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Volume 105 (1995)
- Issue 6 Pages 423-
- Issue 5 Pages 273-
- Issue 4 Pages 191-
- Issue 3 Pages 127-
- Issue 2 Pages 41-
- Issue 1 Pages 1-
Volume 105, Issue 4
Displaying 1-6 of 6 articles from this issue
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Norimichi NAKAHATA1995 Volume 105 Issue 4 Pages 191-197
Published: 1995
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSThe most popular method for determining phosphoinositide hydrolysis is the analysis of watersoluble materials in cells or tissues that have been labeled with [3H] inositol by separating them on anion exchange open columns or HPLC columns. Recently, a radioreceptor assay has become available for the analysis of inositol 1, 4, 5-trisphosphate (IP3) using IP3 receptors and [3H] IP3; this allows the analysis of IP3 in vivo. On the other hand, radiolabeled phosphoinositides are measured by thin layer chromatography to analyze the breakdown or synthesis of phosphoinositide in response to stimuli. The purified enzyme with phospholipid vesicles can be used to hydrolyze [3H] phosphatidylinositol 4, 5-bisphosphate (PIP2) to [3H] IP3, which makes it possible to search for direct action of a drug on phospholipase C.View full abstractDownload PDF (4382K) -
Yukihiro ISOGAI, Masayuki HORI1995 Volume 105 Issue 4 Pages 199-208
Published: 1995
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSTo elucidate the effect of calcitonin on humoral hypercalcemia of malignancy (HHM), we studied the effect of elcatonin, a synthetic eel calcitonin analog, on plasma calcium concentration in hypercalcemic nude mice transplanted subcutaneously with FA-6 pancreas cancer cells and hypercalcemic mice produced by continuous infusion of parathyroid hormone-related peptide (PTHrP). Elcatonin proved to exert a potent hypocalcemic effect in either model for hypercalcemia. The effect reached peaks at 2 hr after its administration, and it was no longer detected at 24 hr. The dose-dependent effects of a single administration of elcatonin were studied in the FA-6 tumor-bearing mice: the hypocalcemic effect of elcatonin at 1-2 hr after administration was dose-relatedly augmented. The effect of daily administration of elcatonin was further studied in the FA-6 tumor-bearing mice: 5-Day daily administration of elcatonin was not accompanied by reduction in its hypocalcemic effect. Moreover, it was suggested that higher the efficacy of elcatonin, the higher were the plasma calcium concentrations in the tumor-bearing mice. These results indicated that elcatonin exerts an immediate hypocalcemic effect even on models for acute and severe hypercalcemia such as FA-6 tumor-bearing mice, that this hypocalcemic effect became more potent depending on their elevation of plasma calcium concentration, and that elcatonin exerts a hypocalcemic effect even on a model for hypercalcemia due to PTHrP, a presumable causative substance of HHM.View full abstractDownload PDF (7033K) -
Tsugio NAKATSU1995 Volume 105 Issue 4 Pages 209-219
Published: 1995
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSThe effect of cepharanthin on the enhancement of mitogen-induced histidine decarboxylase (HDC) activity in mice spleens and the effect of histamine on the production of cytokines were investigated. Cepharanthin enhanced LPS-induced HDC activity in normal mice spleens and also enhanced it in genetically T cell-deficient nude mice spleens and T and B cell-deficient scid mice spleens. Therefore, cepharanthin can exert its effect on macrophages without T cells or B cells. Cepharanthin enhanced LPS-induced cytokine production by macrophages. Histamine induced cytokine production and enhanced LPS-induced cytokines production by macrophages. However, diphenhydramine and cimetidine, histamine receptor antagonists, did not block this process. Alpha-fluoromethylhistidine, a suicide inhibitor of HDC, suppressed LPS-induced cytokine production. These results suggest that cytokine production by macrophages is regulated by both histamine added exogenously and histamine induced by macrophages themselves and that histamine participates in enhancement of cytokine production by cepharanthin.View full abstractDownload PDF (7173K) -
Akihiko SUZUKI, Masaichiro HAGINO, Naohiro YASUDA, Kenji SAGAWA, Tamiy ...1995 Volume 105 Issue 4 Pages 221-229
Published: 1995
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSThe effects of PGE1CD on dimethylnitrosamine (DMN)-induced acute liver damage with intravascular coagulation in rats were biochemically and histopathologically investigated. PGE1·CD was administered i.v. from 30 min before to 24 hr after DMN-intoxication (pretreatment) and from 30 min after or from 4 hr after to 24 hr after DMN-intoxication (post-treatment). Pretreatment with PGE1·CD (0.2-2 μg/kg/min) dose-dependently suppressed the decrease of platelet counts and the elevation of blood biochemical parameters (PT, HP T, GOT, GPT, LDH, LAP, T-Bil) caused by DMN-intoxication. PGE1·CD (0.51 μg/kg/min and over) significantly suppressed the DMN-induced histopathological changes (occurrence of hemorrhage and necrosis). Post-treatment with PGE1·CD (2 μg/kg/min) also suppressed the liver damage. Furthermore, pretreatment with PGE1·CD (2 μg/kg/min) not only suppressed the disruption of hepatocytes, but also prevented the damages of sinusoidal endothelial cells and lysosomal membrane, and it reduced the increase of lipid peroxidation. PGE1·CD (1 μg/kg/min and over) significantly suppressed the decrease of hepatic tissue blood flow caused by DMN-intoxication. These results demonstrate that PGE1·CD has therapeutically efficacy against DMN-induced acute liver damage in rats; Therefore, it will be clinically useful for the treatment of severe hepatitis such as fulminant hepatitis with intravascular coagulation in the sinusoid.View full abstractDownload PDF (7071K) -
Niro INABA, Masahiro SHIBATA, Sadayoshi ONODERA, Masato TANAKA, Takao ...1995 Volume 105 Issue 4 Pages 231-241
Published: 1995
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSThe present study was conducted to investigate the histamine H2-receptor antagonistic property of FRG-8813 by using isolated guinea pig right atria, gastric cells and cerebral cortex preparations. FRG-8813 inhibited the histamine-induced positive chronotropic response of the right atria and shifted the concentration-response curve of histamine to the right with suppression of the maximal response. Although the inhibitory effect of FRG-8813 was enhanced in a time-dependent manner and long-lasting, the antagonism was reversible. The potency of FRG-8813 was 2 times and 50 times greater than those of famotidine and cimetidine, respectively. FRG-8813 decreased the histamine-induced [14C] aminopyrine accumulation in gastric cells. Schild plot analysis showed that the slopes of FRG-8813, famotidine and cimetidine were 1.56, 1.40 and 1.07, respectively, suggesting that the mode of the antagonism of FRG-8813 is also unsurmountable in gastric cells. The lack of effect on dbcAMP and bethanechol-induced [14C] aminopyrine accumulations indicated the selectivity of FRG-8813 for histamine H2-receptor. As in the right atria, the potency of H2-antagonism was 1.5 times and 40 times greater than those of famotidine and cimetidine, respectively. In the [3H] tiotidine binding study of the cerebral cortex preparation, the Ki values showed that the affinity of FRG-8813 was 2 times and 80 times more potent than those of famotidine and cimetidine, respectively. In conclusion, FRG-8813 is an unsurmountable and selective histamine H2-receptor antagonist with 2 times greater potency than famotidine. The antagonistic activity is reversible in spite of the time-dependent increase of the antagonism.View full abstractDownload PDF (7914K) -
Toshinori HIDAKA, Mayumi FURUYA, Yoshihiro TANI, Tomochika OHNO1995 Volume 105 Issue 4 Pages 243-261
Published: 1995
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSWe examined the hemodynamic and neurohumoral effects of carperitide in dogs with low-output heart failure (LHF) produced by volume expansion, ligation of the left anterior descending coronary artery and methoxamine infusion. Carperitide (0.1 ?? 1 μg/kg/min, i.v. infusion for 30 min) decreased pulmonary arterial pressure, right atrial pressure and systemic vascular resistance and increased cardiac output. These pharmacological activities were equivalent to those of nitroglycerin (NG, 3 μg/kg/min). Although most of the animals did not excrete urine after induction of LHF, carperitide, unlike NG, increased urine volume. The plasma level of cyclic GMP was elevated about three times by induction of LHF and further increased after treatment with carperitide (1 μg/kg/min). Carperitide had no effects on plasma renin activity, plasma aldosterone concentration and plasma noradrenaline. These results taken together indicate that carperitide reduces both preload and afterload in association with an increase in cyclic GMP production and improves the untoward hemodynamic alterations in LHF dogs.View full abstractDownload PDF (12020K)
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