachyphylaxis in the PCA test appeared to depend on the doses in internal between predosing and second dosing. The anti-PCA activity of disodium cromoglycate (DSCG) at a dose of 1 mg/kg i.v. decreased significantly by predosing with DSCG (10 mg/kg i.v.) 30 min before the antigen challenge. Cross-tachyphylaxis between Y-12, 141 and DSCG was observed in the PCA test. The tachyphylaxis to Y-12, 141 was more readily induced in the PCA than in the bronchoconstriction. The inhibitory activity of Y-12, 141 (0.3 mg/kg i.v.) given 1 min before the antigen challenge in the PCA and bronchoconstriction was not affected by predosing with Y-12, 141 (1 mg/kg p.o. or s.c.) for 7 days.
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