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Volume 99 (1992)
- Issue 6 Pages 381-
- Issue 5 Pages 267-
- Issue 4 Pages 191-
- Issue 3 Pages 123-
- Issue 2 Pages 63-
- Issue 1 Pages 1-
Volume 99, Issue 2
Displaying 1-7 of 7 articles from this issue
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The histaminergic neuron system in the brainHiroshi WADA1992 Volume 99 Issue 2 Pages 63-81
Published: February 01, 1992
Released on J-STAGE: September 07, 2011
JOURNAL FREE ACCESSThe histaminergic neuron system in the brain has been well-characterized in the last twenty years. This article describes the studies performed by our research groups and discusses the physiological functions of the histaminergic neurons. To demonstrate the distribution of neuronal antibodies against histidine decarboxylase (HDC), the sole enzyme responsible for histamine formation, was used, although the purification of the HDC from fetal rat liver was a difficult task. It took five years to purify the enzyme and another five years to obtain specific antibody suitable for immunohistochemistry. The cell bodies were located in the tuberomammillary nucleus of the posterior hypothalamus. The clusters of cell bodies were designated as E1-5 groups. The fibers that projected from the neurons were distributed in almost all parts of the brain, especially densely in the anterior hypothalamus. α-Fluoromethylhistidine, a specific inhibitor of HDC, is a powerful tool for reducing the neuronal histamine in the brain. Administration of α-fluoromethylhistidine led to changes in various activities of the brain such as arousal state, circadian rhythm, neuroendocrine functions, feeding behavior, body temperature, and vestibular function. These results indicate that the histaminergic neuron system regulates a wide range of physiological functions in the brain by targetting both neurons and glial cells, on which we found histamine H1 and H2 receptors. The molecular structure of the H1-receptor was also discussed.View full abstractDownload PDF (6854K) -
Hideo TSUKAGOSHI, Motohiro KUROSAWA1992 Volume 99 Issue 2 Pages 83-91
Published: February 01, 1992
Released on J-STAGE: September 07, 2011
JOURNAL FREE ACCESSProstaglandin D2 (PGD2) and thromboxane A2 (TXA2) have been suggested to play important roles in the pathogenesis of bronchial asthma. In the present study, effects of i.v.-administration of PGD2 on bronchial hyperresponsiveness in guinea pigs were investigated by the measurement of dynamic compliance and dynamic respiratory resistance with formulae which can exclude the effects of changes of the airway wall thickness.With these formulae, the ratio of bronchial smooth muscle constriction by histamine can be estimated as an index of bronchial hyperresponsiveness. Administration of PGD2 induced airway wall edema. The ratio of bronchial smooth muscle constriction by histamine was enhanced with the administration of PGD2. Moreover, TXA2 antagonists, ONO-NT-126 and ONO-8809, inhibited the effect of PGD2 administration.View full abstractDownload PDF (1076K) -
Kanehiro GHODA, Katsuaki KATO, Yuji NAGAO, Tetsuo OKA1992 Volume 99 Issue 2 Pages 93-107
Published: February 01, 1992
Released on J-STAGE: September 07, 2011
JOURNAL FREE ACCESSWe investigated the effect of ulinastatin, a candidate anti-osteoarthritic drug, in comparison with indomethacin and triamcinolone, two well-known drugs for osteoarthritis, on IL-1 production by monocytes, proteoglycan synthesis by chondrocytes and superoxide generation by leukocytes. Ulinastatin, a glycoprotein purified from human urine, suppressed both the IL-1 production and the IL-1 induced reduction of proteoglycan synthesis. In addition, ulinastatin inhibited superoxide generation. These actions of ulinastatin seemed to be related to its inhibitory actions against serine proteases such as trypsin, a-chymotrypsin, plasmin, leukocyte elastase and leukocyte cathepsin G. Triamcinolone suppressed the IL-1 production more potently than ulinastatin and it also suppressed the IL-1 induced reduction of proteoglycan synthesis. Triamcinolone alone, however, reduced the proteoglycan synthesis, and it did not affect the superoxide generation. In contrast, indomethacin had no effect on proteoglycan synthesis and superoxide generation, although it accelerated the IL-1 production. These results indicate that these three drugs have different mechanisms of action on the factors involved in the pathogenesis of osteoarthritis. Since ulinastatin has broad actions, which are considered to be beneficial for preventing some process of osteoarthritic pathogenesis, ulinastatin is expected to be an useful drug for the treatment of osteoarthritis.View full abstractDownload PDF (9085K) -
Emiko FUJII, Teruko NOMOTO1992 Volume 99 Issue 2 Pages 109-114
Published: February 01, 1992
Released on J-STAGE: September 07, 2011
JOURNAL FREE ACCESSUsing streptozotocin (STZ) -diabetic mice, we examined the respiratory distress induced by arachidonic acid. Male ddY mice were made diabetic by injecting STZ (170mg/kg, i.p.) 2 weeks prior to the experiment. Control mice received the vehicle (citrate buffer, pH 4. 6). The duration of respiratory distress was observed by a slow i.v.-injection of sodium arachidonic acid (AA) into the caudal vein of mice at the dose of 50mg/kg. Aspirin was i.p.-administered 30 min before AA. OKY-046 (specific thromboxane A2 (TXA2) synthetase inhibitor), OP-41483 (stable prostacyclin analog) and 9, 11 epithia-11, 12-methano-TXA2 (STA2, stable TXA2 analog) were i.v.-administered 30 min before AA. The duration of respiratory distress induced by AA was significantly reduced in STZ-diabetic mice. Aspirin (10-50 mg/kg) and OKY-046 (25-100mg/kg) enhanced the AA-induced respiratory distress in STZ-diabetic mice. OP-41483 (1-100μg/kg) reduced the AA-induced effect in both control and STZ-diabetic mice. STA2 (10μg/kg) enhanced the AA-induced effect in both control and STZ-diabetic mice. ONO-1078 (1-10mg/kg) did not affect the AA-induced effect in both control and STZ-diabetic mice. TMK-688 (0.01-1mg/kg) reduced the AA-induced effect in the control mice, but not in the STZ-diabetic mice. These results suggest an involvement of leukotriene in the respiratory response to AA in diabetic mice, especially when cyclooxygenase and TXA2 synthetase are inhibited.View full abstractDownload PDF (1388K) -
Makoto MAYANAGI, Sadao NAKAYAMA, Katsuji OGUCHI1992 Volume 99 Issue 2 Pages 115-121
Published: February 01, 1992
Released on J-STAGE: September 07, 2011
JOURNAL FREE ACCESSEight kinds of hot water extracts (HWE) and 2 kinds of distanninized fractions (DTF) from Umbellzferae herbs were prepared. The effects of HWE and DTF on rat hepatic lipid peroxidation (LPO), aminopyrine N-demethylase (APD) and aniline hydroxylase (ANH) activities were examined in vitro. The APD activity was inhibited by HWE, DTF from Byakushi and HWE from Uikyo, Zenko, Toki, Senkyu, Bofu and Saiko, respectively, whereas DTF from Uikyo caused no significant effect. The ANH activity was inhibited by HWE, DTF from Byakushi, Uikyo and HWE from Bofu, Zenko, Hokushajin and Toki, respectively. LPO was inhibited by HWE from Zenko, Byakushi and Senkyu, but increased by Saiko, Uikyo, Bofu and Hokushajin. The results of Uikyo DTF suggests that the components of Uikyo that altered the activity of APD and ANH are different respectively. Marked inhibitions on the activity of APD and ANH caused by Byakushi indicate that Byakushi might affect the activity of hepatic drug metabolizing enzymes in vivo.View full abstractDownload PDF (1092K) -
1992 Volume 99 Issue 2 Pages b1-b24
Published: February 01, 1992
Released on J-STAGE: September 07, 2011
JOURNAL FREE ACCESSDownload PDF (4020K) -
1992 Volume 99 Issue 2 Pages b25-b49
Published: February 01, 1992
Released on J-STAGE: September 07, 2011
JOURNAL FREE ACCESSDownload PDF (4459K)
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