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Biomedical subjects

A Koda

Publications and source records attributed to A Koda.

At least 127 records · Page 7Linked to original sources
PubMed1987

Inhibition of antigen-induced contraction of guinea pig isolated tracheal muscle with 2-n-butyl-3-dimethylamino-5,6-methylenedioxy indene (MDI-A), indane (MDI-B) and 8-(diethylamino)octyl-3,4,5-trimethoxy benzoate hydrochloride (TMB-8).

The effects of three intracellular calcium antagonists on antigen-induced contraction of sensitized guinea pig tracheal muscle were investigated. The agents employed were: 2-n-butyl-3-dimethylamino-5,6-methylenedioxy indene hydrochloride (MDI-A), 2-n-butyl-3-dimethylamino-5,6-methylenedioxy indane hydrochloride (MDI-B) and 8-(diethylamino)octyl-3,4,5-trimethoxy benzoate hydrochloride (TMB-8). Each of these agents caused a concentration-dependent inhibition of the antigen-induced contraction of sensitized tracheal smooth muscle. Moreover, in histamine and leukotriene D4 (LTD4) incited contractions of guinea pig tracheal muscle, they showed antagonistic action. The induced tracheal muscle contraction, achieved through the addition of compound 48/80 to a solution of ethylene glycol bis (beta-aminoethylether)-N,N,N1, N1-tetraacetic acid (EGTA) in a contained Ca-free medium, was completely inhibited by individual pretreatment with MDI-A, MDI-B and TMB-8. In the case of tracheal muscle contraction induced by CaCl2 in a high potassium, Ca-free medium, only TMB-8 inhibited contraction. Lastly, none of these three intracellular calcium antagonists affected the antigen-induced release of histamine and slow reacting substance of anaphylaxis (SRS-A). These results suggest that MDI-A and MDI-B inhibit the antigen-induced contraction of sensitized guinea pig tracheal muscle by interfering with the contractile responses caused by histamine and LTD4.

Animals↗
PubMed1987

Specific suppression of antigen-antibody reactions by a dialysate from Dermatophagoides farinae.

Mite dialysate prepared from an extract of house dust mite, Dermatophagoides farinae, suppressed 48-h homologous passive cutaneous anaphylaxis (PCA) in rats caused by a non-dialyzable fraction of the mite extract (mite antigen), and the suppression was dose-dependent with a high specificity for the antigen. The mite dialysate itself slightly elicited the PCA. Fraction 3 obtained from the mite dialysate by means of DEAE-Sephadex A-25 column chromatography suppressed PCA in rats and guinea pigs more potently than mite dialysate. Histamine release from sensitized rat peritoneal exudate cells (PEC) induced by the mite antigen was suppressed in a dose-dependent manner when the PEC had been previously incubated with fraction 3. However, incubation of the PEC with fraction 3 caused a significant release of histamine compared to the spontaneous value. Fraction 3 clearly inhibited the passive hemagglutination of the mite antigen-conjugated sheep red blood cells caused by rat hyperimmunized serum. From these results it was considered that certain haptenic substances might be present in the mite dialysate.

Animals↗
PubMed1987

Pharmacological studies on the release of slow reacting substance of anaphylaxis during anti-immunoglobulin E antibody mediated passive peritoneal anaphylaxis in rats.

The release of slow reacting substance of anaphylaxis (SRS-A) by anti-immunoglobulin E(IgE; epsilon)-antibody mediated passive peritoneal anaphylaxis (PPA) in rats was investigated immunopharmacologically. A significant amount of SRS-A was released by anti-epsilon-antibody in the peritoneal cavity of rats passively sensitized with IgE. The amount of SRS-A released by anti-epsilon-antibody was about one third less than that released in an anti-gamma-antibody and IgG2a system. The release of SRS-A was initiated at 2 min and reached its maximum 5 to 10 min after the injection of anti-epsilon-antibody. Disodium cromoglycate, tranilast and ketotifen inhibited the release of both SRS-A and histamine caused by anti-epsilon-antibody mediated PPA. Glucocorticoids (hydrocortisone, prednisolone and dexamethasone) also inhibited the release of both mediators. rho-Bromophenacyl bromide inhibited the release of both mediators. AA-861, a potent 5-lipoxygenase inhibitor, inhibited the release of SRS-A but not histamine. Indomethacin slightly enhanced the release of SRS-A and inhibited the release of histamine. Cytarabine resulted in leucopenia and inhibited the release of histamine but not SRS-A during PPA. Dextran sulfate reduced the number of glass adherent peritoneal cells and inhibited the release of SRS-A but not histamine. These results suggest the suitability of anti-epsilon-antibody mediated rat PPA for investigating the effect of anti-allergic agents on the release of SRS-A.

Anaphylaxis↗
PubMed1987

[Immunopharmacological approach to the modulation of IgE antibody formation].

Soluble factors released by both T and B cells are involved in the class-specific regulation of IgE antibody formation; some factors have affinity for IgE, whereas others do not. The induction phase of the primary and secondary IgE antibody response is highly sensitive to treatment with such factors or some drugs. In contrast, persistent IgE antibody formation is mostly insensitive to the same treatments, indicating that this phase differs apparently from the induction phase. Thus, it is very important to note the marked differences between the regulatory mechanisms of these two phases when drugs responsible for the suppression of IgE antibody response are developed. In the present review, the recent advances pertaining to the regulation of IgE antibody formation in animals and humans are described in view of immunopharmacology.

Animals↗
PubMed1987

Change in the activity of the cyclic AMP-dependent protein kinase in antigen-stimulated sensitized mast cells and effect of drugs inhibiting allergic mediator release.

The activity of cyclic AMP-dependent protein kinase (protein kinase A) in the sensitized rat mast cell was decreased 2 min after antigen challenge when the histamine release exhibited a maximum. Drugs inhibiting allergic mediator release such as disodium cromoglycate, tranilast and theophylline significantly inhibited antigen-induced histamine release and reduced a decrease in the activity of protein kinase A. These results suggest that protein kinase A is involved in the histamine releasing process in the mast cell, and drugs inhibiting allergic mediator release cause their effects partially through the inhibition of protein kinase A.

Animals↗
PubMed1986

Studies on vascular permeability increasing factors involved in 48-hour homologous PCA in the mouse ear.

Several attempts were made to elucidate the possible role of histamine, serotonin, leukotrienes C4 (LTC4) and D4 (LTD4), and prostaglandin E1 (PGE1) as vascular permeability increasing factors involved in 48-hour homologous passive cutaneous anaphylaxis (PCA) in the mouse ear. Increased vascular permeability in the mouse ear caused by the mediator injection or PCA was assessed quantitatively by measuring the amount of extravasated dye. In skin reactions, all of the mediators used in the present study significantly increased vascular permeability. The most potent mediator was serotonin, which increased the vascular permeability from a concentration of 10(-8) g/ml, and the activity was about 100 times higher than that of histamine on a weight basis. Vascular permeability increasing activity of LTC4 was about 10 times higher than that of histamine, and LTD4 and PGE1 were also more potent than histamine. Increases of vascular permeability caused by histamine, serotonin, LTC4 and LTD4 were significantly potentiated by injecting 10(-6) g/ml of PGE1 simultaneously. Histamine-, serotonin- and LTC4-induced skin reactions in the mouse ear were suppressed significantly by the administrations of chlorpheniramine, methysergide and FPL 55712, respectively. In contrast, though chlorpheniramine and methysergide suppressed also mouse ear PCA (about 50 and 40%, respectively), neither FPL 55712, indomethacin nor BW 755C suppressed it. These results strongly suggest that the most important mediator involved in mouse ear PCA is histamine and that serotonin also plays an important role in the increase of vascular permeability caused by PCA. Despite their potent vascular permeability increasing activity LTC4, LTD4 and PGE1 do not seem to play an important role in mouse ear PCA.

4,5-Dihydro-1-(3-(trifluoromethyl)phenyl)-1H-pyraz↗
PubMed1986

Homologous passive cutaneous anaphylaxis in various strains of mice.

Passive cutaneous anaphylaxis (PCA) was elicited both in the ear and in the dorsal skin of 13 strains of mice at the same time and assessed quantitatively by measuring the amount of extravasated dye. Body pigments of colored mice such as DBA/2 (chocolate), C3H/He (brown) and C57BL/6 (black) did not interfere with the measurement of dye. In the ear response, ICR was a higher responder, C57BL/6 and BALB/c-nu/nu were lower responder strains. In the dorsal skin response, however, ICR was a lower responder, BALB/c-nu/nu, Hairless and WBB6F1-+/+ were higher responders. WBB6 F1-W/Wv was a nonresponder in both responses. The ear response was highly reproducible and the dorsal skin response of each strain was 1/2-1/10 of its ear response except for BALB/c-nu/nu. The PCA bluing regions on the dorsal skin of BALB/c-nu/nu were clearly delineated and the response was almost comparable to its ear response.

Animals↗
PubMed1986

Effect of cinnarizine on IgE antibody mediated allergic reaction in mice and rats.

The effect of cinnarizine on immunoglobulin E (IgE) antibody mediated allergic reactions in mice and rats was investigated. Nifedipine and tranilast were used as comparative drugs. The dye leakage caused by IgE antibody mediated passive cutaneous anaphylaxis (PCA) in mouse ear was clearly inhibited by cinnarizine administered both orally and intraperitoneally. The inhibitory action of cinnarizine for PCA was as potent as nifedipine and superior to tranilast. Cinnarizine clearly inhibited the increase in capillary permeability caused by histamine and calcium ionophore A 23187 (A 23187) but not by LTD4 in mouse ear. Nifedipine inhibited the increases of capillary permeability caused by A 23187, histamine and LTD4. Tranilast inhibited A 23187 induced vasculitis but not histamine or LTD4-induced reaction. Cinnarizine had no significant effect on the release of histamine caused by antigen or A 23187 from rat peritoneal mast cells. Nifedipine and tranilast inhibited the release of histamine caused by both antigen and A 23187 from rat peritoneal mast cells.

Animals↗
PubMed1986

Experimental neurogenic bladder in rats and effect of Robaveron, a biological prepared from swine prostate, on it.

An experimental neurogenic bladder was induced in rats by an intraspinal injection of 10% phenol-glycerin solution. The functional and biochemical changes in the bladder were studied in vivo and ex vivo, and the effect of Robaveron, a biological prepared from swine prostate, on these changes were examined. The forced voiding pressure in the control rats which had been caused by the neurogenic bladder was reduced to 1/4-1/5 that of the intact animals. Robaveron recovered a decrease in the pressure, and the effect of 150-250 mg/kg, p.o., corresponded nearly to that of 40 mg/kg, i.m. In the ex vivo study with the strips of isolated neurogenic bladder muscle, the time required to cause 50% of the maximum contraction by transmural electric stimulation prolonged to about four times that of the intact one. Such a prolongation was recovered by Robaveron in a dose-dependent fashion, and the effect of Robaveron given p.o. corresponded to about 1/6 that of the drug given i.m. No change in Ca2+-influx, was found, although Ca2+-efflux was inhibited in the strip of neurogenic bladder muscle. Such an inhibition was significantly relieved in that of animals treated with Robaveron. In the neurogenic bladder rat, the ratio of bladder weight to body weight increased, and the activities of total ChE and AChE in the bladder muscle decreased, on which Robaveron did not show any influence. Phasic and tonic contractions in the strips of intact rat bladder and guinea pig ileum were inhibited by La3+, particularly phasic response in both the strips. Robaveron recovered the inhibition in a dose-dependent fashion. The present study suggests that the urinary dysfunction in neurogenic bladder may be caused not only by nervous disorders but also by changes in the bladder muscle itself. Robaveron was found to be effective for most of such changes. These findings may support the clinical efficacy of Robaveron for improving the attenuated bladder function.

Animals↗
PubMed1986

Inhibition of IgE antibody formation by n-pentyl alpha-L-sorbopyranoside.

Effect of n-pentyl glycosides and alkyl alpha-L-sorbopyranosides on IgE antibody formation in rats and mice were investigated. When n-pentyl alpha-L-sorbopyranoside was given subcutaneously or orally, the IgE antibody formation in rats and mice was suppressed, while no suppression of hemagglutinin formation was observed. The study on timing of administration indicated that n-pentyl alpha-L-sorbopyranoside significantly suppressed the secondary IgE antibody response when administered before the secondary immunization.

Animals↗
PubMed1986

Effects of the new antiallergic drug 11-oxo-11H-pyrido[2,1-b] quinazoline-2-carboxylic acid on immediate allergic reactions.

The effects of 11-oxo-11H-pyrido[2,1-b]quinazoline-2-carboxylic acid (Sm 857) on immediate type, particularly type I allergic reactions were investigated and the following results were obtained. 48-h homologous passive cutaneous anaphylaxis (PCA) in rats was inhibited by oral administration of Sm 857 from the 4th h to the 30th min before antigen challenge and by intravenous administration from the 2nd h to just before antigen challenge. 48-h homologous PCA in rats was inhibited dose-dependently by oral administration of Sm 857 at 1-50 mg/kg 30 min before antigen challenge. On the other hand, the intravenous administration 10 min before antigen challenge showed similar dose-dependent effects on PCA and the effects were significant at doses of 0.5-2 mg/kg. The oral administration of Sm 857 for 1-4 weeks reduced the PCA inhibitory effect in comparison with single administration. Sm 857 injected intravenously twice at intervals of 15-120 min showed no change in inhibitory effect. The PCA inhibitory effect of Sm 857 in adrenalectomized rats was reduced markedly when compared with that in sham-operated rats. On the other hand, adrenalectomy had no influence on the inhibitory effect of tranilast. Sm 857, tranilast and ketotifen inhibited histamin-induced capillary permeability in rats and, in particular, the effect of ketotifen was conspicuous. Sm 857, tranilast and ketotifen significantly inhibited antigen-induced histamine release from the peritoneal cavity of passively sensitized rats. Release of slow reacting substance of anaphylaxis (SRS-A), on the other hand, was inhibited significantly by Sm 857 and ketotifen. Sm 857 showed a tendency to inhibit antigen-induced histamine release from the lung tissue of passively sensitized guinea pigs and significantly inhibited SRS-A release. Sm 857 inhibited histamine- and leukotriene D4 (LTD4)-induced contraction in the lung parenchyma and the tracheal muscle. However, the drug had no effect on contraction of the ileum. Sm 857 showed a tendency to inhibit the Schultz-Dale reaction in the lung parenchyma ana the ileum. Both oral and intravenous administration of Sm 857 showed an inhibitory effect on experimental asthma in guinea pigs, which was similar to that of tranilast.

Animals↗
PubMed1986

A comparative study of the mutagenic activation of N-nitrosopropylamines by various animal species and man: evidence for a cytochrome P-450 dependent reaction.

The mutagenic potential of seven carcinogenic N-nitrosopropylamines was examined by means of Ames' preincubation assay using liver 9000 g superanatant (S9) fractions from rats, hamsters, mice, rabbits, monkeys and humans for metabolic activation. N-Nitroso(2-hydroxypropyl) (2-oxopropyl)amine (HPOP), N-nitrosobis(2-oxopropyl)amine (BOP), N-nitrosobis(2-acetoxypropyl)amine (BAP), N-nitroso-2,6-dimethylmorpholine, N-nitrosomethyl(2-hydroxypropyl)amine (MHP) and N-nitrosomethyl(2-oxopropyl)amine all showed positive mutagenicity in strain TA100 in the presence of liver S9 from each of the uninduced animals, but N-nitrosobis(2-hydroxypropyl)amine was negative. The mutagenic activity of MHP was highest with liver S9 from the hamster, but that of BAP was lowest with hamster liver S9. With regard to the activities of the other N-nitrosopropylamines, there were no significant differences among five animal species. In the presence of liver S9 from humans, HPOP, BOP and MHP showed positive mutagenicity. With the exception of HPOP and BOP, the animal or human liver S9-mediated mutagenicity of these N-nitrosopropylamines was almost completely lost upon removal of NADP+ from the assay system, preincubation in an atmosphere of carbon monoxide, or addition of cytochrome c to the S9 mixture. metyrapone decreased the activities of five compounds (except for BOP) by between 29 and 71%, whereas 7,8-benzoflavone was totally lacking in this effect. These results demonstrated that the phenobarbital-inducible major cytochrome P-450 in animal and human livers is involved in the mutagenic activation of the N-nitrosopropylamines.

Adult↗
PubMed1985

Inhibition of delayed hypersensitivity reactions by a new agent, cis-1-methyl-4-isohexylcyclohexane carboxylic acid (IG-10).

A newly synthesized compound, cis-1-methyl-4-isohexylcyclohexane carboxylic acid (IG-10), has been reported as an inhibitor of delayed hypersensitivity reaction. In the present paper, the mechanisms regarding the inhibitory action of IG-10 was investigated on delayed hypersensitivity reactions. p-Phenylenediamine-induced contact dermatitis in guinea pigs was significantly inhibited when the drug was given in a dose of 100 mg/kg p.o. at various times after challenge with the antigen. IG-10 inhibited both contact dermatitis and monocytes or neutrophils infiltrations induced by picryl chloride in mice. A skin reaction, similar to that seen in the case of delayed hypersensitivity reaction, was induced by an intradermal injection of phytohemagglutinin-P (PHA-P) stimulated lymphocytes in guinea pigs. This reaction was a useful method for assessing the effect of drugs on the release of lymphokines, particularly skin reactive factor (SRF). IG-10 in a concentration of 10(-5) g/ml inhibited the release of SRF as well as the release of migration inhibitory factor (MIF) from guinea pig lymphocytes stimulated by PHA-P. The reduction of delta 4-3-ketone of aldosterone and/or hydrocortisone by rat liver homogenates was not affected with IG-10, unlike that seen in the case of glycyrrhizin.

Aldosterone↗
PubMed1985

Reduction of antigen-induced contraction of sensitized guinea-pig tracheal smooth muscle in vitro by calmodulin inhibitors.

The effect of two calmodulin inhibitors, 1-[bis(p-chlorophenyl)methyl]-3-[2,4-dichloro-beta-(2,4-dichlorobenzylox y) phenethyl]imidazolinium chloride (R 24571) and chlorpromazine (CPZ) on antigen-induced contraction of guinea-pig tracheal smooth muscle was studied. Ketotifen, an anti-allergic compound, was used as a comparative drug. Contraction of sensitized guinea-pig trachea induced by antigen challenge was reduced by all three agents. The two calmodulin inhibitors effected relaxation of contraction of guinea-pig trachea induced by histamine and leukotriene D4 (LTD4). Ketotifen relaxed histamine-induced contraction, but hardly affected LTD4-induced tone. Contrary to chemical mediator induced tone, all examined agents had no effect on resting tone. These three agents shifted histamine- and LTD4-induced concentration-contraction curves to the right. They produced a downward displacement of the maximum, without a parallel shift in histamine- and LTD4-induced concentration-contraction curves. The two calmodulin inhibitors did not affect the antigen-induced release of histamine and SRS-A from sensitized guinea-pig lung tissue. Ketotifen slightly inhibited the release of histamine. These results suggest that R 24571 and CPZ, calmodulin inhibitors, reduced an antigen-induced contraction of sensitized guinea-pig trachea in vitro mainly by affecting the contractility of tracheal smooth muscle by chemical mediators but not by interfering with the release of mediators.

Animals↗
PubMed1985

The inhibition mechanism of histamine release by N-(3,4-dimethoxycinnamoyl) anthranilic acid.

N-(3,4-Dimethoxycinnamoyl) anthranilic acid (N-5') is an inhibitor of IgE-mediated histamine release from mast cells. To elucidate inhibition mechanism, effects of N-5' were examined under various conditions using peritoneal exudate cells and isolated mast cells of rats. N-5' inhibited histamine release induced by antigen, ionophore A23187, ATP, dextran and phospholipase A2. But the release induced by compound 48/80 or ionophore X537A was not inhibited. Influx of Ca++ into mast cells and ATP consumption were inhibited. Based on these results, it is presumed that N-5' interferes with the energy-requiring system and/or Ca++ influx resulting in the inhibition of histamine release.

Adenine Nucleotides↗
PubMed1985

Pharmacological characterization of mouse ear PCA.

Effects of some antiallergic agents on homologous passive cutaneous anaphylaxis (PCA) in mouse ear were investigated by means of assessing the amount of extravasated dye. Antihistamines (chlorpheniramine and diphenhydramine) and antiserotonins (methysergide and cyproheptadine) suppressed mouse ear PCA significantly. In contrast, an antagonist of slow reacting substance of anaphylaxis (SRS-A) (FPL 55712) and an inhibitor of SRS-A synthesis (AA-861) did not suppress the reaction. beta-Adrenergic stimulants (isoproterenol and salbutamol) and theophylline, which elevate cyclic AMP (cAMP) levels, also suppressed mouse ear PCA significantly. The antiallergic agents, N(3',4'-dimethoxycinnamoyl)anthranilic acid(N-5') and ketotifen suppressed mouse ear PCA significantly, but disodium cromoglycate (DSCG) failed to suppress the reaction.

Albuterol↗