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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 6
Displaying 1-7 of 7 articles from this issue
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Tadashi FUJITA, Yohko FUJIMOTO1992 Volume 99 Issue 6 Pages 381-389
Published: 1992
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSThe mechanisms of formation and removal of active oxygen species and lipid peroxides in biological systems have been briefly reviewed. Cytotoxic active oxygen species can be classified into two types: (a) radical species such as O2-· (superoxide) and HO·(hydroxyl radical) and (b) non-radical species such as H2O2 (hydrogen peroxide) and 1O2 (singlet oxygen). The direct or indirect attack of active oxygen species on polyunsaturated fatty acids, essential constituents of biological membranes, has been shown to result in the formation of a number of peroxidative lipid breakdown-products: LOOH (lipid hydroperoxide), LOO·(lipid peroxyl radical) and LO·(lipid alkoxyl radical). The lipid peroxide decomposition is probably dependent on the presence of ferric-ferrous ions. These processes are called lipid peroxidation reactions. In recent years, there has been a renewed interest in the role played by lipid peroxidation in many disease states. The multiple lines of defense against toxic oxygen intermediates consist of enzymatic systems, glutathione peroxidase, catalase and superoxide dismutase, and furthermore involves antioxidant capacities such as those of vitamin E and vitamin C. In biological systems, there are naturally occurring lipid-soluble (vitamin E and ubiquinone) and water-soluble (vitamin C, reduced glutathione and uric acid) antioxidants. Therefore, so long as homeostasis is maintained between the rate of radical generation and the rate of radical dissipation, the cellular generation of radicals may not be harmful. In contrast, this balance can be disturbed if cellular defenses are decreased or if there is a significant increase in the flux of radical generation. Once lipid peroxidation is initiated, the reactive intermediate formed induces cell damage. However, the mechanism of initiation of the lipid peroxidation process in biological systems is still uncertain.View full abstractDownload PDF (8130K) -
Tomohisa HATTORI, Satoko YAMADA, Kazuya FURUTA, Tadashi NAGAMATSU, Mik ...1992 Volume 99 Issue 6 Pages 391-399
Published: 1992
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSEffects of pherodendrin (OB-5) on anti-GBM nephritis were investigated. OB-5 (50 mg/kg/day, i.p.) prevented the urinary protein excretion in original and crescentic-type anti-GBM nephritis in rats. In addition, OB-5 also inhibited the elevation of serum creatinine, urea nitrogen and cholesterol contents in both models of nephritis. Histopathological observations indicated that OB-5 prevented the hypercellularity, crescent formation, adhesion and fibrinoid necrosis in the glomeruli of nephritic rats. OB-5 and cyclosporine A, a positive control drug, prevented the increase in the number of OX-l, CD8 and ED-1 positive cells in the glomeruli. These results indicated that OB-5 may be effective in human glomerulonephritis, and antinephritic mechanisms of OB-5 may be due to its inhibition of the activation of macrophages or cytotoxic T cells.View full abstractDownload PDF (7233K) -
Tetsuaki YAMAURA, Masahiro SHIBATA, Niro INABA, Sadayoshi ONODERA, Yur ...1992 Volume 99 Issue 6 Pages 401-410
Published: 1992
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSWe examined the anti-ulcer effects of FRG 8813, a new type histamine H2-receptor antagonist, on various experimental gastric and duodenal lesions in rats. FRG-8813, administered orally, inhibited the formation of lesions dose-dependently in experimental models with the exception of the Shay ulcer model. The anti-ulcer potency of FRG-8813 was 4 ?? 10 times greater than that of cimetidine when the ED50 values of both compounds were compared. Famotidine and cimetidine inhibited lesion formation at higher doses than the anti-secretory doses. The anti-ulcer action of FRG-8813, however, appeared at even lower doses than those of anti-secretory action. These results suggest that FRG-8813 is able to prevent lesion formation with anti-secretory action plus other mechanisms unlike typical histamine H2-receptor antagonists.View full abstractDownload PDF (7242K) -
Tetsuaki YAMAURA, Masahiro SHIBATA, Yuriko CHIDA, Niro INABA, Sadayosh ...1992 Volume 99 Issue 6 Pages 411-420
Published: 1992
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSWe examined the anti-ulcer effects of FRG 8813, a new-type histamine H2-receptor antagonist, in chronic ulcer models of rats and mice (W/Wv). FRG-8813, given orally twice a day for 7 days, accelerated the healing of gastric or duodenal ulcer induced by acetic acid injection or application at the non-antisecretory doses (0.3 ?? 3 mg/kg). Administration of FRG-8813 to rats with ulcers increased the amounts of mucus in the gastric mucosa. These actions of FRG-8813 were more potent than those of famotidine or cimetidine. In W/Wv mice, several ulcers spontaneously developed on gastric mucosa during the 8 weeks after the birth. The ulcers were aggravated by several unknown factors after the ulcer generation in W/Wv mice. The aggravation of ulcers was inhibited by the 4-week administration of FRG-8813 with diet at the dose of 1 or 10 mg/kg/day, but was not inhibited by cimetidine at the dose of 100 mg/kg/day. From these results, we suggest that FRG-8813 is able to accelerate the healing of ulcers by antisecretory plus increasing actions on the integrity of the gastric mucosal defense mechanisms; therefore FRG-8813 is expected to be a useful drug for the treatment of gastric or duodenal ulcers in humans.View full abstractDownload PDF (8934K) -
Hideto OHHARA, Kohei SAWADA, Toshiaki OGAWA, Mikio TAKEDA, Toshiji IGA ...1992 Volume 99 Issue 6 Pages 421-433
Published: 1992
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSIn anesthetized dogs, loprinone hydrochloride (LP, 10-100 μg/kg, i.v.) dose-relatedly increased cardiac contractility (LV dP/dt max), enhanced cardiac index and decreased systemic vascular resistance with relatively small reduction in mean aortic pressure (MAP) and a mild increase in heart rate (HR). LP also decreased left ventricular internal diameter (ID), increased fractional shortening (LVFS) and caused a leftward shift and an increase in the slope of the LV end-systolic pressure-ID relation. In the heart failure models induced by propranolol, LP rapidly reversed the cardiac depression and the enlargement in cardiac size. The extent of changes in MAP and HR by LP was smaller than those observed with several other cardiotonic agents. In guinea pig cardiac muscles, LP (10-6 ?? 10-4 M) produced a concentration-related increase in contractile force and the maximum rate of rise of Ca2+-action potential. In the sinus nodes, LP induced a concentration-related decrease in action potential duration and increase in the slope of slow diastolic depolarization, resulting in an increase in beating rate. These influences of LP on sinus nodes were smaller than those of milrinone. These results indicate that LP increases LVFS, reduces cardiac size and improves the heart failure due to its cardiotonic and vasodilating properties. Moreover, electrophysiological studies suggest that at least a part of the lower chronotropic effects of LP may be due to the mildness of its direct stimulating effects on sinus nodes.View full abstractDownload PDF (10352K) -
Masako KUROKAWA, Akihisa MORI, Shizuo SHIOZAKI, Tomoyuki KANDA, Rika Y ...1992 Volume 99 Issue 6 Pages 435-443
Published: 1992
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSWe examined the effect of KW 6055 (α-(p-butyrylamino-o-nitrobenzyl) pyridinel, which has antiamnesic activity, on the central cholinergic systems of rat frontal cortex using in vivo brain microdialysis. 1) KW-6055 (40, 160 mg/kg, p.o.) increased the extracellular level of ACh in normal rats (257 ± 23, 202 ± 24%). The stimulating effect of KW-6055 on ACh release was abolished by tetrodotoxin treatment, supporting that the released ACh was due to neuronal firing. Reserpine pretreatment decreased the effect of KW-6055, indicating that KW-6055 acted on cholinergic neurons through catecholaminergic neurons. 2) In basal forebrain-lesioned rats, KW-6055 (40 mg/kg, p.o.) significantly increased the extracellular level of ACh (251±22%) for more than 2 hr, which was longer than in normal rats. In conclusion, these results suggest that the stimulating activity on ACh release may be involved in the mechanism of the antiamnesic effects of KW-6055.View full abstractDownload PDF (7553K) -
Hideki IMOKAWA, Kazumasa ANDO, Takako KUBOTA, Emiko ISONO, Hajime INOU ...1992 Volume 99 Issue 6 Pages 445-450
Published: 1992
Released on J-STAGE: February 13, 2007
JOURNAL FREE ACCESSThe kinetics of bradykinin derived from localized thermal injury on vascular-permeability were investigated in mice with experimental ear burn. The leakage of plasma into the ear tissue by accelerated vascular-permeability reached the maximum at 3 hr and decreased gradually until 6 hr after the thermal injury. The contents of bradykinin increased by the thermal injury and the increment continued up to 24 hr. Although the bradykinin contents in the burned ear decreased by using a protease inhibitor, the hyperpermeability of injured ear vessels was unchanged by protease inhibitors. These results suggest that bradykinin is concerned with the pain reaction rather than vascular-permeability.View full abstractDownload PDF (5369K)
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