Biomedical subjects
Publications and source records attributed to N Inagaki.
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A study was carried out to examine the effect on neurotropin (NSP) on the 4 types of allergic reactions classified by Coombs and Gell. 1) Type 1: NSP inhibited 48-hr homologous passive cutaneous anaphylaxis (PCA) as well as antigen-induced degranulation of rat mesenterium mast cells. The drug also inhibited both experimental asthma and histamine release from lung tissue in guinea pigs, as mediated by IgE antibody. 2) Type 2: NSP slightly suppressed the increase in urinary protein levels caused by nephrotoxic nephritis in rats and showed a tendency to inhibit Forssman shock in guinea pigs. NSP had an anticomplement activity in vitro but did not inhibit the reversed cutaneous anaphylaxis in rats. 3) Type 3: NSP suppressed an increase in the urinary protein level of rats with glomerulonephritis, as induced by immune complex. 4) Type 4: NSP slightly inhibited the increase in the urinary protein level in glomerulonephritic rats pretreated with IgG. However, the drug did not affect picryl chloride-induced contact dermatitis in mice. We conclude that NSP inhibits allergic reactions used in the present study except for reversed cutaneous anaphylaxis and contact dermatitis, and the most potent activity is seen in the case of Type 1 reaction.
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The effects of a novel leukotriene (LT) C4/D4 antagonist, BAY-x-7195 on experimental allergic reactions in airway and skin were compared to that of ONO-1078. BAY-x-7195 showed an antagonistic action to LTD4-induced bronchoconstriction in vitro and in vivo. In in vitro experiments, BAY-x-7195 inhibited LTD4-induced contraction of isolated guinea pig tracheal muscle (pA2 = 8.03). BAY-x-7195 at doses of 3-30 mg/kg clearly inhibited LTD4-induced increases in respiratory resistance (Rrs) in guinea pigs. In contrast, BAY-x-7195 inhibited significantly U-46619-induced increases in Rrs at a dose of 30 mg/kg in guinea pigs. BAY-x-7195 at doses of 3-30 mg/kg inhibited the aerosolized antigen-induced biphasic increase in Rrs in guinea pigs. Moreover BAY-x-7195 inhibited repeated aeroantigen-induced airway hyperreactivity in guinea pigs. In mice, aeroantigen-induced airway inflammation were clearly inhibited by BAY-x-7195. These results show the efficacy of BAY-x-7195 against the antigen-induced increase in airway resistance and antigen-induced airway hyperreactivity in guinea pigs and mice, probably due to anti-LTD4 antagonistic action and the inhibition of antigen-induced airway inflammation.
Recent immunocytochemical studies have identified the histaminergic neuron system in the brain. In the rat brain, histaminergic neuronal cell bodies are located in the tuberomammillary nucleus in the posterior hypothalamus, while histaminergic fibers are distributed in almost all regions of the brain. Similar distributions of histaminergic neuronal cell bodies and fibers have been reported in the brains of other mammals and nonmammalian vertebrates. As expected from the widespread distributions of the efferent fibers, the central histaminergic neuron system seems to be involved in multiple functions in the brain. The results of intracerebral injection of histamine and administration of alpha-fluoromethylhistidine (FMH), which depletes brain histamine level, suggest that the central histaminergic system may modulate feeding, drinking and sexual behaviors, sleep-wakefulness and circadian rhythm, neuroendocrine and cardiovascular controls and thermoregulation.
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Scratching behavior was induced in 12 strains of mice and the frequency was compared. An injection of histamine at a dose of 50 nmol induced frequent scratching behavior only in ICR mice, although the same dose of serotonin induced frequent scratching behavior in all strains of mice except for A/J. Histamine (10 nmol), serotonin (1 nmol), substance P (50 nmol) and passive cutaneous anaphylaxis induced significant vascular permeability increase in BALB/c, ICR, ddY and NC/Nga mice. These four stimuli also induced frequent scratching behavior in ICR mice. However, they failed to induce substantial increase in the incidence of scratching in the other three strains, except for ddY, which exhibited a slight but significant increase against substance P injection. These results suggest that the ICR mouse is a good responder for scratching behavior against various stimuli, especially against histamine. Thus ICR mice may be suitable for studying mediators and/or mechanisms for itching.
We evaluated and characterized the mouse scratching behavior using a new apparatus, MicroAct. Scratching behavior was evoked in ICR and BALB/c mice by compound 48/80, passive cutaneous anaphylaxis or repeated hapten application. Under the present experimental condition, MicroAct detected consecutive scratching behavior (events) consisting of 3 or more beats. Although the detecting standard of MicroAct was not identical to that of an observer, the number of events detected by MicroAct and by an observer were almost comparable with each other. Frequency of events, total scratching time and total number of beats detected by MicroAct increased depending on the intensity of the causing stimuli for scratching. In contrast, the duration of each event and the number of beats in each event increased only slightly, but the scratching speed was almost constant. The present results demonstrate that MicroAct is a useful tool for evaluating mouse scratching behavior. Mouse scratching behavior seems to have a relatively fixed pattern and the causing stimulus increases mainly in the frequency of event without affecting the scratching speed.
The effects of RU-31156 on type I allergic reactions were studied and the following results were obtained. Seven-day homologous PCA in guinea pigs was significantly inhibited by oral doses of this drug. The maximum inhibition was observed when the drug was given 30 minutes prior to challenge. Forty-eight-hour homologous PCA was significantly inhibited in rats, and this inhibition was maximal when the drug was given 10 minutes prior to challenge. Orally-administered RU-31156 gave significant inhibition of induction of experimental asthma symptoms in guinea pigs when it was given one or two hours prior to challenge. In addition, the drug significantly inhibited the asthmatic reaction of experimental asthma in rats when it was given 10 minutes prior to challenge. RU-31156 significantly inhibited histamine and SRS-A release from the lung tissue of passively sensitized guinea pigs. The combined use of isoproterenol or theophylline with RU-31156 did not enhance the inhibitory activity of the drug. RU-31156 did not produce any effect on the histamine release induced by calcium ionophore A 23187. RU-31156 inhibited the Schultz-Dale reaction in the tracheal muscle and the ileum of guinea pigs, but it did not show any antihistaminic in these organs.