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Volume 79 (1982)
- Issue 6 Pages 461-
- Issue 5 Pages 343-
- Issue 4 Pages 237-
- Issue 3 Pages 113-
- Issue 2 Pages 77-
- Issue 1 Pages 1-
Volume 79, Issue 3
Displaying 1-9 of 9 articles from this issue
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Kazuhisa FURUHAMA, Satoshi TAKAYAMA, Takeshi ONODERA1982 Volume 79 Issue 3 Pages 113-121
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSThe experiment was undertaken to make a discrimination between glomerulonephritis (GN, Masugi-type) and tubular damage (TD, cephaloridine-induced) in rats by means of urinary alkaline phosphatase (AlP). Urinary AlP concentrations were increased 13 times in GN rats and 8 times in TD rats, in comparison with the corresponding controls. Cellulose acetate plate electrophoresis before and after neuraminidase digestion revealed that urinary AlP from GN rats migrated similarly to serum and intestinal AlP, while the mobility of urinary AlP from TD rats resembled that of the kidney. The sensitivity of urinary AlP from GN to the inhibitors, L-phenylalanine and urea, was almost equivalent to that of intestinal AlP, and the sensitivity of urinary AlP from TD rats was similar to that from kidney AlP. Histochemically, AlP activity in the kidney appeared normal in GN rats, but it was markedly decreased in TD rats. Those results suggest that the urinary AlP from GN rats is identical to serum AlP originating from intestines, i.e., a selective increase in glomerular permeability in disturbed glomerular filtration occurs. On the other hand, urinary AlP from TD rats originated mainly from the kidney due to the disquamation in the proximal convoluted tubular epithelia. Thus the properties of urinary AlP are important for estimating the site of renal damage.View full abstractDownload PDF (4593K) -
Hajime FUJIMURA, Kaito TSURUMI, Junichi HASEGAWA, Masayoshi YANAGIHARA ...1982 Volume 79 Issue 3 Pages 123-136
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSWe reported in our previous paper that TN-762, a potent inhibitor of prostaglandin biosynthesis, has marked inhibitory activity on acute experimental inflammation. In this paper, the anti-inflammatory, analgesic, and antipyretic activities of TN-762 were assessed in animal models, and compared with those of indomethacin, ketoprofen and ibuprofen. TN-762 inhibited the sustained paw edema induced by mustard in rats during administration for 3 days, but after final administration, the inhibitory activity was decreased rapidly and was less than that of ketoprofen and indomethacin. TN-762 also inhibited the proliferation of granuloma induced by means of cotton pellet and granuloma pouch methods, and the adjuvant arthritis in rats. The inhibitory activity of the compound on inflammatory proliferation was more potent than that of ibuprofen, but slightly less than that of ketoprofen and less than about 1/10 times that of indomethacin. Indomethacin markedly inhibited the body weight gain at a high dose, while TN-762 did not affect it. Therefore, TN-762 was proven to have an inhibitory effect on subacute and chronic inflammation at low doses without toxic effects, but the compound appeared to have a less of an inhibitory effect on secondary or late stages of inflammation than on primary stage inflammation. TN-762 inhibited the acute paw edema induced by nystatin, and the inhibitory activity was the same as that of ketoprofen and indomethacin. The pathogenesis of nystatin edema has been considered to be due to lysosomal labilization. This result suggests that TN-762 has a potent membrane stabilizing action which is considered to be one of the necessary mechanisms in anti-inflammatory action. On the other hand, TN-762 showed the same potent analgesic effect as ketoprofen and indomethacin as observed by the acetic acid writhing and modified Haffner's methods in mice and by the Randall-Selitto's method in rats. However the antipyretic effect of TN-762 was significantly less than that of ketoprofen and indomethacin.View full abstractDownload PDF (6602K) -
Shigeyoshi MORISHITA, Ken-ichi NISHIMURA, Eiichi KATO, Hiroaki SHIRAHA ...1982 Volume 79 Issue 3 Pages 137-146
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSAntihypertensive and diuretic actions of indapamide (SE-1520) were investigated in rats and compared with those of trichlormethiazide (TCMT). In normotensive rats, indapamide in a dose of 100 mg/kg p.o. did not show a significant effect on the blood pressure. In DOCA-saline and uni-nephrectomized DOCA-saline hypertensive rats, indapamide above 1 mg/kg and TCMT above 3 mg/kg with single oral or repetitive administration for 2 weeks reduced the blood pressure level. In spontaneously hypertensive rats (SHR), both indapamide and TCMT lowered the blood pressure with single doses above 10 mg/kg or repetitive doses above 3 and 10 mg/kg, respectively. In the diuretic test using normal rats, indapamide in doses ranging from 0.1 to 30 mg/kg increased urine volume and urinary electrolyte excretion. TCMT showed a more potent diuretic action at a lower dose level. In SHR, indapamide and TCMT produced a greater urine volume and electrolytes excretion. Indapamide inhibited the carbonic anhydrase activity and the potency was about 1/25 of that of acetazolamide in vitro. The antihypertensive activity of indapamide was more potent than that of TCMT and the reverse order to that of their diuretic potencies. It is suggested that the mechanism of antihypertensive effect of indapamide is different from that of TCMT.View full abstractDownload PDF (4802K) -
Takashi HIYAMA, Shigeyuki SHINTANI, Masahiro TSUTSUI, Yoshinobu YASUDA1982 Volume 79 Issue 3 Pages 147-162
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSPharmacological properties of buprenorphine were studied in comparison with those of morphine and pentazocine. Buprenorphine was more potent than morphine and pentazocine in analgesic tests, using chemical, thermal, pressure, and electrical stimulation as the nociceptive stimuli. Buprenorphine exhibited analgesic activity in the D'Amour-Smith's test at high stimulus intensity and in the Haffner's test, while pentazocine exhibited little or no analgesic action in these tests. Buprenorphine showed a bell-shaped dose-response curve in the mouse D'Amour-Smith's test at high stimulus intensity. Analgesic action of buprenorphine was antagonized by naloxone administered before buprenorphine, but not antagonized by naloxone administered after buprenorphine. Duration of the analgesic action of buprenorphine was longer than those of morphine and pentazocine. Buprenorphine decreased the amplitudes of evoked potentials which were recorded from the nucleus ventralis posteromedialis, nucleus centralis lateralis, and periaquaductal central gray. As a naloxone antagonist, Buprenorphine was equivalent or less potent than naloxone and more potent than pentazocine. Tolerance developed to the analgesic activity of buprenorphine, but development of tolerance to buprenorphine was less than that of tolerance to morphine. It was concluded that buprenorphine may be a useful analgesic drug because of its high intrinsic activity and long duration of action.View full abstractDownload PDF (7030K) -
Yoshinobu YASUDA, Yoshihide SHIOYA, Satoru NAKAI, Shigeyuki SHINTANI, ...1982 Volume 79 Issue 3 Pages 163-172
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSInteractions between buprenorphine, narcotic analgesic, and centrally acting drugs were studied in prolongation of halothane-induced sleeping and analgesia using the D'Amour-Smith method in mice, and the effect of buprenorphine on monoamine metabolism was studied in rat brain. Diazepam and chlorpromazine prolonged the halothane-induced sleeping time dose-dependently. Buprenorphine (0.01, 0.1, and 1 mg/kg s.c.) inhibited the effect of diazepam, but not that of chlorpromazine. Pentazocine and naloxone also inhibited the effect of diazepam, but morphine did not. It is suggested that the inhibitory effect of buprenorphine on prolongation of halothane-induced sleeping time by diazepam is due to its opiate antagonistic property. Since narcotic antagonists inhibited the effect of diazepam, the endogenous opiate system seems to be involved in this effect. Diazepam or droperidol had no effect on the analgesia of buprenorphine, morphine, and pentazocine. Buprenorphine analgesia was inhibited by reserpine and p-chlorophenylalanine, potentiated by 5-hydroxytryptophan, and not affected by α-methyl-p-tyrosine or 3, 4-dihydroxyphenylalanine. These results suggest that the serotonergic system plays a modulating role in buprenorphine analgesia. Imipramine and nialamide inhibited buprenorphine analgesia in the test at low stimulus intensity, but potentiated at high stimulus intensity. Buprenorphine (0.1, 1, and 10 mg/kg s.c.) increased the dopamine metabolites, 3, 4-dihydroxyphenylacetic acid and homovanillic acid, in various brain areas and the serotonin metabolite, 5-hydroxyindoleacetic acid, in midbrain.View full abstractDownload PDF (4503K) -
Shigeyuki SHINTANI, Masanao UMEZATO, Yoshifumi TOBA, Yoshiaki YAMAJI, ...1982 Volume 79 Issue 3 Pages 173-191
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSPharmacological properties of buprenorphine were compared with those of morphine and pentazocine. Buprenorphine scarcely showed any effects on spontaneous EEGs and sleep-wakefulness cycles. Buprenorphine tended to depress the recruiting and augmenting responses and the spindle burst, and it also inhibited the hypothalamic arousal response. Buprenorphine had weaker emetic action than morphine and protected against apomorphine-induced emesis in the same manner as morphine. Buprenorphine scarcely affected respiration, blood pressure, heart rate, blood flow, ECG, cardiac contractile force, coronary flow, and intracranial pressure. However, morphine and pentazocine caused depressed respiration, decreased blood pressure, increased blood flow and cardiac contractile force, and elevated intracranial pressure. Buprenorphine, morphine, and pentazocine did not affect bile secretion, but produced contraction of the sphincter of Oddi. Buprenorphine had very little effect on renal function, but morphine and pentazocine reduced this function to depress urine flow. Buprenorphine and morphine inhibited carrageenin-induced edema. Buprenorphine had no effect on blood histamine level, but morphine increased the concentration of histamine. These results indicate that buprenorphine has little effect on the central nervous system, respiratory and cardiovascular system, and renal function.View full abstractDownload PDF (8231K) -
Ryuichi SAZIKI, Iwao ARAI, Yoshihiko ISOBE, Hironaka AIHARA1982 Volume 79 Issue 3 Pages 193-202
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSEffects of a newly synthetized anti-ulcer drug, 2'-Carboxymethoxy-4, 4'-bis(3-methyl-2-butenyloxy)chalcone (SU-88), on gastric blood flow and the cardiovascular system were investigated. Intravenously administered SU-88 dose-dependently increased the blood flow of gastric tissues in rats. In anesthetized dogs, i.a. administered SU-88 also increased the short gastric and the femoral arterial blood flows. SU-88 (1 mg/kg, 3 mg/kg and 10 mg/kg i.v.) caused a mild fall in systemic blood pressure, an increase in heart rate, and a stimulation of respiration; however, these effects were only transient and recovered to the basal level within few minutes. No notable changes were observed in the electrocardiogram except for a shortening of the R-R interval accompanied by an increase in heart rate. The blood flow of the common carotid, the vertebral, the coeliac, the superior mesenteric, and the femoral arteries in dogs were all increased by i.v. administration of SU-88, and among them an increase in the coeliac arterial blood flow was prominent. SU-88 increased the perfusates in isolated rabbit ear and relaxed the contraction of isolated rabbit aorta induced by noradrenaline, but showed no influences on the amplitude, heart rate, and coronary flow of isolated rabbit heart. The hypotensive effect of SU-88 was not abolished by i.v. administered atropine, diphenhydramine, and propranolol and not influenced by vagotomy. Intravertebrally administered SU-88 increased the vertebral blood flow, but showed no influence on systemic blood pressure. Furthermore, SU-88 showed no influence on the rise in blood pressure by both common carotid occlusions. The increase in the femoral and the short gastric arterial blood flow induced by i.a. administration of SU-88 was not inhibited by atropine, diphenhydramine, and propranolol and not influenced by pretreatment with aminophylline. These results suggest that the hypsoensive and vasodilative effects of SU-88 are not mediated by the central nervous system, autonomic nervous system, histamine and the action of adenosine augmentation and further experiments are necessary for precise explanations of its mechanism.View full abstractDownload PDF (4305K) -
Masatoyo KAGOSHIMA, Nobuo SUGURO1982 Volume 79 Issue 3 Pages 203-223
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSThe gastric microvascular changes in reserpine (RES 6 mg/kg s.c.)-induced ulcer in Wistar male rats were studied. Two kinds of water paints were injected through the superior mesenteric vein and celiac artery. Excised stomachs were frozen instantly by cooled methanol (-70°C) and were put into methylsalicylate after 24 hr in order to make transparent preparations. RES caused constriction of the vein from the middle layer till the muscularis mucosae and congestion with ischemia in the gastric mucosa after 1 hr. Even after 3 hr, these vascular changes remained and were accompanied by erosion. After 6 and 9 hr, the erosion became more severe, while ischemia was no longer found and the vessels were rather dilated. These lesions initiated from the fundic-antral border area in the lesser curvature and gradually extended to the greater curvature. The early changes up to 3 hr were inhibited by phentolamine, isoproterenol, C6, metiamide and methysergide, but not by carbachol, atropine, vagotomy and propranolol. Atropine, vagotomy, isoproterenol, propranolol and C6 inhibited erosion in the late stage. Phentolamine, carbachol, diphenhydramine, metiamide and methysergide were not effective. From these results and the gastric movement caused by RES, it is suggested that the vascular changes of the early stage in RES-induced ulcer are due not only to the autonomic nervous system but also to the endogenous biogenic amines, and the erosions in the late stage depend on the hypermotility of the stomach rather than on the hypersecretion of the stomach.View full abstractDownload PDF (11498K) -
Kazunaga FUKAWA, Hideo HONDA, Hideo KUBOTA, Yoshikazu HATANAKA, Takash ...1982 Volume 79 Issue 3 Pages 225-236
Published: 1982
Released on J-STAGE: March 09, 2007
JOURNAL FREE ACCESSEffects of DEM on the cardiovascular, autonomic, and central nervous systems were studied using dogs, rats and rabbits. DEM showed relatively weak effects on the EEG in curarized rabbits and on ambulatory and drinking activities in rats. DEM suppressed dose-dependently the pressor responses induced by norepinephrine, serotonin and bilateral carotid occlusion, but had no effect on the depressor responses induced by acetylcholine and electrical stimulation to the postganglionic vagus nerve in anesthetized dogs. DEM produced a dose-dependent increase in blood pressure, a dose-dependent decrease in heart rate, a transient decrease in respiration rate, and little change in the EGG of anesthetized dogs. The pressor responses induced by DEM were inhibited by phentolamine, methysergide, and indomethacin in anesthetized dogs. With canine femoral arteries, DEM-induced contractions were blocked 10% by phentolamine, 60% by methysergide, and enhanced 10% by indomethacin. On the other hand, DEM-induced contractions of the femoral veins were blocked 30% by phentolamine, 60% by indomethacin, and 10% by methysergide. DEM provoked a significant increase in the level of prostaglandin E in the bathing fluid of the veins but not in that of the arteries. The results suggest that the arterioconstrictor responses induced by DEM are mediated mainly through the serotonin receptors, and the venoconstrictor responses induced by DEM mainly through the enhanced synthesis of prostaglandin E.View full abstractDownload PDF (5172K)
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