Effects of β-stimulant (fenoterol, 0.088-0.150 mg/kg) on EIA were examined. Two types of exercise tolerance tests, i. e. cycle ergometer (300W) and treadmill (10°, 6 km/hr, 6 min) were performed. Its effects were examined not only by the two different types exercise tolerance test, but also in two different asthma severity groups (moderate and severe degree groups). Fenoterol was administered 2 hours prior to exercise. 1)EIA was significantly inhibited in those patients or subjects who were administered fenoterol, not only in the cycle ergometer group but also in the treadmill group. 2)Fenoterol significantly inhibited EIA in both moderate and severe asthmatic groups. 3)Pulse rate did not differ significantly between the fenoterol administered group and the control group, between the two different exercise tolerance tests or between the two groups of asthma severity.

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Neurotropin (NSP) is an extract isolated from vaccinia virus-inoculated and inflamed skin of rabbits. A study was carried out to examine the effect of NSP, an anti-allergic agent, on IgE antibody formation in mice which were immunized with dinitrophenyl-conjugated ovalbumin (DNP-OA) mixed with alum. Short-term administration of NSP did not suppress primary, on-going or secondary IgE antibody formation including both anti-DNP and anti-OA IgE antibodies, although NSP was administered i. v. for 3 days before, with or after immunization. Primary IgG antibody formation, however, was slightly enhanced by NSP given for 3 days with the first immunization. The results of the adoptive transfer experiments indicate that NSP did not affect either T cells or B cells participating in IgE antibody formation. These results suggest that the anti-allergic action of NSP is not responsible for the suppression of IgE antibody formation.

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The antagonistic effects of beta-adrenergic, stimulant, alpha-adrenergic blocker and anticholinergic agent on bronchoconstriction induced by methacholine and histamine aerosol challenge were studied in monkeys. Isoproterenol suppressed an increase of total respiratory resistance due to the aerosol challenge with both methacholine and histamine. Atropine produced an inhibitory effect on bronchoconstriction due to methacholine challenge, but not so significantly with histamine. Phentolamine showed no inhibitory effect on methacholine and histamine induced bronchoconstriction. These data suggest that isoproterenol has not only a myorelaxant action but also an inhibitory effect on the bronchoconstriction through its beta adrenergic effect on bronchial muscle, and that atropine reduces the bronchomotor tone through its antimuscaric action. There is thought to be little participation by alpha adrenergic receptor in bronchial constriction and relaxation.

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One hundred and five asthmatics, who had been treated more than 4 yrs (including over 6 yrs: 52, over 8 yrs: 14, over 10 yrs: 4) in Tokyo Kyosai Hospital and National Medical Center Hospital from 1967 to 1979, were subject to this follow-up study. Thirty-four patients received specific hyposensitization treatement, 11 received non-specific, 50 received combination treatment of specific and non-specific, and 8 were treated only symptomatically. Hyposensitization treatments using extracts of house dust, Candida, Penicillium, Alternalia, Aspergillus and Broncasma Berna were carried out less than 3 yrs on 30 patients, 3-6 yrs on 43 patients and more than 6 yrs on 11 patients. Non-specific treatments using aurothioglucose or -malate, Histaglobulin, Astremedin and Neurotropin were done more than 3 yrs on 37 patients, 3-6 yrs on 21 patients and more than 6 yrs on 3 patients. After 4-12 years' treatment, there were 70 patients (74%) who had no symptoms or only occasional wheezing, including 54 patients (57%) who had been in a state of remission for more than 1 yr. There was no significant difference in remission rate by kind of treatment. It has been shown that asthmatic patients have increased bronchial reactivity to inhaled acetylcholine (Ach) and the respiratory threshold to Ach is very low. The thresholds were checked over period of 4-7 yrs in 6 patient. The initial low threshold rose significantly in 5 patients whose asthma had diminished. After more than 3 years' remission, these patients reacted much less intensely than they had in the former experiment performed at the asthmatic period, but remained hyperreactive to Ach compared to normal subjects.

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Either intact or neuraminidase-treated desialized T cells were mixed with plasma from patients with systemic lupus erythematosus (SLE), counterstained with fluorescein-tagged anti-human IgM, and analysed by indirect immunofluorescence. Reactivity of normal T cells to IgM anti-T cell antibodies from patients with SLE was markedly enhanced by their treatment with neuraminidase. Prior adsorption of the palsma that contained antibodies to both intact and desialized T cells with intact T cells could completely eliminate the ability of the plasma to bind to intact T cells, but only slightly affected its abilities to bind to desialized T cells. The ability of the plasma to bind to either intact or desialized T cells was entirely removed by prior adsorption with desialized T cells. These results indicate that SLE anti-T cell antibodies consist of at least two antibodies with different target cell specificities; one is able to preferentially direct at desialized T cells and the other is able to direct at both intact and desialized T cells. When patients with SLE were studied simultaneously with regard to concanavalin A (Con A)-induced suppressor cell activity produced by their own T cells and with regard to the presence of antibodies to either intact or desialized T cells in their plasma, suppressor T cell activity observed in lymphocytes of SLE patients correlated well with the presence of IgM, but not IgG, antibodies directed at desialized, but not intact, T cells. These results suggest that IgM antibodies to desialized T cells are responsible for the preferential elimination of suppressor T cells. Indeed, prior treatment of desialized, but not intact, T cells obtained from normals with SLE plasma which contained antibodies directed at desialized, but not intact, T cells, plus complement prevented the generation of Con A-induced suppressor cells. We further demonstrated that D-(+)-lactose markedly inhibited the binding of SLE plasma to desialized T cells, but only slightly to intact T cells, and that reactivity of desialized T cells to SLE plasma is markedly inhibited by their treatment with the proteolytic enzyme, pronase. These results also suggest that these antibodies recognize asialo-glycoprotein that is not masked by sialic acid residues on the cell surface.

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[in Japanese]

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The cell populations and the angiotensin-converting enzyme (ACE) activity were examined on the fluids obtained by bronchoalveolar lavage (BAL) in 6 cases with sarcoidosis, 4 with bronchial asthma and 9 control healthy volunteers. The sheep red blood cell rosette-forming cell was detected as T-lymphocyte and the surface immunoglobulin bearing cell as B-lymphocyte. Serum and BAL fluid ACE activity was assayed by Liberman modified method of Cushman and Cheung. Patients with sarcoidosis had a marked increase in the percentage of lymphocytes, mainly T-lymphocytes, in the BAL fluid in comparison with bronchial asthma patients and normal controls. A highly elevated BAL fluid ACE was found in 3 of 6 patients with sarcoidosis not receiving steroids, as compared with normal controls. Bronchial asthma patients showed normal ACE activity. The level of BAL fluid ACE did not correlated with that of serum ACE in sarcoidosis patients. The high ACE level from sarcoid BAL fluid suggests that alveolar macrophages and epithelioid cells in sarcoid granuloma from the lung actively synthesize ACE.

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