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Y Ikoma

Publications and source records attributed to Y Ikoma.

34 records · Page 2Linked to original sources
PubMed1989

[Neurotropic effects of non-ionic contrast media].

Effects of non-ionic contrast media on the central nervous system were compared in order to clarify any differences due to the side-chain structures among iopamidol, iotrolan, iocibidol, iohexol, iopromide, iosimide and metrizamide. The study included a primary screening test based on Irwin's method, antielectric convulsive tests using mice, measurement of the blood pressure using rats and electroencephalography using rats and rabbits. The general behavior of mice in the primary screening test revealed that tolerance to iopamidol, iotrolan and iocibidol was excellent; that to iopromide and iohexol was moderate; and that to iosimide and metrizamide was poor. Iosimide and iohexol suppressed the transient increase of blood pressure upon intravenous administration in the normal rats but not in the pithed rats. Electric stimulus increased the mortality of mice pretreated with iosimide and iohexol. Abnormal EEG with epileptic seizures, slow wave and/or flattening were observed with the administration of iopromide, iosimide or metrizamide as well as ionic contrast media. From these results, it was concluded that iopromide and metrizamide were not well tolerated in general behavior and EEG; iohexol, in general behavior, electroshock and blood pressure; and iosimide, in all experiments, while iopamidol, iotrolan and iocibidol were well tolerated. Therefore, small differences in their side-chain structures among these contrast media are considered to cause different effects on the central nervous system.

Animals↗
PubMed1989

[Effects in animal models of depression of lisuride alone and upon coadministration with antidepressants].

Effects of lisuride, a central dopamine and serotonin agonist of the ergot type, in animal models of depression were investigated in comparison with those of desipramine, mianserin and rolipram. Lisuride, like desipramine and mianserin, inhibited reserpine-induced hypothermia in mice (0.5-5.0 mg/kg, i.p.) and suppressed muricide in olfactory bulbectomized rats (ED50 = 0.16 mg/kg, i.p.) in a dose-dependent manner. The anti-muricidal effect was slightly enhanced by the repeated administration of 0.25 mg/kg lisuride. Lisuride (0.05-0.25 mg/kg, i.p.), like desipramine, dose-dependently reduced the duration of immobility in rats forced to swim, and this effect was antagonized by haloperidol. The reduction of immobility time was enhanced by the repeated administration of lisuride; at the same time, the ambulation in rats increased. Furthermore, the immobility-reducing effects of desipramine and rolipram were markedly enhanced by the co-administration of a low dose of lisuride (0.025 mg/kg, i.p.), which by itself had no effect on the immobility time. These results indicate that lisuride may be useful for the treatment of depression and indicate that a low dose of lisuride may enhance the clinical effectiveness of antidepressants such as desipramine.

Agonistic Behavior↗
PubMed1989

A possible mechanism for the neural adverse reactions caused by metrizamide.

Causality of the metrizamide-induced neural adverse effects was explored among the effects on behavior, electroencephalogram (EEG), and brain glucose utilization in rats. Iotrolan, a new myelographic contrast agent, was used as a reference substance throughout the study. Supracortical subarachnoidal administration of metrizamide caused, within a few minutes, symptoms of sedation and anxiety, which were accompanied by appearance of slow wave or flattening in EEG not only of the cortex, but also of the regions of the hippocampus and thalamus. The rates of local cerebral glucose utilization (LCGU) in a wide range of the brain, measured by using 3H-2-deoxyglucose, were also altered significantly. Despite a limited distribution of metrizamide in the lateral region of the cortex, LCGU was suppressed significantly in the administered side of the parietal cortex, thalamus, subthalamic nucleus, medial geniculate body, and mammillary body and increased in the regions of hippocampus, caudate-putamen, and globus pallidus. It is concluded that, rather than inhibiting the hexokinase reaction in the brain cell, metrizamide appears to cause reduction of a net glucose transport into the cell and that this direct effect on the cortex is amplified and propagated, via neurotransmission, to the regions of the diencephalon and midbrain, causing secondarily various types of disturbance in the mental and motor functions. Iotrolan was proved to lack any biologic activity that may relate to the neural adverse effect observed with metrizamide.

Animals↗
PubMed1988

The effect of a selective phosphodiesterase inhibitor, rolipram, on muricide in olfactory bulbectomized rats.

In order to evaluate the potential usefulness of the drug as an antidepressant, acute and chronic effects of rolipram, a selective inhibitor of Ca2+- and calmodulin-independent cyclic AMP phosphodiesterase were investigated on muricide in olfactory bulbectomized (OB) rats. Upon single administration to OB rats, rolipram at a dosage of 1 mg/kg body weight suppressed the muricide for 2 hr after its administration. As a consequence of daily administration of rolipram, however, the incidence of muricide at 24 hr after the administration was decreased, and more than 60% of the rats did not exhibit the muricide on the 12th day. After the cessation of the administration, the incidence of the muricide returned to the initial level. The suppression of the muricide was not antagonized by several kinds of neurotransmitter blockers. Administrations of phosphodiesterase inhibitors and dibutyryl cyclic AMP as well as desipramine and clomipramine also suppressed the muricide dose-dependently. Repeated administration of desipramine also gave results similar to those of rolipram: repetition of a short suppression on the muricide was followed by the appearance of a long-lasting suppression. Differently from rolipram and desipramine, dibutyryl cyclic AMP did not cause long-lasting suppression, and even the direct effect (75% suppression) observed 30 min after its administration on the first day disappeared during its repeated administration for 14 days. From these results, rolipram was considered to show an antidepressant effect through the inhibition of Ca2+- and calmodulin-independent cyclic AMP phosphodiesterase.

Animals↗
PubMed1983

Changes of metabolism and substrate-binding spectrum of emorfazone between immature and mature guinea-pigs.

Km values for oxidative metabolism at two types of carbon atoms adjacent to nitrogen and oxygen of the morpholino moiety of emorfazone (alpha- and beta-oxygenation) were 1.2 X 10(-2) and 3.0 X 10(-4)M in immature male guinea-pigs, and 8.6 X 10(-3) and 2.5 X 10(-4) M in mature male guinea-pigs, respectively. Vmax values of alpha- and beta-oxygenation were 0.409 and 0.229 mumol/4 nmol cytochrome P-450 in immature male guinea-pigs, and 0.391 and 0.061 mumol/4 nmol cytochrome P-450 in mature male guinea-pigs, respectively. Substrate-binding difference spectrum was composed of type I and reverse type I(RI) spectra both in immature and mature animals, but the spectrum pattern was different. The type RI spectrum was predominant in immature animals, but the spectral pattern in mature animals gradually changed from type RI to type I with increase in substrate concentration. alpha- and beta-Oxygenation may be attributed to two kinds of cytochrome P-450 with different affinities, and the proportions of these cytochrome P-450 species and their spinstate change with maturation of guinea-pigs.

Aging↗
PubMed1982

[Central dopaminergic function in stroke-prone spontaneously hypertensive rats (SHRSP): I. Alteration of locomotor activity and swimming ability].

The possible alteration of central dopaminergic (DA) function, which accompanies the development and persistence of hypertension, was studied in SHRSP by measuring the lisuride-induced locomotor activity and the swimming ability. 1) When administered at a dosage of 50 micrograms/kg, lisuride, a DA agonist, induced significant increases of the locomotor activity in one- and 2-month-old Wistar Kyoto rats (WKY), but not in the 6 month-old rat. Differing from the response of WKY, SHRSP showed only a moderate increase in the locomotor activity at the age of one month (means of systolic blood pressure: 128 mmHg) and apparently no increase at the age of 2 months (176 mmHg). In 6 month-old SHRSP (238 mmHg), hypomotility but not hypermotility was induced by the lisuride administration. 2) Though no significant difference was detected at the age of 4 months, the swimming ability of SHRSP at the age of 8 months was deteriorated significantly as compared to that of WKY, and the impaired swimming performance of SHRSP was improved by the administration of lisuride. These results indicate that some alterations in the synaptic sites of the central DA neuron occurred already at an early stage of the hypertensive development, followed under persistent hypertension by the progressive deterioration of the motor-coordination ability as detected in the swimming ability.

Age Factors↗
PubMed1982

[Central dopaminergic function in stroke-prone spontaneously hypertensive rats (SHRSP): II. Effects of chronic treatment with lisuride on the impaired swimming ability].

Eight month-old SHRSP were treated s.c. with lisuride (50 micrograms/kg per day) for 5 weeks to examine the effect of the central dopaminergic agonist on the deterioration of swimming ability that occurred and progressed under persistent hypertension. General observations on signs and symptoms and histopathological examinations were also carried out with the same rats to evaluate the drug effect on the deterioration of hypertensive symptoms. The poor swimming performance of hypertensive SHRSP was improved significantly by the direct action of lisuride with a maximal effect at the 2nd week of the treatment, although the progress of the deterioration itself was not prevented by the chronic treatment. One week after the drug treatment, 2 out of 8 rats in the control group but none in the lisuride-treated group exhibited the abnormal behavior with aggressiveness, a typical sign of the occurrence of cerebrovascular lesions. Furthermore, macroscopic and histopathological examinations carried out 2 weeks after the drug treatment revealed that severities of the histopathological lesions such as myocardiac necrosis and arteriolosclerosis in the kidney, adrenal and testis were significantly lower in the lisuride-treated group than in the control.

Adrenal Glands↗
PubMed1982

[Effects of an ergot derivative, lisuride, on the central dopaminergic system -- studies of behavioral pharmacology].

The central dopaminergic (DA) activity of lisuride hydrogen maleate (lisuride) was investigated from the view point of behavioral pharmacology in rats and mice. Lisuride exhibited a biphasic action on locomotor activity in mice and rats; with low doses lisuride caused hypomotility, whereas higher doses produced locomotor stimulation. The hypomotility induced by lisuride (0.00625 mg/kg, s.c.) was antagonized by a low dose of sulpiride (10 mg/kg, i.p.) in rats, and the lisuride (0.05 mg/kg)-induced hyperactivity was inhibited with haloperidol (0.1 mg/kg, i.p.). The stimulatory effect of lisuride on locomotion was not affected by the combined pretreatment with reserpine and alpha-methyl-p-tyrosine. The hyperactivity of mice induced by methamphetamine was inhibited by pretreatment with lisuride. In the rat lesioned unilaterally in the nigro striatal pathway by a local injection of 6-hydroxydopamine, a low dose of lisuride induced rotational behavior contralateral to the side of the lesion, and the rotational behavior was inhibited by pretreatment with haloperidol. These results indicate that lisuride at low doses effectively stimulates pre-synaptic DA receptors and the post-synaptic DA receptor under supersensitization in the mesolymbic and nigro striatal systems.

Animals↗