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Biomedical subjects

M Terasawa

Publications and source records attributed to M Terasawa.

At least 73 records · Page 4Linked to original sources
PubMed1988

Effect of etizolam (Depas) on production of superoxide anion by platelet-activating factor and N-formyl-methionyl-leucyl-phenylalanine-stimulated guinea pig polymorphonuclear leukocytes.

Effect of etizolam on platelet activating factor (PAF) and N-formyl-methionyl-leucyl-phenylalanine (FMLP)-induced superoxide anion (O2-) production in guinea pig polymorphonuclear leukocytes (PMNL) was investigated. Etizolam showed the inhibitory effect on PAF-induced O2- production concentration dependently, with an IC50 value of 4.7 microM, but it had no inhibitory effect on FMLP-induced O2- production at 100 microM. These results suggest that etizolam has a selectively strong inhibitory effect on PAF-induced O2- production in guinea pig PMNL.

Animals↗
PubMed1988

Effect of cysteine ethylester hydrochloride (Cystanin) on host defense mechanism (IV): Potentiating effects on the function of peritoneal or spleen macrophages.

L-Cysteine ethylester hydrochloride (ethylcysteine; 30 mg/kg, p.o.) increased the number of la-positive cells (antigen presenting cells) in spleen adherent cells (SAC) and that of Lyt 1.2-positive cells (helper T cells), but not that of Lyt 2.2-positive cells (suppressor T cells) of C57BL/6 mice immunized with sheep red blood cells. The production of hemolytic plaque forming cells (HPFC) in spleens of syngeneic recipient mice was enhanced by the transfer of SAC or spleen lymphocytes of the donor mice pretreated with ethylcysteine. This drug augmented phagocytosis of yeast particles by peritoneal macrophages of ICR mice at concentrations of 1-100 microM. In ex vivo experiments, this drug (30 mg/kg, p.o.) augmented the phagocytosis of yeast particles by mouse macrophages and showed a tendency to increase the macrophage number in the peritoneal cavity. Ethylcysteine (30 mg/kg, p.o.) significantly accelerated the decrease of viable E. coli number in the liver of normal mice 2 and 48 hr after challenge. Furthermore, this drug at the same dose restored the suppression of the decrease of E. coli number in the blood and liver of mice treated with cyclophosphamide (200 mg/kg, i.p.). These results suggest that ethylcysteine augments the functions of macrophages in vitro and ex vivo, and these enhancing effects may lead to the enhancement of host resistance to infections in compromised hosts.

Adjuvants, Immunologic↗
PubMed1988

Chronic granulomatous disease with neutrophil membrane cytochrome b deficiency: demonstration by immunochemical staining with monoclonal antibody.

Cytochrome b deficiency in the peripheral granulocytes of two male patients with chronic granulomatous disease was demonstrated by an immunocytochemical assay using a monoclonal antibody, 7D5, against human neutrophil cytochrome b. A mosaic of cytochrome b positive and negative neutrophils, indicating a carrier state in an X-linked trait, was found in the mother of patient 1 but not in the mother of patient 2.

Antibodies, Monoclonal↗
PubMed1987

[Effect of pranoprofen on sodium urate crystal-induced inflammation].

Effect of a non-steroidal anti-inflammatory drug, pranoprofen (PPF), on sodium urate crystal-induced inflammation was investigated in comparison with standard drugs for treating acute gout in experimental animals. PPF inhibited sodium urate crystal-induced paw edema in both rats (1-10 mg/kg, p.o.) and mice (5-25 mg/kg, p.o.) in a dose-dependent manner. On rat sodium urate crystal-induced paw edema, PPF was found to be almost equally active as indomethacin (IM) and colchicine. In addition, PPF (2.5-10 mg/kg, p.o.) inhibited the accumulation of exudate and decreased the leucocyte numbers and the amount of prostaglandin E2 (PGE2)-like substance in sodium urate crystal-induced pleurisy in rats dose-dependently, with a potency slightly greater than that of IM. The specific anti-gout agent colchicine (5 mg/kg, p.o.) also suppressed the accumulation of exudate and decreased the leucocyte numbers, without affecting the amount of PGE2-like substance. Moreover, in mouse peritonitis, PPF (1-10 mg/kg, p.o.) suppressed the sodium urate crystal-induced increase in vascular permeability in a dose-dependent manner. Furthermore, in experimental models of articular gout, PPF inhibited the pain response (abnormal gait) of sodium urate crystal-induced arthritis in both rats (0.25 and 1 mg/kg, p.o.) and dogs (3 mg/kg, p.o.), with a potency greater than that of IM and phenylbutazone, respectively. These results indicate that as an anti-gout agent, PPF is at least as effective as other standard drugs, so that it should have good clinical potential.

Animals↗
PubMed1987

[Mechanism of the inhibitory effect of pranoprofen on sodium urate crystal-induced inflammation].

The mechanism of the inhibitory effect of pranoprofen on sodium urate crystal-induced inflammation was investigated with several inflammatory parameters using leucocytes stimulated with sodium urate crystals in vitro. At 10(-5) M, pranoprofen tended to inhibit the production of chemotactic factor in guinea pig polymorphonuclear leucocytes (PMNL) stimulated with sodium urate crystals and at 10(-4) M, significantly inhibited it. At 10(-3) M and 10(-4) M, it potentiated the chemotaxis of guinea pig PMNL. Furthermore, it inhibited the production of superoxide anion (O2-) in guinea pig PMNL stimulated with sodium urate crystals, with an IC50 value of 5.0 X 10(-4) M, comparable to that of indomethacin. At 10(-3) M, it inhibited the release of beta-glucuronidase stimulated by sodium urate crystals. From doses as low as 10(-6) M, it inhibited dose-dependently the production of PGE2-like substance by the phagocytosis of sodium urate crystals by rat peritoneal leucocytes, with an IC50 value of 7.5 X 10(-6) M. These results suggest that in inhibiting the production of PGE2 stimulated by sodium urate crystals, pranoprofen shows an inhibitory effect on sodium urate crystal-induced inflammation.

Animals↗
PubMed1987

Antagonistic activity of etizolam on platelet-activating factor in vivo experiments.

The ability of etizolam, 6-(o-chlorophenyl)-8-ethyl-1-methyl-4H-s-triazolo[3,4-c]thieno[2,3-e] [1,4]diazepine (Y-7131), an anti-anxiety drug, to inhibit platelet-activating factor (PAF)-induced reactions was investigated in experimental animals in vivo. Etizolam (0.01-0.3 mg/kg, i.v.) dose dependently inhibited PAF (0.3 microgram/kg, i.v.)-induced bronchoconstriction (Konzett and Rössler's method) in guinea pigs, but even at doses as large as 3 mg/kg, i.v., it had no effect on bronchoconstriction induced by histamine, serotonin, acetylcholine, arachidonic acid, bradykinin, angiotensin l or leukotriene D4. Etizolam (0.1-1 mg/kg, i.v.) also dose-dependently reversed PAF (1 microgram/kg, i.v.)-induced hypotension in anesthetized rats. Injection of PAF into the tail veins of mice produced lethal shock within 10-30 min. Etizolam (0.1-3 mg/kg, i.v. and 1-10 mg/kg, p.o.) protected against the lethal effect of PAF (75 micrograms/kg, i.v.) in a dose-dependent manner. These results indicate that etizolam specifically inhibits the action of PAF in vivo.

Animals↗
PubMed1987

An antagonistic activity of etizolam on platelet-activating factor (PAF). In vitro effects on platelet aggregation and PAF receptor binding.

The antagonistic effect of etizolam, an anti-anxiety drug, on platelet-activating factor (PAF) was investigated in rabbit platelets in vitro. Etizolam inhibited PAF-induced aggregation in a dose-dependent manner, with an IC50 of 3.8 microM, about one tenth that of triazolam (IC50 = 30 microM). At 300 microM, it inhibited both ADP and arachidonic acid-induced aggregation only slightly, while the other anti-anxiety drugs tested had no effect on PAF-induced aggregation even at this concentration. Etizolam and triazolam inhibited the specific binding of 3H-PAF to PAF receptor sites on washed rabbit platelets with IC50 values of 22 nM and 320 nM, respectively. Diazepam and estazolam were inactive even at 1 microM. These results indicate that etizolam is a specific antagonist of PAF.

Animals↗
PubMed1986

Relationship of exercise or pacing induced ST segment depression and myocardial lactate metabolism in patients with hypertrophic cardiomyopathy.

To elucidate a mechanism and clinical implications of chest pain and ST segment depression during exercise in patients with hypertrophic cardiomyopathy (HCM), we investigated myocardial lactate metabolism during atrial pacing in 18 patients with HCM and 7 control subjects with normal coronary arteriograms. At an average peak pacing rate of 146 beats/min, 11 patients with HCM showed the lactate extraction ratio decreasing to less than 5%, and 6 of them produced lactate, suggesting the development of myocardial ischemia. These 11 patients with abnormal lactate metabolism demonstrated ST segment depression (82%) and chest pain (73%) during pacing and also presented abnormal results (55%) on an exercise stress test. These abnormal findings were not observed in the other 7 patients who had ratios of 5% or more at peak pacing. These observations suggest that ST segment depression and chest pain are manifestations of myocardial ischemia even in patients with HCM who have normal coronary arteriograms, and that patients with pacing induced abnormal lactate metabolism are at an increased risk of developing myocardial ischemia during exercise.

Adolescent↗
PubMed1986

Trimethoprim interference in methotrexate assay by an enzyme inhibition assay kit.

Spurious methotrexate (MTX) concentrations in sera and cerebrospinal fluids from leukemia patients who were given trimethoprim (TMP) were estimated using an MTX assay kit which is based on its inhibition of dihydrofolate reductase. The interference of TMP with MTX was confirmed in the assay system. A concentration of 0.17 microgram/ml of TMP gave a value for an apparent MTX of 10 microM.

Diagnostic Errors↗
PubMed1986

Influence of Y-20003, an analgesic agent, on the endogenous opioid peptide system in rats.

Changes of endogenous opioid peptide system by pain stimuli were examined using adjuvant-induced arthritic rats. Following the 5th day after adjuvant inoculation, met-enkephalin (ME)-like peptide content in plasma decreased, while after the 12th day, the peptide content increased in adrenal medulla. A significant correlationship was found between pain threshold and plasma ME-like peptide content. Y-20003, a new nonsteroidal agent without inhibition of prostaglandin biosynthesis, showed an analgesic effect which was significantly antagonized by naloxone or Win 44,441-3, suggesting that endogenous opioid peptide system may be involved in the analgesic mechanism of Y-20003.

Adrenal Medulla↗
PubMed1986

[Factors related to the pathogenesis and clinicopathological findings in dilated cardiomyopathy].

It has been suggested that various factors related to dilated cardiomyopathy (DCM) may concern its onset and/or progression. This study was performed to clarify whether these factors contribute different clinical and morphological characteristics. Subjects were 39 patients with DCM, consisting of 28 men and 11 women whose average age was 46.5 years. The subjects were divided into five groups; namely, the Familial, Myocarditic, Alcoholic, Hypertensive, and Unknown Groups. Clinical parameters including past history, blood pressure, chest radiographs, electrocardiograms, echocardiograms and left ventricular end-diastolic pressures (LVEDP) were evaluated. Morphology of right ventricular endomyocardial biopsy specimens was evaluated in terms of hypertrophy, disarrangement, fibrosis, degeneration, endocardial thickening, interstitial changes, and types of fibrosis. The results were as follows: The Familial Group was characterized by the onset at younger age, highly elevated LVEDP, a lack of myocardial hypertrophy, and proliferation of small vessels. The Myocarditic Group was characterized by the onset at young age, elevated LVEDP, severe fibrosis showing a plexiform pattern in more than half of the patients, cellular disarrangement, and cellular infiltration. The Alcoholic Group showed possible improvement clinically and fatty infiltration in half of the patients. The Hypertensive Group was characterized by high prevalence of a previous alcohol intake, high diastolic blood pressure on admission, clinical improvement, and myocardial hypertrophy with a mild degree of perivascular fibrosis. From these findings, it is thought that each factor related to DCM offers a somewhat different clinical and histological profiles and that these factors may play an important role in the onset and/or progression of DCM. Furthermore, it is highly suggestive that specific therapy against these factors or the removal of these factors is especially necessary for favorable long-term prognosis of DCM.

Adolescent↗
PubMed1986

[Carnitine deficiency: a treatable cardiomyopathy].

This is a report of two brothers, six and five years of age, with systemic carnitine deficiency and cardiomyopathy, whose symptoms were improved after oral administrations of DL-carnitine. They had had progressive muscle weakness since three years of age. The elder brother's radiograph on admission showed cardiomegaly with a cardiothoracic ratio of 60%, and his electrocardiogram showed left ventricular hypertrophy and tall, peaked T waves in the precordial leads. The echocardiogram showed slight thickening of the cardiac muscle and decreased ejection fraction. Skeletal muscle biopsy specimens and sera were assessed for carnitine content. The skeletal muscle specimens revealed lipid storage myopathy, and the carnitine contents of the skeletal muscle and sera were both decreased. Myocardial biopsy for the elder brother revealed mitochondrial accumulation. Cardiomyopathy caused by carnitine deficiency is often fatal, but may be cured. Carnitine deficiency should be considered whenever a patient with cardiomegaly and progressive skeletal muscle weakness is encountered.

Cardiomyopathies↗
PubMed1985

[Anti-inflammatory effect of topically applied pranoprofen-gel].

The anti-inflammatory activity and mode of action of topically applied pranoprofen-gel were investigated in comparison with indomethacin-gel in experimental animals. Applied topically, 0.3 approximately 3% pranoprofen-gel inhibited carrageenin-induced paw edema, fracture-induced paw edema, carrageenin-induced increase in vascular permeability and adjuvant arthritis in rats and ultraviolet ray-induced erythema in guinea pigs dose-dependently, with a potency slightly greater than that of indomethacin-gel. In addition, pranoprofen-gel inhibited dose-dependently the formation of granuloma caused by a cotton pellet implantation, without affecting the weight of the thymus or adrenals and without inducing gastrointestinal lesions. Moreover, applied topically to carrageenin-treated rats, pranoprofen-gel inhibited dose-dependently, and more potently than indomethacin-gel, the production of a prostaglandin E2 (PGE2)-like substance in both the exudate of the carrageenin air pouch and the inflamed synovial membrane. Both drugs inhibited the potentiation of bradykinin-induced vascular permeability in rabbit skin by arachidonic acid, but not by PGE2. Pranoprofen was only one third as potent as indomethacin in inhibiting the production of PGE2 from the phagocytosing of killed bacteria by rat peritoneal leucocytes in vitro. These results show that pranoprofen-gel, applied topically, permeates well from the skin to the deep inflammatory site, relieving potently and long lastingly the inflammation by inhibiting PG production. As a topical anti-inflammatory agent, pranoprofen-gel is at least as effective as indomethacin-gel, so it may have good clinical use.

Administration, Topical↗
PubMed1985

[Effect of traxanox sodium on inflammatory response].

Traxanox was inactive against classic acute and subacute inflammation models such as carrageenin paw edema, UV erythema, 6-hr Evans blue-carrageenin (E-C) pleurisy and cotton pellet granuloma formation, and it failed to inhibit the production of prostaglandin E2 and a slow reacting substance from rat peritoneal leucocytes which phagocytize killed bacteria in vitro. On the other hand, traxanox inhibited the anaphylactoid reaction and decreased the pleural fluid in 24-hr E-C pleurisy. Traxanox (100 mg/kg, p.o.) also showed a tendency to suppress dextran edema and cotton pellet granuloma formation in adjuvant arthritis (AA) in rats. In experimental models of delayed type hypersensitivity (DTH), traxanox (100 mg/kg, p.o.) inhibited the accumulation of the exudate and the leucocyte migration in B. pertussis-induced pleurisy in rats. Traxanox (50 mg/kg) did not show any effect on AA in Lewis rats when administered orally for 21 days after the adjuvant inoculation, but the combined administration of traxanox with hydrocortisone (10 mg/kg, p.o.) or indomethacin (0.25 mg/kg, p.o.) resulted in a synergistic inhibition of AA. When the administration of traxanox was started 21 days before the adjuvant inoculation, it inhibited AA in a dose-dependent manner (50-100 mg/kg, p.o.). On the other hand, traxanox (100 mg/kg, p.o.) enhanced the concanavalin A-induced DTH-like skin reaction in guinea pigs. These results indicate that the mode of action of traxanox on inflammatory responses resembles that of D-penicillamine or levamisole, so that it may prove to be clinically effective in treating rheumatoid arthritis.

Anaphylaxis↗
PubMed1985

[Analgesic effect of topically applied pranoprofen-gel].

The analgesic effect of topically applied pranoprofen-gel (1% and 3%) was investigated in comparison with indomethacin-gel in experimental animals. Applied topically, 1% and 3% pranoprofen-gel inhibited the inflammatory pain induced by Randall and Selitto's method and the pain response (abnormal gait) of concanavalin A-induced arthritis in rats dose-dependently. Furthermore, in antigen (methylated bovine serum albumin)-induced arthritis in rats, pranoprofen-gel had a concentration and application-dependent therapeutic effect on knee joint swelling and the pain response. Pranoprofen-gel had a stronger analgesic effect than indomethacin-gel in these experimental models. Both drugs inhibited the flexor reflexes of the hind limb induced by injecting bradykinin (BK) in combination with arachidonic acid into the common iliac artery of the spinal rat, but failed to do so with BK combined with prostaglandin E2 (PGE2). Moreover, pranoprofen-gel inhibited the BK-induced increase in the firing rate of the saphenous nerve of the spinal cat. These results show that pranoprofen-gel, applied topically, permeates well from the skin to the nociceptor site, relieving the hyperalgesia caused by PGs-induced sensitization of pain receptors by inhibiting their production. As a topical anti-inflammatory and analgesic agent, pranoprofen-gel is at least as effective as indomethacin-gel, so that it should have good clinical potential.

Administration, Topical↗
PubMed1985

An advanced form of familial hypertrophic cardiomyopathy showing massive myocardial fibrosis with intramural small arterial thickening. An autopsy case.

An autopsy case of an advanced form of hypertrophic cardiomyopathy (HCM) showing marked fibrosis with intramural small arterial abnormalities is presented in this report. A 52-year-old woman, who had a positive family history of HCM, was admitted because of palpitations. The chest roentgenogram showed a mildly enlarged cardiac silhouette and the electrocardiogram revealed abnormal Q waves and R wave and T wave abnormalities. The echocardiogram revealed hypokinesis with thinning of the interventricular septum and the anterior wall of the left ventricle. Percutaneous right ventricular endomyocardial biopsies demonstrated moderate interstitial fibrosis with small arterial thickening. At necropsy, the anterior and posterior walls of the left ventricle and the interventricular septum were markedly thinned and showed a massive transmural fibrosis. Moreover, the intramural small arteries, 50-300 microns in diameter, showed marked intimal and medial hypertrophy with proliferation of elastic fibers and smooth muscle cells. From these findings, it is suggested that this was originally a case of HCM which progressed to a decompensated stage because of the abnormal intramural small arteries. The significance of small arterial lesions in HCM is discussed.

Cardiomyopathy, Hypertrophic↗