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Volume 44 (1987)
- Issue 4 Pages 373-
- Issue 3 Pages 233-
- Issue 2 Pages 105-
- Issue 1 Pages 1-
Volume 44, Issue 2
Displaying 1-19 of 19 articles from this issue
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Toshio OBATA, Toru EGASHIRA, Yasumitsu YAMANAKA1987 Volume 44 Issue 2 Pages 105-111
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSIt is known that platelet MAO appears to behave more like the B-form enzyme than the A-form enzyme based on inhibitor sensitivity and substrate specificity. However, dog platelets showed a different substrate specificity such as high activity with 5-HT and β-PEA as substrates. Moreover, dog platelet MAO was sensitive to the drugs clorgyline and harmaline with 5-HT as the substrate, while it was sensitive to the drug deprenyl with β-PEA as the substrate. These results also indicate the existence of two forms of MAO in dog platelets unlike in other platelets such as those from humans. A-form MAO from dog platelets was more stable against heat treatment at 55°C than A-form MAO from dog liver and brain. On the other hand, there was no difference in the heat resistance of the three enzymes with β-PEA as the substrate. After digestion with trypsin at 37°C for 30 min, it was found that MAO from dog platelets, brain and liver were mostly inhibited with 5-HT as the substrate. In contrast, MAO in brain and liver were inhibited about 10%, but platelet MAO was inhibited about 50% with β-PEA as the substrate. From these results, it is considered that dog platelet MAO exists as the two forms of the enzyme and has different enzymic properties in comparison with those of MAO from dog liver and brain mitochondria.View full abstractDownload PDF (352K) -
Hiroyasu SATOH, Masaaki ISHII, Keitaro HASHIMOTO1987 Volume 44 Issue 2 Pages 113-119
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSEffect of cibenzoline, a class I (local anesthetic-type) antiarrhythmic drug, was investigated upon canine ventricular muscle using a conventional microelectrode method. In the presence of cibenzoline at the concentration of 3×10-6 M or higher, the maximum rate of rise of the action potential was inhibited and the action potential duration was lengthened significantly in a concentration-dependent manner. The effective refractory period was also prolonged. From its effect on the action potential duration, cibenzoline should belong to la, according to the Vaughan Williams classification of antiarrhythmic agents. On the other hand, cibenzoline inhibition of the maximum rate of depolarization was greater with an increase in stimulation frequency (a use-dependent block). In the presence of cibenzoline concentrations of 3×10-6 M and 8×10-6 M, which blocked the maximum rate of depolarization by 36% and 67% at 180 beats/min, the rates of onset of inhibition of the maximum rate of depolarization were 0.109±0.027 and 0.146±0.070 AP-1 (mean±S.D.), respectively. From the kinetics of inhibition of the maximum rate of depolarization, these results suggest that cibenzoline should be classified as an intermediate drug with the prolongation of the action potential duration.View full abstractDownload PDF (370K) -
Takashi ITO, Shigetoshi CHIBA1987 Volume 44 Issue 2 Pages 121-126
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe effects of calcium antagonists, diltiazem (DI) and verapamil (VE), on α-adrenoceptor-mediated contractile responses of the isolated and perfused canine intermediate auricular artery were examined by use of the stainless steel cannula inserting method. KCI (3 mg)-induced contractile responses were dose-dependently inhibited by DI and VE. Norepinephrine (0.1 μg)-induced vasoconstrictions were also dose-dependently inhibited by both DI and VE. DI and VE shifted dose-response curves for phenylephrine and clonidine to the right with suppression of maximal responses. At large doses, DI and VE suppressed clonidine-induced contractions more than phenylephrine-induced ones, but not significantly. It is concluded that 1) not only α1- but also α2-adrenoceptor mediated vasoconstrictions of the canine intermediate auricular artery are dependent on the influx of extracellular calcium ions, 2) the present results may provide in vitro proof for the effectiveness of calcium antagonists on skin circulatory disturbances such as Raynaud's phenomenon and 3) the isolated and perfused canine intermediate auricular artery would be a good in vitro model for investigating responsiveness of the skin supplying artery.View full abstractDownload PDF (335K) -
Masahiko HAYASHI, Junko KIMURA, Sachiko OH-ISHI, Susumu TSUSHIMA, Hiro ...1987 Volume 44 Issue 2 Pages 127-134
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSCV-3988 inhibited the vascular permeability increase induced by C16-PAF and C18-PAF in rat skin in a dose-dependent manner. The inhibition was shown to be specific and competitive with PAF on its receptor by the following observations: 1) Parallel shift of the dose-response curve; 2) Crossing of double reciprocal plots on the intersection of the ordinate; and 3) No inhibition on other autacoids such as bradykinin, histamine, 5-hydroxytryptamine and LTC4. PAF-induced blood pressure fall in rats was also suppressed by pretreatment with CV-3988 selectively.View full abstractDownload PDF (360K) -
Sadao NAKAYAMA, Atsufumi MANABE, Junichi SUZUKI, Koji SAKAMOTO, Tetsuy ...1987 Volume 44 Issue 2 Pages 135-143
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSHypolipidemic effects of the usual γ-oryzanol (γ-OZ) and a new γ-OZ (N-γ-OZ) with a different sterol composition from γ-OZ were investigated on the hyperlipidemia induced by ingestion of a high cholesterol diet (HCD) containing 1 % cholesterol for 12 days in male Sprague-Dawley rats. Treatment with γ-OZ for 6 days significantly inhibited the increase in serum total cholesterol (TC) and phospholipids (PL) induced by HCD, while the treatment with γ-OZ for 12 days did not inhibit the increase of TC and PL. Treatment with N-γ-OZ at 100 or 1000 mg/kg for 6 days slightly inhibited the increase of TC by HCD. The decrease of TC in high density lipoprotein (HDL-TC) was markedly inhibited by treatment with N-γ-OZ for 12 days, but N-γ-OZ for 6 days and γ-OZ for 6 and 12 days did not inhibit the decrease of HDL-TC. Treatment with N-γ-OZ for 12 days significantly inhibited the increase of PL and free cholesterol (FC) by HCD. γ-OZ at 1000 mg/kg for 12 days also inhibited the increase of FC. N-γ-OZ significantly reduced the atherogenic index using TC and HDL-TC by affecting the HDL-TC increase. γ-OZ at 100 mg/kg and N-γ-OZ at 100 mg/kg for 6 days reduced the atherogenic index using TC and HDL-TC by the inhibition of TC increase. The atherogenic index using PL and HDL-PL was only reduced by the treatment with N-γ-OZ at 1000 mg/g for 12 days. The increase of triglyceride (TG) by HCD was inhibited by the treatment of N-γ-OZ for 6 days (all doses) and 12 days (500, 1000 mg/kg), and γ-OZ at 500 mg/kg for 6 and 12 days also inhibited the increase of TG by HCD. γ-OZ and N-γ-OZ had no effects on liver lipid contents. The hypolipidemic effect of N-γ-OZ was slightly more potent than that of γ-OZ. The inhibition of decrease in HDL-TC and increase in FC by HCD in the treatment with N-γ-OZ was more potent than that of γ-OZ, and these effects of N-γ-OZ may be related to the acceleration of HDL function in the serum.View full abstractDownload PDF (435K) -
Makie HIGUCHI, Takeo ASAKAWA1987 Volume 44 Issue 2 Pages 145-153
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSEffects of nipradilol on hemodynamics and transmural energy metabolism of underperfused (ischemic) canine hearts were investigated. The ischemic heart was prepared by constricting a tube connecting the circumflex coronary artery with the carotid artery for 10 min so that the perfusion pressure (CPP) was reduced to 30 mmHg. The reduction in CPP resulted in decreases in coronary blood flow (CBF) by 70%, regional myocardial contractile force (MCF) by 30%, myocardial ATP contents by 32% (inner layer)-22% (outer) and creatine phosphate by 75% (inner)-60% (outer). Increases in the left ventricular end diastolic pressure (LVEDP) by 4.8 mmHg, myocardial inorganic phosphate contents by 1.9 times (inner)-1 .3 (outer) and lactate by 4.3 times (inner)-2.4 (outer) were also observed. In dogs with normal hearts, an infusion of nipradilol (10 μg/ kg/min, i.v., for 1 5 min) decreased CPP by 25%, CBF by 40%, cardiac effort index by 45% and MCF by 30 to 40%, and it slightly increased LVEDP without affecting myocardial high-energy phosphate and lactate levels. In ischemic hearts, nipradilol infusion starting 5 min before ischemia attenuated the ischemia-induced elevation of LVEDP to 1.8 mmHg, and the ischemia-induced changes in high-energy phosphate contents to 1/2 (inner)-1/3 (outer) and changes in lactate to 1 /6 (inner)-1/10 (outer). These results indicate that nipradilol improves the ischemic derangement of both transmural energy metabolism and hemodynamics.View full abstractDownload PDF (470K) -
Harumi MITSUHASHI, Kentaro AKIYAMA, Keitaro HASHIMOTO, Yoshio SAWA, Yo ...1987 Volume 44 Issue 2 Pages 155-162
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSAntiarrhythmic effects of a new antiarrhythmic drug, E-0747, were examined using four canine ventricular arrhythmia models: digitalis-, adrenaline- and two-stage coronary ligation-induced arrhythmias and a newly developed locally-induced digitalis arrhythmia. The minimum effective plasma concentration of E-0747 was determined for the first three arrhythmia models. E-0747 suppressed those arrhythmias, and the minimum effective plasma concentrations for arrhythmias induced by digitalis, adrenaline, 24 hr coronary ligation, and 48 hr coronary ligation were 1.4±0.6, 1.8±0.4, 1.6±0.4 and 2.2±0.2 μg/ml, respectively (mean±S.D., n=5-10). The aforementioned minimum effective plasma concentrations of E-0747 for these arrhythmias were almost equal to the reported concentration in vitro to suppress the Na channels of isolated canine ventricular tissues. The class 1 property of E-0747 was also shown in a newly developed locally-induced digitalis arrhythmia. Thus E-0747 suppresses arrhythmia by inhibiting Na channels of cardiac cells and is expected to become a clinically useful anti-arrhythmic drug.View full abstractDownload PDF (423K) -
Koji TAKEUCHI, Osamu FURUKAWA, Hironori TANAKA, Hideyuki NISHIWAKI, Su ...1987 Volume 44 Issue 2 Pages 163-170
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe effects of hemorrhagic shock (HE) on duodenal pH, acid-neutralizing capacity and mucosal tolerance to acid were investigated in anesthetized rats, and they were compared with those of indomethacin. HE was performed by bleeding from the carotid artery to reduce arterial blood pressure to about 55 mmHg (3 ml of bleeding per 200 g of body weight), and indomethacin was given s.c. in a dose of 5 mg/kg. Duodenal pH was determined in the outflow from the proximal duodenum (1.7 cm) which was perfused with 10-4 M HCl, and acid-neutralizing capacity was measured by back-titration of the perfusate to pH 4.0 with 10 mM HCl. Under these conditions, duodenal pH was kept at around 6.0 as the result of neutralization in the loop (8 μEq/hr). Both HE and indomethacin significantly decreased the pH and acid-neutralizing capacity. Administration of 16, 16-dimethyl prostaglandin E2 (16-dmPGE2: 30 μg/kg, s.c.) significantly increased both pH and acid-neutralizing capacity in normal and indomethacin-treated rats, but failed to affect these parameters in rats under HE conditions. When the duodenal loop was perfused with 50 mM HCl for 1.5 hr, both HE and indomethacin induced extensive damage in the mucosa. Pretreatment with 16-dmPGE2 significantly reduced the formation of duodenal lesions induced by indomethacin but not by HE. These results suggest that HE as well as indomethacin impaired duodenal acid-neutralizing capacity to reduce the tolerance to acid of the mucosa. The deleterious effects of H E on the mucosa may be mainly due to a decreased mucosal blood flow, but not due to a deficiency of endogenous prostaglandins.View full abstractDownload PDF (456K) -
Fukio KONNO, Masataka KUSUNOKI, Issei TAKAYANAGI1987 Volume 44 Issue 2 Pages 171-178
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSA series of imidazolines and norepinephrine were used to characterize and differentiate the presynaptic alpha2-adrenoceptors in the rabbit vas deferens and the guinea pig Heal longitudinal muscle using pharmacological procedures. Based on pEC50-values (the negative log of the 50% effective concentration) for each imidazoline, a rank order of potency of p-aminoclonidine>oxymetazoline≥clonidine>naphazoline>phentolamine was obtained in the rabbit vas deferens and an order of p-aminoclonidine>clonidine>naphazoline>oxymetazoline was obtained in the guinea pig ileum. In the rabbit vas deferens, phentolamine, which is generally considered to be a competitive alpha1- and alpha2-adrenoceptor antagonist, acted as a full alpha2-adrenoceptor agonist. The dissociation constants of oxymetazoline and yohimbine were significantly lower in the rabbit vas deferens than in the guinea pig ileum. These results suggest that the presynaptic alpha2-adrenoceptors in these tissues are different. Furthermore, the pKB-value of yohimbine against norepinephrine was significantly one log unit lower than those obtained using a series of imidazolines. Data from our studies add to increasing evidence of the existence of high and low affinity binding sites on the alpha2-adrenoceptors in the rabbit vas deferens.View full abstractDownload PDF (499K) -
Yasufumi OHKURA, Yasuhiro MIZOGUCHI, Yoshihide SAKAGAMI, Kenzo KOBAYAS ...1987 Volume 44 Issue 2 Pages 179-185
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSTJN-101, which is a lignan component isolated from schisandra fruits, inhibits hepatotoxic chemicals-induced liver injuries. In this study, effects of TJN-101 on immunologically induced liver injuries were investigated in vivo and in vitro. When a small dose of lipopolysaccharide was injected into mice previously injected with heat-killed Propionibacterium aches, most of the animals died with acute hepatic failure which was produced by cytotoxic factors from activated adherent cells, and liver cells were injuried by antibody-dependent cell-mediated cytotoxic (ADCC) reaction or activated macrophages in vitro. TJN-101 reduced the mortality of the mice with acute hepatic failure dose-dependently. Histologically, necrosis was supressed by the treatment of TJN-101, but infiltration of nonspecific inflammatory cells was not. TJN-101 inhibited the isolated liver cell injuries induced by ADCC reaction or activated macrophages in vitro. These results suggest that TJN-101 can be markedly protective against immunological liver injuries.View full abstractDownload PDF (428K) -
Mitsuhiro YOSHIOKA, Haruhisa YAHAGI, Masaru MINAMI, Hideya SAITO1987 Volume 44 Issue 2 Pages 187-196
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSPrevious data on budralazine, 1-[2-(1, 3-dimethyl-2-butenylidene)-hydrazino]-phthalazine, has indicated that it is a direct-acting vasodilating agent that does not produce marked tachycardia. The present study was undertaken to elucidate what effects may be seen on the central sympathetic nerve activity when budralazine is given systemically to rats. Budralazine (0.5, 1.0 and 5.0 mg/kg, i.v.) produced a dose-dependent reduction of mean arterial pressure. At doses of 0.5 and 1.0 mg/kg, budralazine induced bradycardia accompanied with a decrease in cardiac sympathetic nerve activity. Preganglionic adrenal sympathetic nerve activity was also reduced by budralazine (1.0 mg/kg, i.v.). A dose of 0.5 mg/kg of budralazine neither influenced carotid sinus nerve activity nor augmented aortic depressor nerve activity. On the contrary, a high dose of budralazine (5.0 mg/kg) produced simultaneous increases in the heart rate and cardiac sympathetic nerve activity along with a marked suppression of aortic depressor nerve activity. Plasma norepinephrine and epinephrine concentrations were also increased at a dose of 5.0 mg/kg. These findings suggest that budralazine doses of 0.5 and 1.0 mg/kg may reduce the sympathetic outflow that is mediated via central sympathoinhibitory action. Baroreceptor-mediated tachycardia occurred after high dose budralazine (5.0 mg/kg) administration in anesthetized rats.View full abstractDownload PDF (406K) -
Miwa MISAWA, Kiyoteru TAKENOUCHI, Yukiko SHIRAKAWA, Saizo YANAURA1987 Volume 44 Issue 2 Pages 197-205
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSDevelopment of a nonimmunologically induced experimental asthma model using compound 48/80 was attempted. Male mongrel dogs anesthetized with pentobarbital-Na were immobilized with decamethonium bromide under artificial respiration. Airway resistance was measured with a modified Konzett-Rössler method and expressed as a change in ventilation overflow (VO). Inhalation of compound 48/80 caused no change in VO even in high concentrations up to a 1 % solution. Infusion of compound 48/80 into the bronchial artery at a dose of 0.2 mg/min for 10 min by using the right bronchial perfusion method caused a marked increase in VO accompanied by decreases in perfusion pressure and systemic blood pressure. The compound 48/80-induced bronchoconstriction was inhibited 58% by surgical vagotomy and was almost abolished by chlorpheniramine (10 mg/kg, intraduodenally (i.d.)). Disodium cromoglycate (inhalation of 1% solution along with 5 mg/kg, i.v.), tranilast (300 mg/kg, i.d.) and NCO-650, a new antiallergic drug (100 mg/kg, i.d.) significantly inhibited the compound 48/80-induced bronchoconstriction. These results indicate that 1) compound 48/80 infusion into the bronchial artery produces an asthma-like bronchoconstriction, 2) the main chemical mediator involved in this response would be histamine acting through H1-receptors, and 3) effects of mast cell stabilizers can be evaluated with this model.View full abstractDownload PDF (505K) -
Tatsuji FURUTA, Tatsuro SHIGEI1987 Volume 44 Issue 2 Pages 207-210
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSEndothelium-dependent relaxations of canine veins isolated from 15 different sites were examined. Acetylcholine (ACh, 10-10-10-6M) caused marked endothelium-dependent relaxations in the external jugular vein, superior vena cava, brachiocephalic vein, segment A (supradiaphragmatic portion) and D (infrarenal portion) of the inferior vena cava. However, only contractile responses were induced by ACh in the portal, mesenteric veins and the segment C of the inferior vena cava (between liver and renal veins) with or without endothelium. The other 7 veins showed only small endothelium-dependent relaxations (10-20%). These results indicated that the endothelium-dependent responses of canine veins to ACh are regionally different.View full abstractDownload PDF (202K) -
Norio INOMATA, Norio OHNUMA, Mayumi FURUYA, Yujiro HAYASHI, Yasushi KA ...1987 Volume 44 Issue 2 Pages 211-214
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSProtective effect of α-human atrial natriuretic peptide (α-hANP) on pulmonary edema was investigated using an isolated perfused lung model. Infusion of α-hANP (1.7 to 22 ng/ml or 0.56 to 7.3 nM) prevented the edema induced in isolated lung from guinea pig by repeated treatment of 50 μg of arachidonic acid at 30 min intervals via the pulmonary artery. The antiedematic action of α-hANP was considered to be receptor mediated because the effective concentration was close to the Kd value of the binding of the ANP receptors in the lung homogenate.View full abstractDownload PDF (227K) -
Isamu OKUNO, Kiyohisa UCHIDA1987 Volume 44 Issue 2 Pages 215-217
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe effects of latamoxef, cefamandole, carbenicillin and cefotaxime on fibrinolytic system in rats were examined under feeding of an ordinary diet or a vitamin K-deficient diet for eight days. No obvious change was observed in UK-induced plasma clotlysis time, euglobulin lysis time and antiplasmin level in plasma. These findings of the in vitro and ex vivo studies suggest that these antibiotics cause no enhancement of fibrinolytic activity.View full abstractDownload PDF (175K) -
Toshihiko IIJIMA, Masao ENDOH, Norio TAIRA1987 Volume 44 Issue 2 Pages 218-221
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSIn canine atrial muscles, carbachol and nicorandil hyperpolarized the resting membrane potential and shortened the action potential duration. In the presence of carbachol or nicorandil, isoproterenol further hyperpolarized the resting membrane potential and shortened the action potential duration. Isoproterenol significantly increased the plateau duration in the presence of nicorandil, but further abbreviated it in the presence of carbachol. This increase in the plateau duration by isoproterenol in the presence of nicorandil probably reflects the increase in the slow inward current.View full abstractDownload PDF (193K) -
Masafumi OSHITA, Tetsuo OHASHI, Kouji MORIKAWA, Hideo KATO, Yasuo ITO, ...1987 Volume 44 Issue 2 Pages 222-224
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSThe affinity and selectivity of a novel spasmolytic agent, tiquizium bromide (HSR-902), for muscarinic receptors were studied by the radioligand binding technique using 3H-quinuclidinyl benzilate. The parameters (Kj, nH) of HSR-902 obtained from competition experiments in cerebral cortex and heart muscarinic receptors showed that HSR-902 was an atropine-type, nonselective muscarinic antagonist. The affinity of HSR-902 toward the stomach and ileal muscarinic receptors was about 3-4 times more potent than atropine.View full abstractDownload PDF (156K) -
Hitoshi OHMORI, Midori IENAGA, Itaru YAMAMOTO1987 Volume 44 Issue 2 Pages 225-227
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSWe have devised a new culture medium that is made of RPMI-1640 medium, 500 μg/ml β-cyclodextrin (β-CD) and 1% fetal calf serum (FCS) (β-CD medium). Murine lymphocytes stimulated with sheep erythrocytes in vitro developed antibody-forming cells in β-CD medium as efficiently as in 10% FCS-containing RPMI-1640 medium (10F medium). Immunostimulating agents (SA96 and levamisole) and immunosuppressive agents (hydrocortisone and D-penicillamine) showed similar immunomodulating effects on the antibody responses in both media. In addition, the enhancing effect of levamisole varied drastically depending on the lot of FCS used in 1OF medium, but a clear enhancement was always observed in β-CD medium containing any lot of FCS tested.View full abstractDownload PDF (141K) -
Hachiro USUI, Kazuyoshi KURAHASHI, Hiroaki SHIRAHASE, Kiyoshi FUKUI, M ...1987 Volume 44 Issue 2 Pages 228-231
Published: 1987
Released on J-STAGE: September 15, 2006
JOURNAL FREE ACCESSIn the canine basilar artery, noradrenaline-induced contraction was markedly decreased by intimal rubbing. Scanning electron microscopic studies showed that the rubbing procedure had scrapped away the endothelial cells from the intimal surface of the artery. Prazosin (10-7 M) reduced the noradrenalineinduced contraction in intact arteries, but did not significantly affect the contraction in the scrapped arteries. Yohimbine (10-7 M) strongly inhibited the contraction in both intact and scrapped arteries. The endothelium-dependent vasocontraction produced by noradrenaline was inhibited by aspirin (5×10-5 M), OKY-046 (10-5 M) and ONO-3708 (5×10-9 M). The present experiments provided evidence for endothelium-dependence of the vasocontraction produced by noradrenaline in canine basilar arteries, and they suggested that the endothelium-derived contracting factors might be arachidonic acid metabolites such as TXA2; they also suggested that alpha1 adrenoceptors might be preferentially distributed on the endothelium, while alpha2 adrenoceptors are preferentially located in smooth muscle.View full abstractDownload PDF (285K)
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