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Volume 54 (1990)
- Issue 4 Pages 345-
- Issue 3 Pages 257-
- Issue 2 Pages 97-
- Issue 1 Pages 1-
Volume 54, Issue 2
Displaying 1-20 of 20 articles from this issue
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Tetsuo MATSUI, Ikuko KIMURA, Masayasu KIMURA1990 Volume 54 Issue 2 Pages 97-103
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSAcetylcholinesterase activity and pseudocholinesterase activity were examined in plasma and in striated muscles (whole heart and diaphragm muscles) of diabetic KK-CAy mice. Both activities of acetylcholinesterase in heart muscle and pseudocholinesterase in plasma were significantly increased in diabetic KK-CAy mice compared to pre-diabetic KK-CAy mice. Both acetylcholinesterase and pseudocholinesterase activities in skeletal muscle were not changed by the diabetic state. The increases in activity of plasma pseudocholinesterase was significantly correlated to the increase in blood glucose level in alloxan-, streptozotocin (STZ)-diabetic ddY mice and diabetic KK-CAy mice. The increase was not correlated to the body weight in non-diabetic female-KK-CAy mice. Furthermore, the activity of heart acetylcholinesterase was significantly correlated with the activity of plasma pseudocholinesterase (r=0.79, P<0.01 ). The activities of acetylcholinesterases in heart muscles from STZ and alloxan-diabetic ddY mice also tended to increase. The hypersensitivity of the pulse rate to a low dose (1 mg/kg) of acetylcholine was correlated to the activity of plasma pseudocholinesterase (r=-0.51, P<0.05). These results demonstrate that the activities of plasma pseudocholinesterase were increased by the diabetic state being associated with the increasing alteration of cardiac sensitivity to acetylcholine in the whole body.View full abstractDownload PDF (391K) -
Jerry J. BUCCAFUSCO, Nevine F. MAKARI, Alan C. HAYS1990 Volume 54 Issue 2 Pages 105-112
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSCentral cholinergic pressor neurons exist at several levels of the neuraxis. Activation of these neurons in spontaneously hypertensive rats (SHR) can lead to an exaggerated hypertensive response when compared with normotensive control animals (WKY). Our earlier studies demonstrated that intravenous injection of the indirect acting agonist physostigmine, but not the direct agonist arecoline, resulted in an exaggerated pressor response in SHR. The purpose of this study was to determine whether discrete injection of cholinergic agonists directly into the CNS would also result in an exaggerated pressor response in SHR. Cholinergic pressor neurons in the posterior hypothalamus may be activated following injection of cholinergic agonists into the lateral cerebral ventricles (I.c.v. injection). Cholinergic pressor neurons in the medulla may be activated following injection of agonists into the cisterna magna (i.c. injection). L.c.v. injection of arecoline in freely-moving animals evoked a pressor response in both SHR and WKY rats that was not significantly different between the two strains. Prior depletion of brain acetylcholine with hemicholinium-3 did not affect the pressor response to I.c.v. arecoline, confirming the postsynaptic site of action of the agonist. Surprisingly, I.c.v. injection of physostigmine also did not result in an exaggerated pressor response in SHR. In contrast, injection of physostigmine into the cisterna magna did produce an enhanced hypertensive response in SHR compared to WKY rats. These results are consistent with the presence of two cholinergic pressor systems; however, only the medullary cholinergic system appears to play a prominent role in spontaneous hypertension. Also the hypothalamic (rostral) cholinergic system does not appear to directly interact with the caudal system.View full abstractDownload PDF (464K) -
Naoya SATOH, Jyunko SUZUKI, Hideki BESSHO, Yoshimi KITADA, Akihiro NAR ...1990 Volume 54 Issue 2 Pages 113-119
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSEffects of betaxolol, a cardioselective β-adrenoceptor antagonist, on cardiohemodynamics and coronary circulation were investigated in two kinds of anesthetized open-chest dog preparations in comparison with those of atenolol and propranolol. When administered intravenously, betaxolol, atenolol and propranolol produced dose-dependent decreases in the heart rate (HR), maximum left ventricular dP/dt ((+)dP/dt), cardiac output (CO) and mean arterial pressure (MAP). Although all three drugs were almost equipotent in decreasing HR, betaxolol was much less potent than atenolol and propranolol in decreasing (+)dP/ dt. Betaxolol decreased the total peripheral resistance (TPR), whereas atenolol and propranolol increased it. In another series of experiments, when administered intravenously, betaxolol, atenolol and propranolol all produced a decrease in the myocardial oxygen consumption (MVO2) and an increase in the atrioventricular conduction time (AVCT). All three drugs were nearly equipotent in decreasing MVO2, although betaxolol was less potent than the other two drugs at higher doses (>300 μg/kg). Prolongation of AVCT with propranolol was stronger than those with betaxolol and atenolol. These results suggest that, unlike atenolol and propranolol, the decrease in TPR as well as β1-adrenoceptor blockade may be responsible for both the hypotensive effect of betaxolol and the decrease in MVO2 with betaxolol. The result that the cardiodepressant effect of betaxolol was much less potent than those of atenolol and propranolol suggests that betaxolol would be more beneficial than the others in the treatment of ischemic heart desease.View full abstractDownload PDF (374K) -
Masami FUJIWARA, Kazutaka MITSUI, Itaru YAMAMOTO1990 Volume 54 Issue 2 Pages 121-131
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSMixed lymphocytes reactions (MLR) and concanavalin A (Con A)- or phytohemagglutinin (PHA)-stimulated proliferative responses were dose-dependently inhibited by salazosulfapyridine (SASP) and cyclosporin A (CsA) in the concentration ranges of 1×10-5-5×10-4 M and 10-1000 ng/ml, respectively. Such a significant inhibition was not observed with metabolites of SASP, sulfapyridine (SP) and 5-aminosalicylic acid (5-ASA). In addition, SASP and CsA inhibited the production of interleukin 2 (IL-2) from splenocytes in these experiments. The inhibitory effect of CsA on IL-2 production practically correlated with that on proliferative responses, whereas SASP showed a less marked inhibitory effect on IL-2 production than on proliferative responses. Neither SP nor 5-ASA inhibited the IL-2 production. In the Con A-induced proliferative response, SASP showed a full inhibition even when added after 4-8 hr of culture, but CsA did not. The splenocytes that were pulsed with Con A for 4 hr could proliferate in response to Con A-supernatant or purified IL-2. CsA exhibited the inhibitory activity only when present during the time of Con A-pulsing, while SASP acted on the subsequent stage of the response, exerting its inhibitory effect. These findings suggest that SASP down-regulates the immune response by a mechanism apparently distinct from that of CsA.View full abstractDownload PDF (562K) -
Eisaku SATOH, Teruyuki YANAGISAWA, Norio TAIRA1990 Volume 54 Issue 2 Pages 133-141
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSThe mode of antagonism by glibenclamide, a potassium channel blocker, of the negative inotropic effects of potassium channel openers, cromakalim, pinacidil and nicorandil, was investigated in canine atrial muscle. Glibenclamide shifted the concentration-negative inotropic effect curves for cromakalim, pinacidil and nicorandil to the right without affecting the basal force of contraction. Schild analysis yielded uniform pA2 values of 6.06-6.35 for glibenclamide against the three potassium channel openers. The force of contraction of atrial muscles previously reduced by cromakalim was also antagonized by increasing concentrations of glibenclamide. Glibenclamide affected neither the concentration-negative inotropic effect curves for carbachol, an opener of the muscarinic receptor-coupled potassium channel, nor those for nifedipine, a calcium channel blocker. From these results, it became evident that glibenclamide behaved as a pharmacological antagonist of cromakalim, pinacidil and nicorandil in cardiac inotropy. The antagonism seems to involve competition of glibenclamide and these potassium channel openers, presumably at the ATP-sensitive channel in canine right atrial muscles.View full abstractDownload PDF (429K) -
Minoru KAWAMURA, Masahito IMANISHI, Yohkazu MATSUSHIMA, Satoshi AKABAN ...1990 Volume 54 Issue 2 Pages 143-149
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSThe present study was designed to examine and compare the acute effects of lisinopril (20 mg) and enalapril (10 mg) after a single oral administration on the inhibition of the renin-angiotensin system (RAS) in eight normal subjects. Serum concentration of lisinopril and enalaprilat, an active metabolite of enalapril, reached the respective maximal levels at 6 and 4 hr after administration of the drugs. At 24 hr, the serum concentration of lisinopril was higher than that of enalapril; thus the rate of disappearance of lisinopril was retarded, in comparison to that of enalapril. The reduction of serum angiotensin I converting enzyme (ACE) activity was consistent with the pattern of increase of concentration of the drugs in the serum. However, with these two drugs, the concentration of plasma ANG II was decreased in a similar manner, and it returned to the pretreatment level within 24 hr. Thus, there was no significant difference in ANG II levels throughout the 24 hrstudy between the lisinopril and enalapril treatment. The results indicate that a single administration of 20 mg lisinopril and 10 mg enalapril show similar potency for lowering the circulating ANG II level, although lisinopril exerts a more sustained inhibition of serum ACE activity. The measurement of ANG II provides useful informations for evaluating the efficacy of ACE inhibitors for the inhibition of circulatory RAS.View full abstractDownload PDF (352K) -
Noriko KINJO, Katsuhiko NOGUCHI, Kiyotake HIRAYAMA, Matao SAKANASHI1990 Volume 54 Issue 2 Pages 151-161
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSCharacteristics of the cardiovascular effects of habu venom were studied in vivo and in vitro in rats. Aortic pressure (AoP), heart rate (HR) and renal cortical blood flow (RCBF) assessed by a laser-Doppler flowmeter were measured in anesthetized rats. Administration of habu venom (0.2-1.6 mg/kg, i.v.) dose-dependently produced a fall in AoP without a marked change in HR. RCBF decreased significantly along with the decline in AoP. Heated habu venom (70°C for 5 min) or the residual venom by dialysis produced similar hemodynamic responses to nonheated crude habu venom. Although habu antivenin significantly reduced the effects of habu venom, indomethacin, aprotinin, atropine, captopril and chlorpheniramine did not. Methylprednisolone significantly attenuated these effects. Habu venom (10-5 to 3×10-4 g/ml) produced dose-dependent relaxations of the isolated rat aorta preparations precontracted with norepinephrine or KCl, which were not affected by indomethacin, nordihydroguaiaretic acid, p-bromophenacyl bromide, mepacrine, methylene blue or de-endothelialization. These results indicate that habu venom, particularly its heat-stable component(s) which has at least more than 10, 000 molecular weight, produces hypotensive and vasorelaxant effects in rats, and suggest that eicosanoids, kinins, histamine, ACh, and endothelium are scarcely involved in these effects.View full abstractDownload PDF (540K) -
Hisashi KURIBARA, Takayasu ASAMI, Takashi SAITO, Iturou IDA, Sakutaro ...1990 Volume 54 Issue 2 Pages 163-170
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSEffects of repeated administration of mergocriptine (CBM36-733: CBM), a long-acting ergot derivative with an agonistic action on both dopamine D1 and D2 receptors, as well as interaction between CBM and methamphetamine (MAP2 mg/kg, s.c.), were investigated by ambulatory activity in mice. CBM at 4 mg/kg significantly suppressed the ambulatory activity, but significantly increased it at 16 mg/kg in the drug-naive mice. However, 4 and 8 mg/kg of CBM were effective for increasing the ambulatory activity when these doses were repeatedly administered for 9 times at intervals of 7 days. The same treatment with 16 mg/kg of CBM produced a reverse tolerance to the ambulation-increasing effect. The mice that had received CBM at 1 and 2 mg/kg, but not 4-16 mg/kg, demonstrated a significantly lower sensitivity to MAP than the saline-experienced mice. On the other hand, the repeated MAP administration induced not only a reverse tolerance to itself, but also a cross reverse tolerance to 8 and 16 mg/kg of CBM. Furthermore, the established reverse tolerance to MAP was scarcely attenuated by the repeated treatment with any doses of CBM, but rather enhanced by 8 and 16 mg/kg of CBM. The present results indicate that, although the dose-effect relations are partially different, the behavioral characteristics of CBM were almost idential with those of bromocriptine, another long-acting ergot derivative having antagonistic and agonistic actions on dopamine D1 and D2 receptors, respectively.View full abstractDownload PDF (369K) -
Masako OKAZAKI, Hideharu SAKAMOTO, Akira OHTSUKI, Katsuji OGUCHI1990 Volume 54 Issue 2 Pages 171-178
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSBrain lipid composition was studied in thiamine deficient rats treated with thiamine antimetabolites (oxythiamine: OT, and pyrithiamine: PT) and thiamine deficient diet (TDD). After intraperitoneal injection of OT (40 mg/kg/day) or TDD feeding for 6 days, body weight gain decreased. However, the PT (500 μg/kg/day) treated rats or the pair fed control (PFC: TDD+thiamine of 5 mg/kg, i.p.) showed no decrease in body weight gain compared with the regular diet control (C). Brain lipid levels (total lipid, total cholesterol, triglyceride, phospholipid, sphingomyelin and cerebroside) were examined in four brain regions (cerebral cortex, subcortical structure, brain stem and cerebellum). Total lipid level increased in four regions in OT or TDD treated rats, but total lipid level in the cerebellum in PT treated rats decreased. Total cholesterol level increased in all treated rats, while the triglyceride level in the brain stem decreased dramatically in OT or TDD treated rats. Cerebroside levels of four regions in the PT, OT or TDD group remarkably decreased, and PFC rats showed a significant improvement of the decrease in cerebroside level. It is conceivable that these changes in brain lipid composition provided some clues for the histological and morphological changes of the brain as manifested by the myelin degradation in acute thiamine deficiency.View full abstractDownload PDF (452K) -
Tomoaki TAMURA, Toshietsu TANIGUCHI, Tetsuo MIYAMOTO, Masaru AOKI, Isa ...1990 Volume 54 Issue 2 Pages 179-185
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSEffects of eptazocine on cerebral metabolic changes due to a sublethal dose of KCN were investigated in mice. KCN (2 mg/kg, i.v.) induced a temporary loss of consciousness being moderated by eptazocine (1-10 mg/kg) in a dosedependent manner. The KCN injection decreased the contents of phosphocreatine (PCr), ATP and glucose and increased the contents of AMP and lactate, resulting in a 34% decrease in energy charge potential (ECP) and an increase in lactate/ pyruvate (L/P) ratio. Such changes were improved by eptazocine (10 mg/kg) and EKC (3 mg/kg), but not by pentazocine (10 mg/kg) and morphine (3 mg/kg), and the improving effect of eptazocine was completely inhibited by MR-2266 (3 mg/kg), a relatively selective opioid κ-receptor antagonist. On the other hand, eptazocine (3, 10 mg/kg) was found to increase the glucose content in normal mice, but not to give significant changes in the contents of glycolytic metabolites and high-energy phosphates. These results suggest that eptazocine may improve anoxic changes in cerebral energy metabolism.View full abstractDownload PDF (341K) -
Yu YAMAGUCHI, Kaori YAMADA, Satomi KITAGAWA, Masaru KUNITOMO1990 Volume 54 Issue 2 Pages 187-196
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSA mouse model of atherosclerosis was produced by feeding a 1.5% cholesterol diet with 0.4% β-aminopropionitrile (BAPN) fumarate, a chemical lathyrogen, for 10 weeks, and the pharmacological sensitivity and specificity of this model were evaluated biochemically with various hypolipidemic drugs and calcium antagonists. Histological findings on this model showed typical angiolathyrism with foam cells in the media of the thoracic aorta. Uniform and marked accumulation of cholesterol, notably esterified cholesterol, in the aorta was observed, although it was much less in mice receiving a high-cholesterol diet or BAPN alone. The reduction in elastin contents in the aorta was a characteristic feature of this model. Clofibrate, cetaben and elastase tended to prevent the increase of cholesterol contents in the aorta, together with their significant hypocholesterolemic effects. Nifedipine, diltiazem and verapamil showed a slight preventive effect on the cholesterol accumulation and on the reduction of elastin content in the aorta without a cholesterol lowering effect in the serum. MgCl2 was more effective than other calcium antagonists and even had a hypocholesterolemic effect. The results indicate that this mouse atherosclerosis model may be usable for primary drug evaluation.View full abstractDownload PDF (626K) -
Keiji MIYATA, Takeshi KAMATO, Akira FUJIHARA, Masaaki TAKEDA1990 Volume 54 Issue 2 Pages 197-204
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSFamotidine has been already demonstrated to be a competitive H2-receptor antagonist in the stomachs of dogs and cats. The present experiments were carried out to examine the effects of famotidine on changes in blood pressure induced by dimaprit and several other agonists in vagotomized, anesthetized dogs and on changes in gastric acid secretion induced by histamine in stomach-perfused, anesthetized rats. Famotidine caused a parallel displacement of the dimaprit dose-response curve to the right with a DR10 value of 0.059 μmol/kg, indicating that famotidine is 166 times more potent than cimetidine in vascular H2-blocking activity. On the contrary, famotidine did not affect the depressor responses to 2-pyridylethylamine and histamine that were antagonized by mepyramine. The histamine dose-response curve was displaced to the right more markedly after simultaneous administration of mepyramine and famotidine than after mepyramine alone. The effects of methacholine, phenylephrine and isoproterenol on blood pressure were not influenced by famotidine in doses up to 720 nmol/kg. In rats, famotidine also caused a parallel displacement of the acid dose-response curve to histamine to the right with a DR3 value of 24 μmol/kg/hr in stomach-perfused rats anesthetized with pentobarbital, exhibiting a potency 108 times greater than that of cimetidine. Analysis of the acid dose-response curve with the Edie-Hofstee transformation showed that famotidine, like cimetidine, was a competitive H2-receptor antagonist.View full abstractDownload PDF (416K) -
Toshio HARAUCHI, Toshio YOSHIZAKI1990 Volume 54 Issue 2 Pages 205-215
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSA simple, useful method was developed for detecting drug nephrotoxicity in rats. Rat urine excreted by stimulation of the sacral part of the back was collected in a beaker, and enzymes in 0.2 ml of the urine were partially purified by centrifugal ultrafiltration using an Amicon MPS-1 kit. Activities of N-acetyl-β-D-glucosaminidase (NAG), alanine aminopeptidase (AAP), γ-glutamyltranspeptidase (γGTP) and lactate dehydrogenase (LDH), and the protein concentration of the enzyme preparation suspended in phosphate-buffered saline were represented as creatinine ratios. A marked increase in these enzyme activities and protein concentration were observed in rats with kidneys damaged by treatment with cephaloridine, HgCl2, cisplatin or gentamicin. The patterns of increase of these indicators differed with the drug, but in general, LDH showed the highest response and NAG, the longest lasting one. These data agreed with the results reported by other researchers using dialyzed 24-hr urine. Thus, we concluded that this method is an efficient one for determining drug nephrotoxicity in rats.View full abstractDownload PDF (515K) -
Miwa MISAWA, Susumu IWAMURA1990 Volume 54 Issue 2 Pages 217-226
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSThe effects of inhaled PAF on the guinea pig nasal mucosa were investigated. Intranasal pressure (INP) was recorded as an index of intranasal resistance. To access the capillary premeability of nasal mucosa, exudation of Evans blue into the nasal lavage fluid was determined. Inhalations of histamine and PAF markedly and significantly increased INP and dye exudation into the nasal cavities. The two responses to PAF were about 20-fold and 70-fold stronger than those of histamine, respectively. A PAF antagonist, CV-3988, significantly antagonized both the PAF-induced increases in INP and dye exudation. Indomethacin and OKY-046 had no effect on the PAF-induced responses. FPL-55712 inhibited the PAF-induced increases in INP and dye exudation by 52% and 40%, respectively. Ovalbumin (OA) antigen challenge by inhalation to sensitized guinea pigs resulted in significant increases in both INP and dye exudation. These two responses to 30 mg/ml OA were inhibited by CV-3988 (10 mg/kg, i.v.) by 55% and 40%, respectively. From the above results, it is indicated that: 1) inhalation of PAF evokes rhinitis-like symptoms through activation of PAF receptors, 2) the PAF-induced rhinitis is, in a part, mediated by leukotrienes, and 3) PAF might be involved in allergic rhinitis.View full abstractDownload PDF (496K) -
Koji TAKEUCHI, Tetsuo TANAKA, Syuichi WAKABAYASHI, Seiichiro MOCHIZUKI ...1990 Volume 54 Issue 2 Pages 227-235
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSEffects of intragastric application of azuletil sodium (KT1-32), a novel antiulcer drug, on transmucosal potential difference (PD) and acid secretion were investigated in the rat stomach. The stomach was mounted on a Lucite chamber and perfused with saline before and after exposure to KT1-32 for 10 min. KT1-32 (3-30 mg/kg) produced an elevation of PD in a dose-dependent manner with a rise of the luminal pH. The increased PD response caused by KT1 -32 (10 mg/kg) persisted after removal of the agent from the stomach, but this PD generating effect was significantly mitigated by pretreatment with omeprazole (60 mg/kg, i.p.). KT1-32 raised PD under basal conditions, but did not significantly affect the reduced PD response caused by 30% ethanol. In addition, topical application of KT1-32 significantly reduced acid secretion caused by histamine (4 mg/kg/hr, i.v.) and carbachol (20 μg/kg/hr, i.v.). In the in vitro study, KT1-32 at 3.9×10-4 M showed 50% inhibition of the H/K ATPase activity prepared from the hog gastric mucosa. These results suggest that KT1-32 exerts locally antisecretory and PD generating effects. The latter may be accounted for by the antisecretory action, which is probably related to the H/K ATPase inhibition.View full abstractDownload PDF (454K) -
Hachiro USUI, Yoshinobu AKIMOTO, Kazuyoshi KURAHASHI, Hiroaki SHIRAHAS ...1990 Volume 54 Issue 2 Pages 237-240
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSThe stable thromboxane A2 analogue, STA2, caused concentrationdependent contractions in the canine basilar artery. In Ca2+-free medium containing EGTA (0.1 mM) and nifedipine (10-6 M), the addition of Ca2+ (2.5 mM) in the presence of STA2 (10-8 M) caused a tonic contraction (nifedipine-resistant Ca2+-induced contraction). In the basilar artery, nitroglycerin did not significantly affect such nifedipine-resistant Ca2+-induced contractions, but nearly abolished the contraction in the coronary artery. The present experiments suggest that the regulatory mechanism of mobilized Ca2+ for the nifedipine-resistant Ca2+-induced contraction produced by STA2 in the basilar artery is different from that in the coronary artery.View full abstractDownload PDF (199K) -
Michiko SHINKAI, Issei TAKAYANAGI1990 Volume 54 Issue 2 Pages 241-243
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSThe contractile responses to substance P (SP), neurokinin A (NKA), Tyr0-neurokinin B (Tyr-NKB), senktide (NK3 receptor selective agonist) and SP methyl ester (SPOMe, NK1 receptor selective agonist) were investigated in detrusor strips from guinea pigs. Except for senktide, all drugs induced a concentrationrelated contraction with the following rank order of potency: SPOMe>SP>NKA≥Tyr-NKB. After desensitization of NK1 receptors with SPOMe, the rank order of potency was NKA≥Tyr-NKB>SP>SPOMe. Both NK1 and NK2 receptors exist in the detrusor strip from guinea pigs.View full abstractDownload PDF (174K) -
Katsuhiko NOGUCHI, Yoshihiko OJIRI, Noriko KINJO, Hidehiko MOROMIZATO, ...1990 Volume 54 Issue 2 Pages 244-249
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSThe effects of superoxide dismutase modified with polyoxyethylene (SOD-POE) on impairment of myocardial segment shortening (SS) during coronary stenosis plus pacing-induced tachycardia (CSPT) and the recovery after reperfusion was examined in anesthetized dogs. SOD-POE or saline was administered i.v. 30 min before reperfusion. Changes in hemodynamic variables and SS by CSPT were similar in both groups. However, the SOD-POE group showed improved recovery of SS compared with the control group. Results indicate that oxygenderived free radicals may partially be involved in the genesis of myocardial dysfunction after CSPT-induced regional ischemia.View full abstractDownload PDF (306K) -
The Anticonflict Effect of MK-801, an NMDA Antagonist: Investigation by Punishment Procedure in MiceHisashi KURIBARA, Suguru FUJIWARA, Hideko YASUDA, Sakutaro TADOKORO1990 Volume 54 Issue 2 Pages 250-252
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSThe NMDA antagonist MK-801 at 0.3 mg/kg, i.p. increased the punished response under a MULT VI 1.5/FR 5-punishment schedule of food reinforcement in mice. Furthermore, although neither MK-801 (0.1 mg/kg, i.p.) nor diazepam (0.25 mg/kg, s.c.) was without effect when separately administered, a significant increase in the punished response appeared after the combined administration of these two drugs. The present results suggest that MK-801 not only shows an anticonflict effect, but also enhances the anticonflict effect of benzodiazepine anxiolytics in mice.View full abstractDownload PDF (179K) -
Isao KISHI, Fumiaki HATA, Tadayoshi TAKEUCHI, Toshiaki ISHII, Osamu YA ...1990 Volume 54 Issue 2 Pages 253-256
Published: 1990
Released on J-STAGE: August 25, 2006
JOURNAL FREE ACCESSStimulation of the hypogastric nerve to the guinea pig vas deferens induced biphasic contraction consisting of a rapid transient phase (mediated by ATP) and a delayed tonic phase (mediated by norepinephrine, NE), whereas stimulations in the presence of selective antagonists caused each contractile phase separately. Stimulation in the absence of antagonist induced a larger rapid transient contraction than that induced by stimulation in the presence of α1-antagonist. Results obtained in separate or simultaneous additions of exogenous ATP and NE showed synergism in the rapid transient contraction. These findings indicate that NE assisted ATP in inducing the hypogastric nerve-mediated contractile response in guinea pig vas deferens, but not vice versa.View full abstractDownload PDF (216K)
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