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Volume 82 (1983)
- Issue 6 Pages 411-
- Issue 5 Pages 303-
- Issue 4 Pages 223-
- Issue 3 Pages 171-
- Issue 2 Pages 103-
- Issue 1 Pages 1-
Volume 82, Issue 6
Displaying 1-7 of 7 articles from this issue
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(1) Establishment of in vitro culture system and effect of 6-mercaptopurine on development of early stage embryoKohachi KAMATA, Shuetsu SUZUKI, Sachiko OH-ISHI1983 Volume 82 Issue 6 Pages 411-418
Published: 1983
Released on J-STAGE: March 07, 2007
JOURNAL FREE ACCESSThe basal conditions for culture of early mouse embryo in vitro were examined for drug evaluation. Among the media tested, BMOC-III was most suitable for mouse embryo culture. Changing the medium at 1 or 3 hr after culture was harmfull to the survival and/or development of early staged embryos, whereas at 12 or 24 hr after culture, changing of the medium showed slight effect on embryo development. Eight-cell staged embryos were more resistant to changing medium than two-cell staged ones. Preliminary work using a suitable culture system established that exposure to 6-mercaptopurine for 12 or 24 hr resulted in a prolonged developmental rate at each stage. The effects showed a dose-dependent relationship with the 24 hr exposure. It was suggested that inhibition of the developmental rate during exposure resulted from a direct toxic effect on the cell and that the inhibition after exposure resulted from metabolic toxicity.View full abstractDownload PDF (4239K) -
(2) Differential staining of sister chromatids of blastocyst cellKohachi KAMATA, Sachiko OH-ISHI1983 Volume 82 Issue 6 Pages 419-427
Published: 1983
Released on J-STAGE: March 07, 2007
JOURNAL FREE ACCESSA method for differential staining ofsister chromatids of cell from mouse blastocyst was devised. Mouse embryo was cultured for 24 hr in BMOC-III medium from the 8 cell stage and then transferred into the medium containing 5-bromodeoxyuridine (BrdU) for a further 24 hr. At 4 hr prior to the termination of culture, colchicine was added to arrest the cell division in metaphase. Cells were fixed on a slide glass, air-dried, stained with Hoechst 33258, lighted with a mercury light, and stained with Giemsa. Basic conditions for the differential staining such as the concentration of BrdU and lighting were examined. When the mercury light (400 W) was used at 15 cm distance for 60-90 min, sister chromatids could be clearly differentiated with a BrdU concentration of 3-30 ng/ml. Under these concentrations of BrdU, the frequency of sister chromatid exchange (SCE) was almost the same as the control level. Thus the concentration could not affect the SCE frequency. This method can be used for the evaluation of drug toxicity of genetic or mutational effects on mammalian embryos.View full abstractDownload PDF (3733K) -
Keiji NAKAGAMI, Toyokazu KOBAYASHI, Noriyasu TAKAYANAGI, Joji YANO, Ma ...1983 Volume 82 Issue 6 Pages 429-441
Published: 1983
Released on J-STAGE: March 07, 2007
JOURNAL FREE ACCESSIntravenous injection of Forssman antiserum produced a diphasic increase in pulmonary resistance in guinea pigs. The first increase (phase I) occurred with 20 sec latency after injection of Forssman antiserum. The second increase (phase II) occurred immediately thereafter, and this lasted more than 30 min and was irreversible. In the lung, hemorrhages and edema were evident. Hemorrhagic fluid was noted in the bronchiole and the alveoli. Polymorphonuclear leucocytes aggregated in the capillary lumen. The endothelial lining of the venule had been destroyed. Phases I and II were not blocked by DSCG. These were completely blocked by cobra venom factor and carrageenin. Isoproterenol, salbutamol and aminophylline selectively blocked phase I. Also, aminophylline weakly blocked phase II. Cyproheptadine blocked phase I, but chlorpheniramine did not. In contrast, indomethacin and aspirin selectively blocked phase II. Superoxide dismutase significantly blocked phase II, but inactivated superoxide dismutase and catalase did not. The present findings suggest that activation of the complement system appears to be essential for the induction of the increase in pulmonary resistance mediated by Forssman antiserum. Phase I is probably due to the contraction of the respiratory tract. Serotonin may be one of the substances for this contraction. In contrast, phase II is due to disintegration of the endothelial lining and extravasation of hemorrhagic exudates into the respiratory tract. Prostaglandins and/or superoxide radical may take part in the phase II response.View full abstractDownload PDF (6858K) -
Masakatsu NOZAKI, Masayuki NIWA, Junichi HASEGAWA, Hajime FUJIMURA1983 Volume 82 Issue 6 Pages 443-450
Published: 1983
Released on J-STAGE: March 07, 2007
JOURNAL FREE ACCESSThe opioid receptor affinities of butorphanol (BT) and its main metabolites, norbutorphanol(NB) and hydroxybutorphanol(HB), were determined by an in vitro receptor binding assay using crude synaptosomal membrane preparations of rat brain. BT showed high affinities to all types of the receptor except the a type (phencyclidine binding site), resulting in displacements of the bindings of μ (dihydromorphine)-, δ (D-Ala2D-Leu5-enkephalin)-and κ (ethylketocyclazocine)-ligands with more potency than morphine and ketocyclazocine, and it preferentially bound to μ and κ-opioid receptors. NB bound to the μ-binding site with affinity higher than that of pentazocine and to the κ-binding site with the lowest affinity. HB exclusively bound to the μ-binding site with lower affinity. The affinities of BT, NB, HB and morphine to the σ-site were smaller than those of pentazocine and ketocyclazocine. In the presence of 100 mM NaCl or by treating with 500 μM 5, 5'-dithiobis (2-nitrobenzoic acid), the binding capacity of the membrane preparation was altered, and BT behaved as a typical antagonist. NB showed an agonistic property, and HB behaved as an antagonist. BT appears to be a μ-opioid receptor antagonist and has a κ-receptor agonist-like character.View full abstractDownload PDF (3430K) -
Masayuki NIWA, Masakatsu NOZAKI, Keita KAMIKUBO, Hajime FUJIMURA, Tosh ...1983 Volume 82 Issue 6 Pages 451-463
Published: 1983
Released on J-STAGE: March 07, 2007
JOURNAL FREE ACCESSAfter the intravenous injection of butorphanol or norbutorphanol in rats every lhr for 3 days, naloxone-induced body weight loss and withdrawal syndrome were observed to some degree. A slow-released emulsion containing each of the test drugs was injected subcutaneously in guinea-pigs, and naloxone was administered after 2 or 3 days. BT caused little jumping response even at a dose of 600 mg/kg, and the reaction was significantly weaker than that of pentazocine. No jumping responses were recognized in the cases of NB (600 mg/kg). In morphinized rats, the injection of BT or HB caused potent body weight loss, and these rats exhibited withdrawal syndrome which was more potent than that by pentazocine at the same dose. The body weight losses by the injection of NB and pentazocine were to the same degree, and these changes were significantly different from that of the saline control. BT inhibited the adenylate cyclase activity of the rat caudate nuclei, and the effect was weaker than that of pentazocine. NB showed a slight inhibition, and HB had no effect on the activity. These results suggest that the physical dependence liability of butorphanol is less than that ofpentazocine, and the potent μ-antagonistic character of butorphanol is based on the liability. NB, a μ-agonist, makes dependence production possible. The ability of HB is negligible.View full abstractDownload PDF (5312K) -
Kazuhiro SHIMIZU, Shuichi TANAKA, Takeshi HANDA, Shoichi KAWAZOE, Seni ...1983 Volume 82 Issue 6 Pages 465-474
Published: 1983
Released on J-STAGE: March 07, 2007
JOURNAL FREE ACCESSModels of post-ischemic acute renal failure were prepared in rats. The effects of adenosine triphosphatemagnesium chloride (ATP-MgCl2) administration following renal ischemia on possible changes in renal function and renal cellular metabolism following ischemia were studied using the model. The results obtained revealed the following: 1) Over 40 minute-renal ischemia led to significant lowerings of renal cellular ATP level and energy charge (EC) by as much as 45 to 57% and 4.1 to 7.4% of the control, respectively, at 90 min following re-establishment of renal blood flow. Significant increases in Na+ in renal tissues were observed, but no changes in K+. Further, lactate level in renal tissues tended to increase with prolonged ischemic time by as much as 27 to 31% of the control, with a renal cellular anaerobic metabolism observed. On the other hand, at 24 hr following recirculation of the kidney, plasma creatinine (P-Cr), blood urea nitrogen (BUN) and fraction excretion of sodium (FENa) increased significantly, and creatinine clearance (C-Cr) and urine osmotic pressure decreased significantly, as compared with the control, indicating ischemic acute renal failure. 2) Intravenous injection of ATP-MgCl2 at a dose of 25 μmole/kg and a rate of 1.0 μmole/min after 40 min of renal ischemia led to significant lowerings of P-Cr, BUN and FENa to 36, 35 and 35%, %, of the control (injected with physiological saline solution), respectively, and to significant elevation of C-Cr and urine osmotic pressure by as much as 41 to 31% of the control respectively, at 24 hr after reperfusion. The above results suggested that the ischemic acute renal failure was caused by the decreases in renal cellular ATP and EC with ischemia, resulting in renal cellular metabolic disturances. It was further suggested that ATP-MgCl2 administered for such a pathological condition could make significant improvements in renal function.View full abstractDownload PDF (4395K) -
Shiroh KISHIOKA, Yoshiyuki IGUCHI, Masanobu OZAKI, Hiroyuki YAMAMOTO1983 Volume 82 Issue 6 Pages 475-484
Published: 1983
Released on J-STAGE: March 07, 2007
JOURNAL FREE ACCESSIt was confirmed that the nucleus reticularis gigantocellularis (NRGC), including the nucleus reticularis paragigantocellularis (NRPG), was a highly sensitive site in the production of morphine analgesia by the microinjection technique (ED50=8.5 ng/rat). The NRGC of SD male rats (280-350 g) was bilaterally lesioned by direct current (0.5 mA for 40 sec). The body weight was decreased by NRGC destruction, while no abnormality in motor activity was obseved in NRGC-destructed rats. The size of lesion area was decreased in relation to the days after operation. The size of the destructed area immediately after operation was about 30% of the NRGC area. Morphine analgesia was estimated by tail pinch and hind paw pressure tests. No change in control pain threshold was produced by NRGC lesioning. Morphine analgesias due to 5, 10 and 15 mg/kg s.c. were depressed almost equally by NRGC lesioning, and depression % was 60-70%. Time course of the morphine effect in NRGC-destructed rats was similar to that in sham operated rats. The degree of depression of morphine analgesia by NRGC lesioning was dependent on the extent of NRGC lesioning, i.e., the more the destructed area of NRGC was extended, the more the morphine analgesia was depressed. Reduction of morphine analgesia in rats in which the position of destruction had deviated from the NRGC was smaller than that in rats in which the destruction was exactly at the NRGC. These results suggest that the NRGC, including the NRPG, plays an important role in morphine analgesia.View full abstractDownload PDF (4377K)
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