Folia Pharmacologica Japonica
Online ISSN : 1347-8397
Print ISSN : 0015-5691
ISSN-L : 0015-5691
Volume 85, Issue 6
Displaying 1-9 of 9 articles from this issue
  • Toshihiko IIJIMA
    1985 Volume 85 Issue 6 Pages 415-423
    Published: 1985
    Released on J-STAGE: March 02, 2007
    JOURNAL FREE ACCESS
    Understanding of the electrophysiological properties of the calcium channel in cardiac cell membranes has been hampered because of the difficulties in interpreting voltage-clamp data. Recently, new techniques for isolation of adult heart cells, internal dialyzation of the cell and analysis of the single ion channel current have been established. Some of the previous results and concepts obtained in intact cardiac tissues have been confirmed and new understanding of the nature of the calcium channels has been gained by the techniques. In this article, the author reviews the electrophysiological and electropharmacological properties of the calcium ion channels in cardiac cell membranes. Especially, emphasis is placed on new information gleaned from the new techniques.
    Download PDF (7322K)
  • Takao KUBO
    1985 Volume 85 Issue 6 Pages 425-433
    Published: 1985
    Released on J-STAGE: March 02, 2007
    JOURNAL FREE ACCESS
    The nicotinic acetylcholine receptors present in the mammalian brain have received less attention than those in other areas of the nervous system. However, recent studies have reported the pharmacological character and regional distribution of a high-affinity binding of [3H]acetylcholine or[3H]nicotine. In this review, the pharmacological characters and physiological functions of the brain nicotinic receptors were discussed with special reference to central cardiovascular regulation.
    Download PDF (7784K)
  • Yoshitaka KUDO, Yoshimitsu ICHIKAWA, Hiroyuki SUGIURA, Keigo NISHINO, ...
    1985 Volume 85 Issue 6 Pages 435-441
    Published: 1985
    Released on J-STAGE: March 02, 2007
    JOURNAL FREE ACCESS
    Experimental cerebral infarction accompanying altered cerebral energy metabolism and cerebral edema was produced in rats by injecting arachidonate into the left carotid artery. In the present study, the effects of 3-isobutyryl-2-isopropylpyrazolo[1, 5-α]pyridine (KC-404) on these ischemic insults as well as on the regional cerebral blood flow (r-CBF) were studied. 1) Cerebral metabolism: On the 7th day of infarction, a significant decrease in ATP content and an increase in glucose content were observed, especially in the left hemisphere. There were no significant changes in lactate and puruvate contents as compared with normal rat brain. Treatment with KC-404 (10 mg/kg, p.o.) once on the 7th day or twice on the 6th and 7th days of infarction caused a significant increase in ATP content and a decrease in lactate content. Increased content of glucose tended to be suppressed by KC-404. In normal rats, KC-404 (10 mg/kg, p.o.) caused slight but significant increases in cerebral ATP, glucose and pyruvate contents. 2) Cerebral edema: On the 4th day of infarction, significant increases in water content and Na+/K+ ratio and a decrease in K+ content were observed in the left hemisphere. Treatment with KC-404 (10 mg/kg, p.o.) for three preceding days showed a significant suppression of increased water content with a tendency to improve altered electrolyte levels. 3) r-CBF: KC-404 (0.05 mg/kg/min) infused i.v. for 15 min increased more markedly the r-CBF in the affected left hemisphere as compared with that in normal brain. These results show that KC-404 exerts therapeutic effects on altered cerebral metabolism and cerebral edema in rats with arachidonate-induced cerebral infarction when administered during the restitution period of the lesion. Furthermore, it is suggested that enhancement of cerebral blood flow in the affected hemisphere would contribute, at least partly, to these observed effects of KC-404.
    Download PDF (5508K)
  • Nobuyuki HARA, Susumu OKABE
    1985 Volume 85 Issue 6 Pages 443-446
    Published: 1985
    Released on J-STAGE: March 02, 2007
    JOURNAL FREE ACCESS
    The effects of gefarnate on several acute gastric lesions were studied in rats. Gefarnate, given at either 100 ?? 1000 mg/kg orally or intraduodenally, dose-dependently inhibited the formation of gastric lesions induced by HCl-ethanol, HCl-taurocholate and aspirin. Cimetidine, given at 30 ?? 100 mg/kg as a reference drug, also significantly inhibited both HCl-ethanol and aspirin-induced lesions. The present study suggests that gefarnate, as well as cimetidine, is useful for the treatment of acute gastric lesions in man.
    Download PDF (2754K)
  • Yasumi UCHIDA, Tsuneaki SUGIMOTO
    1985 Volume 85 Issue 6 Pages 447-451
    Published: 1985
    Released on J-STAGE: March 02, 2007
    JOURNAL FREE ACCESS
    During the search for a new antihypertensive substance, the author and his co-workers found that SGB 1534 has a potent vasodepressor action. However, its pharmacological properties are not well-known. Therefore, we examined the cardiovascular effect and the site of action of this substance. In anesthetized beagle dogs, SGB 1534 (0.01 μg/kg, i.v.) caused a 8% fall in mean systemic blood pressure. It caused a transient increase in aortic blood flow. Heart rate was increased transiently and was decreased thereafter. Systemic vascular resistance was reduced, but Vpm and time constant “T” were little influenced by this substance. The phenylephrine-induced vasopressor effect was eliminated by SGB 1534. In dogs pretreated with propranolol and prazosin, the norepinephrine-induced vasopressor effect was supressed by yohimbine, but not by SGB 1534. In dogs pretreated with prazosin and yohimbine, isoproterenol-induced increase in heart rate was not influenced by this substance. The results indicate that SGB 1534 is a potent α1-adrenoreceptor blocking substance.
    Download PDF (4624K)
  • Yoshiyuki IGUCHI, Masanobu OZAKI, Shiroh KISHIOKA, Sadako TAMURA, Hiro ...
    1985 Volume 85 Issue 6 Pages 453-465
    Published: 1985
    Released on J-STAGE: March 02, 2007
    JOURNAL FREE ACCESS
    In order to investigate the involvement of pituitary fi-endorphin in electroacupuncture analgesia (EAA), the effects of hypophysectomy, dexamethasone (Dex) and adrenalectomy on the analgesia and the increase in plasma corticosterone (Cort) and ACTH levels produced by electroacupuncture (EA) were studied in male SD rats. In saline-treated and Dex-treated rats, plasma Cort levels were correlated with plasma ACTH levels. In non-treated rats, the time course of EA-induced increase in pain threshold was similar to that of EA-induced elevation of plasma Cort levels. In the hypophysectomized rats, EAA was significantly reduced and the EA-induced increase in plasma Cort was also abolished. Single administration of a large dose of Dex tended to reduce EAA and significantly reduced the EA-induced increase in plasma Cort and ACTH. Further suppression of pituitary functions by 4 days-treatment with Dex resulted in further reduction of EAA and the EA-induced increase in plasma Cort and ACTH. On the other hand, hind-paw pressure test without EA produced an increase in plasma Cort and ACTH to the same extent as that produced by EA and produced no analgesia. In the adrenalectomized rats, EAA was reduced, and the plasma ACTH level, which was sixteen times higher than that of nonoperated rats, was further elevated 2-fold higher by EA. No correlation between plasma ACTH levels and the increase in pain thresholds was observed in individual rats of the saline-treated and Dex-treated groups. Control pain thresholds were not influenced by hypophysectomy, Dex or adrenalectomy. These results suggest that pituitary β-endorphin may not be mainly involved in EAA.
    Download PDF (8702K)
  • Shiroh KISHIOKA, Yoshiyuki IGUCHI, Masanobu OZAKI, Hiroyuki YAMAMOTO
    1985 Volume 85 Issue 6 Pages 467-480
    Published: 1985
    Released on J-STAGE: March 02, 2007
    JOURNAL FREE ACCESS
    The development of tolerance to and dependence on morphine over 1 ?? 8 days treatment with morphine were studied with time in rats in which the nucleus reticularis gigantocellularis (NRGC), including the nucleus reticularis paragigantocellularis, were electrically destructed. The NRGC of SD male rats was bilaterally lesioned (DC, 0.5 mA, 40 sec), and morphine analgesia was estimated by the tail flick method. Morphine analgesia in NRGC-destructed rats (D-rat) was reduced to about 50% of that in sham-operated rats (S-rat). The dose of morphine to produce equi-analgesia increased 2 ?? 21.8 times during 1 ?? 8 days treatment with morphine in S-rat. Throughout this period, ratios of the equi-analgesic dose in D-rat to that in S-rat were almost the same, i.e., the rate of tolerance development to morphine analgesia in D-rat was to the same degree as that in S-rat. Administration of naloxone after 1 ?? 6 days treatment with morphine elicited body weight loss and increase in plasma corticosterone (Pcs), degrees of which were dependent on the dose of naloxone or the period of morphine treatment. No difference in these abstinence signs were detected between S and D-rat, i.e., the rate of development of dependence on morphine in D-rat was to the same degree as that in S-rat. These results suggest that the NRGC participates in the development of morphine analgesia, but does not participate in the development of tolerance to and dependence on morphine.
    Download PDF (9758K)
  • Ryuichiro ANDOH, Akihiko YONEZAWA, Tadashi FUJII, Shinobu SAKURADA, Ts ...
    1985 Volume 85 Issue 6 Pages 481-486
    Published: 1985
    Released on J-STAGE: March 02, 2007
    JOURNAL FREE ACCESS
    Desensitizing effects of vanillyl n-nonoylamide, one of the synthetic capsaicinoids, were investigated by algogenics induced vocalization in conscious guinea pigs. Intra-arterial administration of bradykinin, acetylcholine and capsaicinoids (capsaicin, dihydrocapsaicin, vanillyl n-nonoylamide) evoked strong vocalization responses. Increasing doses (50 mg/kg, 100 mg/kg, 200 mg/kg, 400 mg/kg) of vanillyl n-nonoylamide were given to guinea pigs by subcutaneous administration for 4 days. Consecutive administration of vanillyl n-nonoylamide produced a weak but not significant desensitizing effect on bradykinin, acetylcholine-evoked vocalization at several doses. However, a complete suppressive effect on capsaicinoidsevoked response was observed in animals treated with serial administration of vanillyl n-nonoylamide. A weak vocalization response reappeared by three kinds of capsaicinoids (3 μg), but there were statistically significant effects on vocalization count when compared with the control values. It was therefore concluded that serial administration of vanillyl n-nonoylamide had a selective desensitizing action on chemonociceptors.
    Download PDF (4416K)
  • Mitsuo EGAWA, Noriko HASHIMOTO, Akihiro TOBE
    1985 Volume 85 Issue 6 Pages 487-492
    Published: 1985
    Released on J-STAGE: March 02, 2007
    JOURNAL FREE ACCESS
    Cerebral protective effect of MCI-2016 and influence of age on survival time in the cerebral ischemic model induced by bilateral-carotid-arterial ligation in male Mongolian gerbils were studied. Of all animals (6 to 40 weeks old), the mean survival time of the immature group (6 to 7 weeks) was long (3.6 hr), but variable, and that of the 10 to 40 weeks group was relatively stable (1.9 ?? 2.4 hr), but that of the older group (30 ?? 40 weeks) inclined to be reduced. Effects of drugs on this model were studied in 10 to 15 weeks old male Mongolian gerbils. The mean survival time in the control groups was 2.3 ?? 2.4 hr. After a single administration of MCI-2016 at doses of 25 mg/kg, i.p., and 100 mg/kg, p.o., the mean survival time were 8.1 and 6.4 hr, respectively. In these cases, some animals survived over 12 hr, while no animals surviving over 12 hr were observed in the control group. In this model, animals showed severe neurological symptoms. This, however, tended to be depressed by the administration of MCI-2016 at a dose of 25 mg/kg, i.p., which was observed early after ligation. A cerebral metabolic activator, Ca-hopantenate, slightly increased the survival time at a dose of 100 mg/kg, i.p., and a cerebral vasodilator, ifenprodil, was not effective. Subsequently, consecutive administration of MCI-2016 at a dose of 25 and 50 mg/kg, p.o., was more effective than a single administration of MCI-2016 at each dose. The mechanism for the cerebral protective effect of MCI-2016 was discussed.
    Download PDF (4045K)
feedback
Top