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Volume 108, Issue 5
Displaying 1-4 of 4 articles from this issue
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Masaru MINAMI, Toru ENDO, Masahiko HIRAFUJI1996 Volume 108 Issue 5 Pages 233-242
Published: 1996
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSThere are now abundant evidence to confirm the role of serotonin (5-HT) and in particular, 5-HT3 receptors in the control of cisplatin-induced emesis. Emesis caused by cisplatin is associated with an increase in the concentration of 5-HT in the intestinal mucosa and in the area postrema. The intestinal mucosa contains enterochromaffin (EC) cells that synthesize and secrete approximately 80% of all 5-HT produced in the body. A selective 5-HT3 agonist, 2-methyl-5-HT, induced a dose-dependent increase in 5-HT level from the ileum. Furthermore, a selective 5-HT4-receptor agonist, 5-methoxytryptamine also induced a concentration-dependent increase of 5-HT level. Both 5-HT3 and 5-HT4 receptors may be involved in intestinal 5-HT release. It is proposed that anticancer drugs cause 5-HT release from the EC cells and that the released 5-HT stimulates the 5-HT3 receptors on the afferent vagal fibers, resulting in their deporalization. Electrical stimulation of the abdominal vagal afferents is capable of inducing emesis, and abdominal vagotomy suppresses cisplatin-induced emesis. These results indicate that the vagus is the major afferent pathway involved in the detection of emetic stimuli.View full abstractDownload PDF (9790K) -
Hideyuki FUNATO, Yukio KATSUKI, Takashi YANO, Hiroyuki KAWANO, Yasushi ...1996 Volume 108 Issue 5 Pages 243-257
Published: 1996
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSWe examined the cerebral protective effects of lacidipine (L) using three different types of cerebral ischemia models, and the effects were compared with those of nicardipine (N). (1) In the transient forebrain ischemia model of the rat, oral administration of L (0.3 and 1 mg/kg) before ischemia significantly decreased the number of acidophilic neurons in CA1 regions of the hippocampus 7 days after ischemia. N (3 mg/kg, p.o.) before ischemia also produced a significant reduction in the number of acidophilic neurons, and it's effectiveness was almost the same as that of L (1 mg/kg). (2) In the focal cerebral ischemia model of the rat, oral administration of L (1 and 3 mg/kg) before of after left middle cerebral artery occlusion (MCAO) significantly reduced infarct size at 24 hr after MCAO. Such an ameliorative effect was also observed when N was administered orally. However, the effect of N at 30 mg/kg was less than that of L at 1 mg/kg. (3) In the delayed cerebral vasospasm model of the dog after subarachnoid hemorrhage (SAH), intravertebral artery injection of L (10 μg/kg) or N (10 μg/kg) dilated the contracted basilar artery 3 days after SAH to the level before SAH. Finally, while both L and N increased cerebral blood flow (CBF) in a dose-dependent manner in conscious normal rat, the increment of CBF induced by L at a given level of reduced-blood pressure was greater than that induced by N. These results indicate that lacidipine may be a potential therapeutic agent that exerts a protective effect against brain damage after cerebral ischemia.View full abstractDownload PDF (12522K) -
Isami KIMURA, Shinobu NAGAHAMA, Maki KAWASAKI, Mikiko KATAOKA, Makoto ...1996 Volume 108 Issue 5 Pages 259-266
Published: 1996
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSWe have already confirmed that symptoms in the experimental UC model in rats induced by ingesting DSS resembled those of human UC. In the present study, to clarify the participation of chemical mediators concerned with the development and etiology of the experimental UC model, we investigated the effects of superoxide dismutase (SOD), 5-aminosalicylic acid (5-ASA), AA-861, an LTB4-receptor antagonist (LTB4-ra), indomethacin (Ind) and OKY-046 on the DSS-induced UC model in rats. The UC model was produced by giving rats drinking water containing 3% DSS, and animals were selected when bloody stool was observed in more than 90% of the animals. After selection, drugs were intrarectally administered once a day, for 7 days, to UC rats that were given drinking water containing 1 % DSS. SOD, 5-ASA, AA-861 and LTB4-ra inhibited the formation of erosions in the large intestine. Furthermore, SOD, 5-ASA and LTB4-ra improved the length of the large intestine of rats that had been shortened by ingesting DSS. On the other hand, neither Ind nor OKY-046 improved the shortening and erosion of the large intestine. From these results, it is concluded that the free radical and lipoxygenase metabolites of arachidonic acid may be partially involved in the DSS-induced UC model in rats.View full abstractDownload PDF (7467K) -
Naoki FUJIKURA, Tatsuro YOKOYAMA, Yukinori MASUDA, Ken-ichi SHIKADA, S ...1996 Volume 108 Issue 5 Pages 267-274
Published: 1996
Released on J-STAGE: February 06, 2007
JOURNAL FREE ACCESSEffect of efonidipine hydrochloride (efonidipine) on myocardial oxygen tension (PO2) was investigated in open-chest anesthetized dog and compared with those of nifedipine and nisoldipine. P02 was measured by a membrane-coated platinum wire, which was inserted into the myocardium. Intravenous administration of efonidipine (10 and 30 μg/kg) decreased mean blood pressure to a similar extent to that induced by nifedipine (1 and 3 μg/kg) or nisoldipine (1 and 3 μg/kg). Efonidipine increased coronary blood flow (CBF) and decreased the double product (DP) dose-dependently. Similar results were observed in nisoldipine-treated animals. Nifedipine produced a transient increase in CBF and a transient decrease in DP. The duration of action of efonidipine on CBF was longer than that of nifedipine or nisoldipine. Efonidipine increased PO2, and the effect was more pronounced in the endocardial region than in the epicardial region. Nifedipine had no significant effect on the PO2, while nisoldipine significantly increased PO2 in the endocardial region. The effect of efonidipine on the PO2 was greater than that of nisoldipine and the duration of action of efonidipine was longer than that of nisoldipine. These results suggest that efonidipine may increase PO2 by mediating, at least in part, a long-lasting increase in oxygen supply and a decrease in oxygen demand in dog heart.View full abstractDownload PDF (6867K)
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