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Volume 29 (1979)
- Issue 6 Pages 821-
- Issue 5 Pages 687-
- Issue 4 Pages 503-
- Issue 3 Pages 319-
- Issue 2 Pages 151-
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Volume 29, Issue 4
Displaying 1-25 of 25 articles from this issue
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Heitaroh IWATA, Satoru YAMAGAMI, Eibai LEE, Toshio MATSUDA, Akemichi B ...1979 Volume 29 Issue 4 Pages 503-507
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSWe determined the effect of physiological stimulation on taurine contents in three regions (cerebral cortex, brain stem and cerebellum) of the brain of El mice, a genetically epileptic strain. Taurine contents in all regions of the brain increased significantly at the onset of convulsions, as induced by tossing the animals up many times. Levels in the cerebral cortex and cerebellum increased markedly in the early stage of the stimulation, yet convulsion did not occur. Taurine contents in the cerebral cortex and brain stem returned to the resting level within 30 min after the onset of convulsions, while levels in the cerebellum remained high for 3 hr. Concentration of taurine in the plasma also increased with the onset of convulsions. On the other hand, taurine administration increased the threshold of convulsion by the stimulation in El mice.View full abstractDownload PDF (289K) -
Hideo NAKAGAWA, Kyung Rak MIN, Kimiko NANJO, Susumu TSURUFUJI1979 Volume 29 Issue 4 Pages 509-514
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSEffect of progesterone (1 mg/kg) on the inflammation in rats induced by carrageenin was studied. Progesterone inhibited the vascular permeability and the formation of granulation tissue in the early phase of the inflammation. In the chronic proliferative phase, progesterone suppressed the vascular permeability and there was an active resorption of the granulation tissue. Increased degradation of noncollagen protein was observed in the treated group without apparent influence on the metabolism of collagen or on the synthesis of noncollagen protein. The mode of action of progesterone was compared with that of a potent anti-inflammatory steroid, hydrocortisone acetate.View full abstractDownload PDF (430K) -
Yasuo GOMI, Hiroaki SHIRAHASE, Hideyuki FUNATO1979 Volume 29 Issue 4 Pages 515-524
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSEffects of 1-(2-chloro-4-hydroxyphenyl)-2-t-butylaminoethanol hydrochloride (HOKU-81), one of the metabolites of tulobuterol, on isolated trachea and atria of guinea pigs were compared with those of various bronchodilators. All test drugs abolished the resting tone of tracheal muscle completely. The potencies of test drugs which induced relaxation were in the order of: trimetoquinol > HOKU-81 ≥ isoproterenol > salbutamol > terbutaline ≥ tulobuterol > metaproterenol > clorprenaline. In acetylcholine-, histamine- or potassium-stimulated preparations, the intrinsic activities of 2-chlorophenyl derivatives were less than those of 3, 4- or 3, 5-dihydroxyphenyl derivatives and that of HOKU-81, 2-chloro-4-hydroxyphenyl derivative, lay between two groups. HOKU-81 showed weak positive chronotropic and inotropic actions and the potency ratio of HOKU-81 to isoproterenol was about 3/100 and less than 3/1000, respectively. Both chronotropic and inotropic actions of 2-chlorophenyl derivatives, including HOKU-81, were weak and the inotropic actions of drugs with N-t-butylamino radical were weaker than chronotropic actions. Effects of test drugs on trachea and atria were antagonized by propranolol 1 × 10-6 or 1 × 10-7 M. HOKU-81 appears to be a potent and selective β2-stimulant with a slight inotropic action.View full abstractDownload PDF (617K) -
Matao SAKANASHI, Makie HIGUCHI, Fumio TAKENAKA1979 Volume 29 Issue 4 Pages 525-530
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSThe relationship between responsiveness and high-energy phosphate metabolism was observed in isolated dog coronary arterial strips before and after equilibration, under aerobic conditions. The strips responded slowly to potassium, norepinephrine, isoproterenol and 5-hydroxytryptamine before being equilibrated but did respond quickly to these drugs after being equilibrated for 1 hour under aerobic conditions. The contents of ATP, creatine phosphate (CP) and lactate were not significantly altered before and after equilibration for 1 hr. It is proposed that, before being equilibrated under aerobic conditions, coronary arteries may be unable to utilize ATP and CP due to injury of contractile or relaxant mechanisms resulting in a weak vascular responsiveness.View full abstractDownload PDF (336K) -
Taketoshi SAIJO, Yasuko ASHIDA, Hisashi KURIKI, Morio KANNO, Yoshitaka ...1979 Volume 29 Issue 4 Pages 531-540
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSThe antiallergic action of 6-ethyl-3-(1H-tetrazol-5-yl)chromone (AA-344) was studied on isolated rat peritoneal mast cells. AA-344 clearly inhibited the IgE-mediated release of histamine caused by various concentrations of antigen and the 50% inhibitory concentration was 0.1 μM. On the IgGa-mediated release of histamine, a peak inhibition of AA-344 was observed at 10 μM. The histamine release induced by chemical agents such as concanavalin A, dextran and compound 48/80 was depressed by AA-344 at the range of 0.1-1 mM. The results obtained in this study indicate that the antiallergic action of AA-344 is due to selective inhibition on the immunological release of the chemical mediator from mast cells.View full abstractDownload PDF (699K) -
Toshio SUGA, Masahiko SUZUKI, Masami SUZUKI1979 Volume 29 Issue 4 Pages 541-552
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSIn order to elucidate the mechanism of the central hypertensive action of angiotensin II (ATII), the effects of ATII on the medullary neurons of rabbits were studied by the technique of electrophoretic application. ATII gave rise to excitatory effect on some neurons of medulla and this effect was antagonized by a specific ATII antagonist, 1-sarcosine-8-alanine-ATII. The ATII sensitive medullary neurons showed no specific response to acetylcholine, norepinephrine or isoproterenol, but there was a significant increase in the excitatory response to norepinephrine in comparison with the ATII non-sensitive neurons. The excitatory effect of ATII was not blocked by atropine, phentolamine and propranolol. The ATII sensitive neurons in the medulla apparently do not have a topograhically or functionally characteristic distribution related to the central vasomotor control mechanisms. The neurons in the area postrema did not respond to electrophoretically applied ATII, while microinjection of ATII in this region produced remarkable hypertensive responses. These results suggest that the mechanism of the central hypertensive action of ATII administered into the vertebral artery is primarily mediated by the chemoreception of the area postrema. The mechanism of central cardiovascular effect of ATII and of the effects of acetylcholine and catecholamines on the medullary neurons are discussed.View full abstractDownload PDF (779K) -
Kiyohisa UCHIDA, Haruto TAKASE, Masumi KADOWAKI, Yasuharu NOMURA, Taka ...1979 Volume 29 Issue 4 Pages 553-562
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSChanges of cholesterol, phospholipid, triglyceride or bile acid levels in serum, liver, bile and feces after the treatment with alloxan were examined in Wistar strain male rats. Serum cholesterol, phospholipid and triglyceride levels and liver cholesterol level markedly increased but liver phospholipid and triglyceride levels remained unchanged. The lipid levels in serum very low density and low density lipoproteins were elevated but those in high density lipoprotein were not. Bile flow was not changed but biliary secretion of cholesterol, phospholipid and bile acids markedly increased. Among the biliary bile acid components, cholic acid markedly increased but the amount of chenodeoxycholic acid was similar to that of normal rats. Fecal excretion of deoxycholic acid increased but that of lithocholic and hyodeoxycholic acids decreased, and α-, β- and ω-muricholic acids did not change, thus, the total amount of fecal bile acids remained unchanged. Hepatic cholesterol synthesis was markedly depressed, while cholesterol 7α-hydroxylase activity did not change and cytochrome P-450 content was elevated by about 40 %. From such evidence, it was apparent that synthesis of cholic acid increased while that of chenodeoxycholic acid decreased and the total amount of bile acids synthesized did not change in the diabetic rats. Furthermore, marked increase of the pool size of cholic acid and hepatic secretion of cholic acid stimulated the absorption of lipids and produced a hyperlipidemia in the diabetic rats.View full abstractDownload PDF (667K) -
Takasuke NAKANO, Norio TAIRA1979 Volume 29 Issue 4 Pages 563-571
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSExperiments were conducted on II loosely restrained, conscious dogs which responded with vocalization in a dose-dependent manner to bradykinin (0.6-10 nmol) or acetylcholine (0.1-10 μmol) injected into the femoral or the mesenteric artery through a chronically indwelling arterial catheter. Vocalization was taken as being to reflect the algogenic action of these substances. Administration of captopril (1 mg/kg, i.v.) potentiated the algogenic action of bradykinin but not that of acetylcholine injected into either artery. The magnitude of potentiation of the algogenic action was about 3-fold for bradykinin injected into the femoral artery and about 10-fold for that injected into the mesenteric artery. The potentiation can be interpreted in terms of inhibition of kininase II by captopril. The difference in potentiation by captopril of the algogenic action of bradykinin injected into the two arteries may reflect the difference in kininase II activity in the two arterial beds. Possible involvement of E-series prostaglandins in the potentiation was also discussed.View full abstractDownload PDF (535K) -
Noriaki KONDO, Issei TAKAYANAGI, Yutaka KASUYA1979 Volume 29 Issue 4 Pages 573-579
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSAn increase of intracellular cyclic AMP levels induced by 1-isoprenaline (1-Iso) was significantly depressed in coexistence with BuTMA or histamine, but not with KCl or BaCl2. An analysis of steady state data for d, l-[3H]-isoprenaline binding to single cells of taenia from guinea pig caecum in the presence of histamine or KCl by Scatchard plots was performed. The affinity of 1-Iso for β-adrenoceptor sites was decreased in the presence of histamine but not in the presence of KCl. These results suggest that the interaction of 1-Iso with the β-adrenoceptors is interfered with by histamine and butyltrimethylammonium, for which the specific receptors were postulated, but not with KCl and BaCl2, nonspecific smooth muscic stimulants. These phenomena demonstrate the heterotropic negative cooperativity among the heterogeneous receptors.View full abstractDownload PDF (409K) -
Masako MORIKAWA, Michiko INOUE, Minoru TSUBOI, Mamoru SUGIURA1979 Volume 29 Issue 4 Pages 581-586
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSWe studied the aspirin-hydrolyzing activity in human serum and found a difference between the sexes in the aspirin-hydrolyzing activity expressed in mU salicylic acid released from ml of serum. However, aspirin-hydrolyzing activity expressed in mU salicylic acid per ml albumin showed no such difference. In cases of chronic hepatitis, liver cirrhosis and nephrosis, the aspirin-hydrolyzing activity was much lower than that seen healthy persons. In disc electrophoretic experiments, the aspirin-hydrolyzing activity was found to be located in pseudocholinesterase and albumin and this activity in the cholinesterase region was inhibited by eserine sulfate. When the albumin from human serum was purified by chromatography on DEAE-cellulose and Sephadex G-100, the purified albumin hydrolyzed aspirin and this aspirin-hydrolyzing activity of purified albumin, although not inhibited by eserine sulfate and diisopropyl fluorophosphate, was inhibited by treatment with acetic anhydride. These results suggest that the aspirin-hydrolyzing activity from human serum included the pseudocholinesterase activity and acetylation effect of aspirin.View full abstractDownload PDF (397K) -
Yoko UCHIDA1979 Volume 29 Issue 4 Pages 587-596
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSEffects of chlorpromazine (CPZ) on lipolysis in brown (interscapular: IBAT) and white (epididymal: EWAT) adipose tissues in cold-exposed rats were studied in vitro. Adult male Wistar-Imamichi rats were exposed to 4°C for 1 (acute cold-exposed) or 30 (cold-acclimated) days. The spontaneous free fatty acid (FFA) release from interscapular brown adipose tissue (IBAT) of control rats, was three fold higher than epididymal white adipose tissue (EWAT). FFA release from the EWAT of acute cold-exposed rats was significantly higher than that of control rats. After cold acclimation, FFA release from IBAT increased up to three times that of the control level. CPZ (10-4, 10-3 M) suppressed the elevated lipolytic activity in IBAT of cold-acclimated rats. However CPZ had no effect on FFA release from EWAT or IBAT in all other groups. A single intravenous administration of 10 mg/kg 6-hydroxy-dopamine (6-OHDA) produced a marked decrease in the concentration of noradrenaline and dopamine in IBAT and EWAT of cold-acclimated rats. FFA release from IBAT in 6-OHDA treated, cold-acclimated rats decreased to 50 % of untreated, cold-acclimated rats. A further decrease in lipolytic activity in the IBAT of 6-OHDA treated, cold-acclimated rats was produced following CPZ treatment. CPZ also depressed the lipolysis stimulated by the added noradrenaline (3×10-5 M). These results suggest that the effect of CPZ on the lipolysis in the IBAT from cold-acclimated rats is mediated by a modification of sympathetic activity.View full abstractDownload PDF (632K) -
Kazushige SAKAI1979 Volume 29 Issue 4 Pages 597-603
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSExperiments were conducted on rat isolated, small intestine perfused at a fixed flow rate through the superior mesenteric artery with arterial blood from a donor rat, to determine the responses of the ileum to different peptides. Drugs were closely injected into the superior mesenteric artery. Single injections of bradykinin produced monophasic fast contractions of the ileum preceded by an initial fall and a subsequent rise of tone. The fast contraction was abolished by tetrodotoxin (TTX), morphine and hexamethonium (C6), but was resistant to blockade by atropine or mepyramine. Changes in ileal tone induced by bradykinin remained evident even in the presence of these blocking agents, thereby suggesting a direct action on smooth muscle fibers of the ileum. The fast contraction in response to substance P was not influenced by either TTX, morphine, C6, atropine or mepyramine. The present results indicate that bradykinin induces the fast contraction of the ileum by excitation of myenteric neuronal elements involving cholinergic interneurons, while substance P produces the contraction by a direct stimulation of smooth muscle fibers of the ileal region.View full abstractDownload PDF (409K) -
Katsuhiko MIYASAKA, Yoshio HIRAMATSU, Takayuki TAKEZAKI1979 Volume 29 Issue 4 Pages 605-622
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSVasodepressor mechanism of lycorenine (an alkaloid of Lycoris radiata Herb.) was investigated in anesthetized rats. Lycorenine (1-10 mg/kg i.v.) produced dose-related decreases in blood pressure and heart rate and tachyphylaxis developed with repeated injections. In the blood-perfused rat hindquarters, lycorenine (62.5-500 μg i.a.) produced dose-related decreases both in mean blood pressure and in perfusion pressure, and the lycorenine-induced decrease in perfusion pressure was abolished by phenoxybenzamine or hexamethonium. Lycorenine (more than 1 mg/kg i.v.) blocked the pressor response to sympathetic nerve stimulation, but failed to block the tachycardia induced by sympathetic nerve stimulation. Lycorenine (7.5 or 15 mg/kg i.v.) reduced the spontaneous splanchnic nerve activity. Lycorenine when given intracerebroventricularly produced decreases in blood pressure and heart rate only in large doses (over 500 μg). The maximal bradycardia induced by lycorenine was abolished by bilateral vagotomy. It is suggested that lycorenine may produce a decrease in blood pressure as the result of alpha-adrenergic blockade in conjunction with the reduction of the spontaneous sympathetic nerve activity, and produce bradycardia by modifying vagal activity.View full abstractDownload PDF (1274K) -
Eijiro TAGASHIRA, Tomoko IZUMI, Saizo YANAURA1979 Volume 29 Issue 4 Pages 623-630
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSThe antagonistic mode of levallorphan in rats dependent on morphine or codeine was studied from the viewpoints of the doses of morphine and the lengths of administration and also from the standpoint of timing of the challenge. In morphine-dependent rats on morphine-admixed food (60-100 mg/kg/day) for 1, 3 and 6 weeks, the rate of maximum weight loss on application of levallorphan (2 mg/kg, s.c.) did not correlate with the length of morphine treatment. The rate of weight loss on single application of levallorphan 0, 6, 12 or 24 hours after withdrawal of morphine was lower with the passage of time after the withdrawal. Rats which were given levallorphan 3 times in succession, i.e., at 0, 5 and 10 hours after morphine withdrawal showed such a pattern of weight loss that the first application of levallorphan resulted in 7 % loss, while with the second and third applications there was little weight loss. Despite the continued withdrawal, the animals began to gain body weight as early as 14 hour, and body weight was totally recovered before the withdrawal in 24 hour. In conclusion, it is advisable to challenge with levallorphan at 0 hour of withdrawal to obtain qualitative and reproducible results. In addition, the application of levallorphan to morphine-dependent rats at adequate intervals provides for the early recovery of abstinence signs.View full abstractDownload PDF (556K) -
Minoru INABA, Kunie KAMATA1979 Volume 29 Issue 4 Pages 631-638
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSTo determine the influence of colchicine on adrenocortical function in vivo, we gave significant amounts subcutaneously to rats and observed the distribution to the anterior pituitary and adrenal glands. Corticosteroids in the serum and adrenal gland were increased remarkably by the administration of colchicine in a dose-dependent manner. Maximum elevation was achieved around 2.5 hours after the injection and continued for at least 4 hours. Maximum levels produced by the injection of 1 mg/kg body wt. of colchicine were the same as those elicited by the injection of 0.1 U/rat of adrenocorticotropic hormone, the latter producing temporary increases in corticosteroids in the serum and adrenal gland. A significant augmentation of corticosteroids in the serum and adrenal gland resulted when colchicine was administered 60 minutes prior to the injection of adrenocorticotropic hormone. The pattern of intracellular distribution of corticosteroids in the adrenal glands of rats given colchicine was the same as that seen in rats given adrenocorticotropic hormone. In the in vitro experiment, only high concentrations of colchicine such as 10-3 M added to the incubation system of the adrenal quarters suppressed the release of corticosteroids from the adrenal gland. Thus, the continuous stimulation of the synthesis and secretion of adrenocortical hormone seen with the administration of colchicine may explain why this drug is effective in the treatment of gouty arthritis.View full abstractDownload PDF (468K) -
Yutaka TAKATA, Hirosi KURIYAMA1979 Volume 29 Issue 4 Pages 639-651
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSThe effects of angiotensin II (Ag-11) and 1-sar., 8-isoleu. angiotensin 11 (anti-Ag-11) on the membrane and mechanical properties of smooth muscle cells of the rat portal vein were investigated in three different age groups (6-8 weeks, immature rat; 3-5 months old, young rat and 13-15 months old, adult rat). Application of Ag-11 (10-10 g/ml) did not depolarize the membrane, but did increase the spike frequency and potentiated the frequency and amplitude of twitch contraction. In a concentration of more than 10-9 g/ml Ag-II, the membrane was depolarized and a phasic contracture was developed in three age groups. Depolarization of the membrane produced by Ag-II could be classified into two components, i.e. phasic and tonic depolarizations. In adult rats, Ag-II produced the highest amplitude of the depolarization in three age groups but tonic depolarization showed nearly the same amplitude as that observed in immature rats. These phenomena indicate that the sensitivity of smooth muscle cell membrane to Ag-II increases with age up to 3-5 months and that an increased sensitivity is accompanied by a generation of desensitization. Tachyphylaxis to Ag-II was also observed by repetitive applications, but the appearance depended on the stimulus conditions. Anti-Ag-II, itself slightly increased the spike frequency and the amplitude of twitch contraction. However, under pretreatment with anti-Ag-II (10-9 or 10-7 g/ml), the actions of Ag-II on the electrical and mechanical activities were markedly suppressed in the three age groups. When the dose-response curve was obtained from the mechanical response produced by Ag-II, the relation shifted to the right in the presence of anti-Ag-II in all age groups. In the presence of 10-7 g/ml anti-Ag-II, no contracture was evoked by application of 10-6 g/ml Ag-II in three age groups. Anti-Ag-II seems to possess a higher affinity to the angiotensin receptor than does Ag-II.View full abstractDownload PDF (796K) -
Hiroichi NAGAI, Akihide KODA1979 Volume 29 Issue 4 Pages 653-659
Published: 1979
Released on J-STAGE: December 19, 2006
JOURNAL FREE ACCESSA comparative study was carried out on the histamine release from rat neutrophils and mast cells by calcium ionophore A 23 187 (Ionophore). A maximum release of histamine from neutrophils was induced by 10-6 g/ml Ionophore and that from mast cells was 5×10-6 g/ml. A fairly good correlation was found between the 45Ca incorporation into and the histamine release from both cells . The Ionophore-induced histamine release from both cells was decreased in Ca2+-free Tyrode's solution and by pretreatment with 0.05 M EDTA. Effects of different drugs on Ionophore-induced histamine release from neutrophils were similar to those seen in mast cells. Dibutyl cyclic adenosine monophosphate, theophylline, isoproterenol and prostaglandin E1 had no or only a slight inhibition on the release. The dose dependent inhibition of release was observed with disodium cromoglycate, N-(3', 4'-dimethoxycinnamoyl) anthranilic acid and disodium baicalein phosphate, in experiments using both cells. Colchicine did not inhibit the reaction in these cells, however phosphatidylserine enhanced the reaction. On the other hand, the effect of concanavalin A was different in each type of cells, the release from mast cells was inhibited while the release from neutrophils was potentiated. These findings suggest the similarity of biochemical events in Ionophore-induced histamine release from neutrophils and mast cells.View full abstractDownload PDF (421K) -
Takahiko SUMI, Yuri UMEDA1979 Volume 29 Issue 4 Pages 661-663
Published: 1979
Released on J-STAGE: December 19, 2006
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Yasuo ISHII, Machiko TERADA1979 Volume 29 Issue 4 Pages 664-666
Published: 1979
Released on J-STAGE: December 19, 2006
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Toshiaki NAKASHIMA, Yasuchika BAN, Kinya KURIYAMA, Tatsuro TAKINO1979 Volume 29 Issue 4 Pages 667-670
Published: 1979
Released on J-STAGE: December 19, 2006
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Yutaka KASUYA, Tetsuro URUSHIDANI, Susumu OKABE1979 Volume 29 Issue 4 Pages 670-673
Published: 1979
Released on J-STAGE: December 19, 2006
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Wataru TSUKADA, Yuichi RYOKAWA, Haruo TACHIZAWA1979 Volume 29 Issue 4 Pages 674-676
Published: 1979
Released on J-STAGE: December 19, 2006
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Toru EGASHIRA, Kazuya KAMIJO1979 Volume 29 Issue 4 Pages 677-680
Published: 1979
Released on J-STAGE: December 19, 2006
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Kinya KURIYAMA, Makoto MURAMATSU, Meiko NAGANO1979 Volume 29 Issue 4 Pages 680-683
Published: 1979
Released on J-STAGE: December 19, 2006
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Masaki TAKAHASHI, Hiroshi KOGO, Yoshio AIZAWA1979 Volume 29 Issue 4 Pages 684-686
Published: 1979
Released on J-STAGE: December 19, 2006
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