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Biomedical subjects

N Inagaki

Publications and source records attributed to N Inagaki.

At least 235 records · Page 13Linked to original sources
PubMed1988

Inhibition of vascular permeability increase in mice. An additional anti-allergic mechanism of glucocorticoids.

Effects of glucocorticoids on IgE antibody-mediated 48-hour homologous passive cutaneous anaphylaxis (PCA) and skin reactions caused by mediator releasers and vascular permeability increasing factors were investigated comparatively. Both PCA and skin reactions were evoked in the mouse ear and these reactions were quantitatively evaluated by measuring the amount of dye extravasated into the ear. The glucocorticoids hydrocortisone, prednisolone and dexamethasone inhibited the PCA significantly. The maximum inhibitory effects of these glucocorticoids were obtained when administered 8 h prior to the antigenic challenge. Dexamethasone significantly inhibited the skin reactions caused by compound 48/80, Ca ionophore A 23187 and hypotonic salt solution. Dexamethasone also significantly inhibited the skin reactions caused by histamine, serotonin, platelet-activating factor, leukotrienes C4 and D4, and bradykinin. The maximum inhibitory effects of dexamethasone on these skin reactions were observed when administered 12-6 h before. These results support the previous observations that glucocorticoids inhibit the increase of vascular permeability caused by various stimuli, and indicate that the inhibition of vascular permeability increase contributes at least in part to the inhibitory effects on the PCA and the mediator releaser-induced skin reactions. Furthermore, the inhibition of vascular permeability increase by glucocorticoids might play an important role in their anti-allergic actions.

Animals↗
PubMed1988

Comparative study of 1.5-hour and 48-hour homologous passive cutaneous anaphylaxis in the mouse ear.

To characterize passive cutaneous anaphylaxis (PCA) in the mouse ear, reactions caused by non-heated and heated antiserum were compared to those caused by monoclonal immunoglobulin E antibody (mc-IgE) and monoclonal immunoglobulin G1 antibody (mc-IgG1). Heat treatment at 56 degrees C did not alter the activity of antiserum or mc-IgG1 to elicit the 1.5-h PCA. The 1.5-h PCA mediated by mc-IgE and 48-h PCA's mediated by both antiserum and mc-IgE were abrogated almost completely by heating at 56 degrees C for 2 h. The 48-h PCA was not elicited by mc-IgG1. The sensitized state persisted at least for 7 d when mice were sensitized with non-heated antiserum or mc-IgE. In contrast, the sensitized state disappeared rapidly in cases of heated antiserum and mc-IgG1. In 48-h PCA's mediated by antiserum and mc-IgE, extravasated dye in the ear was detected 5 min after challenge and the reaction was terminated in 15 min. In contrast, in the 1.5-h PCA mediated by heated antiserum, the accumulation of dye in the ear was delayed slightly when compared to the 48-h PCA. In mc-IgG1-mediated 1.5-h PCA, the delay was significant. Both 1.5-h PCA's mediated by heated antiserum and mc-IgG1, and the 48-h PCA's mediated by antiserum and mc-IgE were not observed in WBB6 F1-W/Wv mice, which lack mast cells. All these PCA's were inhibited equally by tranilast, an inhibitor of mediator release from mast cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Inhibitory effects of glucocorticoids on increased vascular permeability caused by passive cutaneous anaphylaxis and some chemical mediators in rats.

Effects of hydrocortisone, prednisolone and dexamethasone on IgE antibody-mediated homologous passive cutaneous anaphylaxis (PCA) and mediator-induced skin reactions were investigated. PCA and skin reactions were evoked at the same time in the dorsal skin of a rat. Administrations of glucocorticoids inhibited not only the PCA but also the skin reactions caused by histamine, serotonin and leukotriene (LT) C4 significantly. It is suggested, therefore, that glucocorticoids inhibit the increase of vascular permeability non-specifically. This action of glucocorticoids might contribute at least in part to its inhibitory effect on the PCA.

Animals↗
PubMed1988

Superoxide anion production by neutrophils in myelodysplastic syndromes (preleukemia).

Superoxide anion (O2-) production by neutrophils from 14 untreated patients with acute nonlymphocytic leukemia (ANLL) was significantly less than that of healthy controls (4.93 +/- 1.99 vx 6.20 +/- 1.53 nmol/min/10(6) neutrophils, p less than 0.05). In 10 patients with myelodysplastic syndrome (MDS), however, it was not significantly different from the control level although 6 of the 10 patients had low levels, when individual patients were compared with the lower limit of the control range. An inverse correlation between the O2- production of neutrophils and the percentage of leukemic cells in the marrow existed in ANLL (r = -0.55, p less than 0.01), but not in MDS. Three of 4 MDS patients who died of pneumonia prior to leukemic conversion showed a low level of O2- production. The impaired O2- production by neutrophils from some MDS patients, probably due to the faulty differentiation from leukemic clones, may be one of the causes of enhanced susceptibility to infection.

Aged↗
PubMed1988

[Clinical effects of K-18 (IgG-melphalan) in hypoplastic leukemia: a case report].

Five cases of hypoplastic acute myelocytic leukemia were treated with an IgG-melphalan conjugate, K-18. Eight tablets of K-18, containing 30 mg per tablet, were given daily. One patient, a 68-year-old female, obtained complete remission with a duration of 1.5 + months. Among the four remaining patients without remission, one showed a decrease in leukemic cells in the peripheral blood. No side effects of K-18 were observed except in one patient, showing a slight increase in serum GOT and GPT levels. Further studies with a large group will be necessary to clarify the effect of this drug on hypoplastic leukemia.

Administration, Oral↗
PubMed1988

[A case of advanced penile cancer treated with multimodal therapy--combination with tensor fascia lata myocutaneous flap].

A 40-year-old male with advanced penile cancer, whose left inguinal node was ulcerated at the time of initial presentation, underwent multimodal therapy. Four cycles of chemotherapy were given from September 20, 1984 to February 8, 1985. Partial penectomy and left ilioinguinal lymphadenectomy with removal of left groin ejaculation were performed on February 20, 1985, followed by right ilioinguinal lymphadenectomy on March 20, 1985. The skin defect of the left groin was covered with tensor fascia lata myocutaneous flap. The patient is alive with no evidence of disease 30 months after the surgery.

Adult↗
PubMed1987

The histaminergic innervation of the mesencephalic nucleus of the trigeminal nerve in rat brain: a light and electron microscopical study.

Histaminergic fibers in the mesencephalic nucleus of the trigeminal nerve of Long-Evans rats were examined by light and electron microscopy after peroxidase-antiperoxidase immunocytochemical staining for histidine decarboxylase (HDC) as a marker. By light microscopy, neurons in the mesencephalic nucleus of the trigeminal nerve were seen to be surrounded by a number of HDC-like immunoreactive (HDCI) fibers, suggesting the presence of axo-somatic contact. This finding was supported by immunoelectron microscopic demonstration of synaptic contact of some HDCI fibers with the soma of the neurons in this nucleus. These findings indicate that histamine is involved in the sensory regulation of movement of the masticatory muscles at the level of the trigeminal mesencephalic nucleus.

Animals↗
PubMed1987

Immunocytochemical localizations of cytosolic and mitochondrial glutamic oxaloacetic transaminase isozymes in rat primary sensory neurons as a marker for the glutamate neuronal system.

The localization of cytosolic (s-) and mitochondrial (m-) glutamic oxaloacetic transaminase (GOT) was examined in the rat trigeminal, jugular and dorsal root ganglia by means of an indirect immunofluorescence method using antibodies specific for s- and m-GOT. Staining of s-GOT-like immunoreactivity was seen in giant, large, medium and small cells in these ganglia. On the other hand, m-GOT-like immunoreactivity was not seen in them. The distribution of GOT suggests that glutamate may be a transmitter released from primary sensory neurons.

Animals↗
PubMed1987

Role of thromboxane (Tx) A2 in guinea pig Forssman shock and the effect of OKY-046, Tx A2 synthetase inhibitor.

To study the role of thromboxane (Tx) A2 in Forssman systemic shock (FSS) in guinea pig, the effect of (E)-3-[p-(1H-Imidazol-1-ylmethyl)phenyl]-2-propenoic acid hydrochloride (OKY-046), a specific Tx A2 synthetase inhibitor, was studied. OKY-046 administered intravenously clearly prolonged survival time and protected against fatal shock. In shocked animals, definite decreases in serum complement hemolytic activity (CH50), leucocyte counts and platelet counts and an increase in lactate dehydrogenase (LDH) activity were observed. In addition, a significant increase of Tx B2 and incoagulability of blood were observed after shock. Whereas OKY-046 had no effect on the decreases in CH50, platelet counts and leucocyte counts, it inhibited the increase of Tx B2 and increased the amount of 6-keto PG F1 alpha. When Forssman antibody (half a lethal dose) was injected, a diphasic increase in airway resistance was observed. OKY-046 inhibited this diphasic increase in airway resistance. These data suggest a pathophysiological role for Tx A2 in FSS. OKY-046 inhibited the Forssman antibody induced respiratory disorders probably due to the inhibition of Tx A2 synthesis after shock.

Acrylates↗
PubMed1987

Effect of cinnarizine on IgE antibody-mediated experimental allergic reactions in guinea pigs.

The anti-allergic activity and mechanism of cinnarizine was investigated in guinea pigs. Nifedipine, a calcium antagonist, and tranilast, a potent, orally active anti-allergic agent, were used as comparative drugs. Cinnarizine protected against fatal systemic anaphylactic shock in guinea pigs passively sensitized with IgE antibody. Cinnarizine reduced many of the features of severe respiratory disorders. Nifedipine and tranilast showed similar effects. Cinnarizine and nifedipine inhibited the contractile response to antigen of sensitized tracheal smooth muscle when the challenge was carried out at low antigen concentrations. Tranilast showed a tendency to inhibit the antigen-induced contraction of tracheal smooth muscle. Cinnarizine and nifedipine inhibited Ca-induced contraction in potassium-depolarized tracheal smooth muscle, tranilast had no effect. Cinnarizine showed antagonistic action to the contraction by histamine or leukotriene D4 (LTD4) of tracheal muscle. Nifedipine showed similar antagonistic action, although its potency is lower than cinnarizine. Tranilast showed slight antagonistic action to LTD4. Antigen-induced release of histamine and slow reacting substance of anaphylaxis (SRS-A) from sensitized lung tissues was inhibited by nifedipine and tranilast but not by cinnarizine. The release of histamine and SRS-A from lung tissues by calcium ionophore A23187 was inhibited by nifedipine and tranilast but not by cinnarizine. These results suggest that the anti-allergic action of cinnarizine is mainly due to the antagonistic action to allergic mediators and not by interfering with the release of mediators. Cinnarizine's mechanism seems to be related to its antagonistic action to Ca in smooth muscle, but not to the transport of Ca in releasing the anaphylactic chemical mediators in mast cells and other target cells.

Animals↗
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

[Clinical study of ofloxacin (OFLX) on urinary tract infections].

Fifty-three patients with urinary tract infections (UTI) were treated with Ofloxacin, a new oral synthetic antimicrobial agent, and its clinical efficacy was studied. Ofloxacin (600 mg/day) was administered to 35 patients with acute simple cystitis for more than three days, and to 17 patients with complicated UTI for more than five days except a case in which the treatment was interrupted for side effects. Acute simple cystitis: In ten cases meeting the criteria of UTI committee, overall effectiveness rate was 100%. All of the 26 strains isolated from 26 patients disappeared after the treatment. In all of acute simple cystitis cases, 94.3% were evaluated as excellent or as moderate by attending doctors. Complicated UTI: In 11 cases treated during five or seven days, 63.6% of patients showed improvement on pyuria. Seven out of nine strains isolated from seven patients disappeared. However, two strains of P. aeruginosa and P. cepacia persisted after the treatment. In all of the complicated UTI cases, 38.9% of patients were evaluated as excellent or as moderate by attending doctors. Some slight side effects were observed in four out of 53 cases. This study showed that Ofloxacin is effective against urinary tract infections.

Acute Disease↗
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↗