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Volume 84 (1984)
- Issue 6 Pages 471-
- Issue 5 Pages 411-
- Issue 4 Pages 327-
- Issue 3 Pages 259-
- Issue 2 Pages 155-
- Issue 1 Pages 1-
Volume 84, Issue 5
Displaying 1-6 of 6 articles from this issue
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Enhancement effect of bacterial pyrogen on the fetal toxicity of salicylic acidTakafumi ITAMI, Seizaburo KANOH1984 Volume 84 Issue 5 Pages 411-416
Published: 1984
Released on J-STAGE: March 07, 2007
JOURNAL FREE ACCESSWe reported previously that the acute and fetal toxicities of aspirin (ASA) were enhanced by bacterial endotoxin (LPS). In order to clarify the mechanism of the enhancement by LPS, the effects of LPS on the toxicities of salicylic acid (SA), the main metabolite of ASA, were investigated in rats. The following results were obtained: 1) The acute toxicity of SA was significantly potentiated by LPS in male rats. The LD50 of SA with LPS was about one third of that of SA alone. 2) The increase of maternal body weight was inhibited significantly after administration of SA (383 mg/kg, p.o.) with LPS (20 μg/kg, i.v.), but not after administration of SA alone. 3) The fetal toxicity of SA including fetal death, resorption, growth retardation and skeletal variations was slightly observed in the dam receiving a single dose of SA on the 15th day of pregnancy, but it was markedly increased by LPS (20 μg/kg, i.v.). 4) The half-life period of SA in plasma was increased significantly by the coadministration of LPS in male rats after administration of ASA or SA. All of these phenomena in the rats given SA closely resembled the phenomena previously reported in the rats given ASA. These results suggest that SA might play a main role in the acute and fetal toxicities of ASA, and one of the mechanism of the enhancement effect by LPS on ASA-induced fetal toxicity might be related to the increase of SA concentration in the fetus.View full abstractDownload PDF (3131K) -
IV. Effects on coagulation, platelets and fibrinolysisYoshiko KOSHIYAMA, Masayuki OZEKI, Akemi MOTOYOSHI, Mitsunobu FUJITA, ...1984 Volume 84 Issue 5 Pages 417-428
Published: 1984
Released on J-STAGE: March 07, 2007
JOURNAL FREE ACCESSInhibitory effects of FUT-175 (nafamstat mesilate) on coagulation, platelets and fibrinolysis were examined. 1) FUT-175 prolonged activated partial thromboplastin time, thrombin time and prothrombin time in rabbit plasma. 2) FUT-175 prolonged these coagulation times in human plasma at lower concentration than in rabbit plasma. 3) FUT-175 inhibited platelet aggregation induced by a variety of aggregation agents in rabbit plateletrich plasma (PRP). 4) In human PRP, FUT-175 inhibited platelet aggregation induced by a variety of aggregation agents at lower concentration than in rabbit PRP. 5) Lipopolysaccharide induced a dose-dependent platelet aggregation in dog PRP. FUT-175 showed an inhibitory effect on this aggregation. 6) FUT-175 inhibited clot retraction in rabbit plasma. 7) The fibrinolysis activity was measured on fibrinolysis of rabbit plasma activated by urokinase. FUT-175 prolonged this fibrinolysis time. 8) Inhibitory effects on coagulation and fibrinolysis were also found ex vivo. 9) FUT-175 prolonged bleeding time in mice. These results indicate that FUT-175 has potent inhibitory effects on coagulation, platelets and fibrinolysis.View full abstractDownload PDF (4925K) -
Yutaka GOMITA, Yasuyuki ICHIMARU, Minehiro MORIYAMA1984 Volume 84 Issue 5 Pages 429-439
Published: 1984
Released on J-STAGE: March 07, 2007
JOURNAL FREE ACCESSEffect of amantadine, an adamantane derivative, was investigated on intracranial self-stimulation behavior and cerebral glucose utilization (CGU) in rats. The experiments were performed on Wistar strain male rats. The low rate responses induced by low current brain stimulation on lateral hypothalamic self-stimulation behavior in a Skinner box were increased by p.o. administration of amantadine at doses of 5 and 10 mg/kg, but were decreased at doses of over 50 mg/kg. Amantadine at doses of 5 and 10 mg/kg, p.o., increased the running speed in run-way performance of animals rewarded with electric stimulation of the medial forebrain bundle in the lateral hypothalamus. On a “conflict” situation induced by combining the hypothalamic selfstimulation with midbrain dorsal central gray stimulation in a Skinner box, amantadine at doses of 5 and 10 mg/kg, p.o. caused an increase of lever pressing in the unpunished period without affecting the punished responses. The CGU measured by [14C] 2-deoxyglucose autoradiography was increased by i.p. administration of 5 mg/kg. In addition, amantadine at a dose of 5 mg/kg, i.p., decreased the high optic density in bilateral habenulae induced by pimozide at 0.75 mg/kg, i.p. These results indicate that amantadine facilitates the intracranial self stimulation behavior related to a dopaminergic mechanism at low doses, and inhibits the high local CGU of bilateral habenulae induced by pimozide.View full abstractDownload PDF (5034K) -
Tadao NAKAMURA, Tatsumi TSUMAGARI1984 Volume 84 Issue 5 Pages 441-451
Published: 1984
Released on J-STAGE: March 07, 2007
JOURNAL FREE ACCESSThe effects of nizofenone, a new compound with cerebral protective properties, were compared with those of quinidine on various types of experimental arrhythmia in dogs. Pretreatment with nizofenone (3 and 10 mg/kg, i.v.) markedly increased the amount of ouabain needed to cause cardiac toxicity in pentobarbital-anesthetized dogs, to the same degree as quinidine (10 mg/kg, i.v.). Nizofenone (1, 3 and 10 mg/kg, i.v.) was effective in reversing established ouabain-induced ventricular tachycardia in pentobarbital-anesthetized dogs. In contrast quinidine (3 and 10 mg/kg, i.v.) showed only weak activity in this test. Nizofenone (3 and 10 mg/kg, i.v.) significantly reduced the ectopic ventricular rate in pentobarbital-anesthetized dogs 24 hr after a two-stage ligation of the anterior descending coronary artery. Quinidine (10 mg/kg, i.v.), however, was more potent in this test. In addition, nizofenone, like quinidine, caused hypotension and bradycardia and prolonged the electrocardiogram QTc interval. On the other hand, nizofenone (1 and 10 mg/kg, i.v.) was inactive against epinephrine-induced arrhythmias in halothane-anesthetized dogs. Quinidine (10 mg/kg, i.v.) was effective in this test and also antagonized the pressor response induced by epinephrine. The effects of quinidine on adrenergically-induced arrhythmias are considered to be mediated through a blocking of the adrenergic α-receptors. Nizofenone did not show the adrenergic a-receptor blocking effect. Accordingly, the above findings suggest that the antiarrhythmic action of nizofenone may result from depressant effects on the cardiovascular system and from a membranestabilizing effect.View full abstractDownload PDF (5181K) -
(1). Nephrotoxicity of gentamicin and mercuric chlorideRyoji KOJIMA, Yoshio SUZUKI1984 Volume 84 Issue 5 Pages 453-462
Published: 1984
Released on J-STAGE: March 07, 2007
JOURNAL FREE ACCESSThe present study was designed to find useful markers for detection of renal damage due to gentamicin (GM). Following the administration of 80 mg/kg GM, there were singificant increases in urinary protein contents and alkaline phosphatase, N-acetyl-β-glucosaminidase, lactate dehydrogenase, γ-glutamyl transpeptidase and lysozyme activities. Alterations of these parameters had a peak at the 7th or 10th day and values restored to near normal levels by the 15th day. Light microscopic observations of the kidney on the 10 th day showed mainly the necrosis of proximal tubular epithelial cells in the renal outer cortex, and there was regeneration of epithelial cells on the 15th day. In addition, when 1 mg/kg HgCl2 was given to rats, there were increases in urinary enzyme activities and protein contents, and BUN. The kidney of rats that received HgCl2 showed the necrosis of tubular epithelial cells in the renal inner cortex. It is considered from these results that determination of the activities of various urinary enzymes may be useful markers to detect tubular damage induced by GM.View full abstractDownload PDF (5267K) -
Protective effect of latamoxef against gentamicin nephrotoxicityRyoji KOJIMA, Yoshio SUZUKI1984 Volume 84 Issue 5 Pages 463-469
Published: 1984
Released on J-STAGE: March 07, 2007
JOURNAL FREE ACCESSEffects of gentamicin (GM) alone and in combination with latamoxef (LMOX), an oxacefem antibiotic, were studied in rat kidney in order to determine the effect of combinations of nephrotoxic drugs. Groups of 7 male Sprague-Dawley rats, weighing approx. 230 g, were given daily s.c. doses of GM (80 mg/kg) or 80 mg/kg GM plus LMOX (500, 1000 or 2000 mg/kg) for 15 days. Treatment with GM alone resulted in marked increases in urinary lactate dehydrogenase, N-acetyl-β-glucosaminidase and lysozyme activities, urinary protein contents and blood urea nitrogen contents, which peaked on the 10th day. The combination of GM plus LMOX significantly suppressed the increases in these biochemical parameters with GM alone. In this case, the suppressions were roughly dependent on the dose of LMOX. Although GM alone caused pronounced histological changes in proximal tubules between the 7th and 15th days, the combination with LMOX apparently protected against these changes. These results indicate that the combination with LMOX obviously protects the kidney from the nephrotoxicity of GM.View full abstractDownload PDF (4330K)
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