Pharmacological studies on sufoxazine (Y-8894). II. Anti-anoxic effect.

Izumi, Noriyoshi; Yasuda, Hiroshi

doi:10.1254/fpj.86.323

Cited by 4 publications

(2 citation statements)

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“…Moreover, the compound shows both antiamnesic and anti-anoxic effects in experimental animals (Anami et al, 1985;Izumi et al, 1985). Quantitative pharmaco-EEG findings in humans demonstrate that Y-8894 is indeed a psychoactive drug as it induced an increase in alpha activity and decrease in fast beta activity (M. Saito, personal communication).…”

Section: Introductionmentioning

confidence: 99%

Clinical pharmacology of a new antidepressant, Y‐8894 in healthy young and elderly volunteers.

Ogura

Kishimoto

Kunimoto

et al. 1987

Brit J Clinical Pharma

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1 In the first experiment the influences of a single oral administration of a new antidepressant, Y-8894 50 mg, nortriptyline 50 mg, and placebo on physiological and psychological parameters were evaluated by a double-blind, crossover method in 10 healthy male volunteers. As the second experiment eight elderly healthy men were also recruited to examine the clinical pharmacology of Y-8894. 2 Y-8894 50 mg showed no significant anticholinergic, sedative, or cardiovascular effect on any of the measures used in young subjects. 3 In the elderly Y-8894 50 mg increased pulse rate (P < 0.05-0.01), lowered systolic blood pressure (P < 0.05-0.005), and decreased salivary flow (P < 0.05) compared with those of pre-drug baseline. C.f.f. was improved after Y-8894 50 mg, but not significantly. 4 Neither psychomotor performance nor immediate memory was influenced after either treatment in young subjects. Furthermore, in the elderly Y-8894 50 mg did not affect these parameters.5 In the elderly both k21 and ke were smaller, t½,z was longer, and AUC was larger compared with young subjects (P < 0.01). 6 In conclusion, Y-8894 50 mg seemed to lack the anticholinergic, sedative and cardiovascular effects which were observed after nortriptyline 50 mg in young subjects. In the elderly some affects were recognized, in part, due to pharmacokinetic alteration.

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Section: Introductionmentioning

confidence: 99%

Clinical pharmacology of a new antidepressant, Y‐8894 in healthy young and elderly volunteers.

Ogura

Kishimoto

Kunimoto

et al. 1987

Brit J Clinical Pharma

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“…Theniloxazine antagonizes in rat the C0,-, electroconvulsive shock-, and scopolamine-induced amnesia (Anami et al, 1985), shortening the time of KCN-induced coma; prolonging the survival time in hypobaric hypoxia-loaded mice (Izumi and Yasuda, 1985); reducing the alterations in rat brain phosphocreatine, glucose, and lactate concentrations, and keeping ATP, AMP, and ECP at nearly their normal values in KCN-induced energetic derangement (Yasuda et al, 1986). Theniloxazine inhibits in vitro the norepinephrine uptake to mouse cerebral synaptosomes and inhibits norepinephrine uptake in vivo, but not dopamine or serotonine uptake (Setoguchi et al, 1987).…”

Section: Discussionmentioning

confidence: 98%

Effect of intermittent mild hypoxia and drug treatment on synaptosomal nonmitochondrial ATPase activities

Benzi

Gorini

Arnaboldi

et al. 1993

J of Neuroscience Research

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Synaptosomal nonmitochondrial ATPases linked to the energy-utilizing systems were evaluated in cerebral cortex from normoxic rats and rats submitted to mild intermittent normobaric hypoxia [12 hr daily exposure to N2:O2 (90:10) mixture for 4 weeks]. The activities of Na+,K(+)-ATPase; high- and low-affinity Ca(2+)-ATPase; basal Mg(2+)-ATPase; and Ca2+, Mg(2+)-ATPase were assayed in synaptosomes and synaptosomal subfractions, namely, synaptosomal plasma membranes and synaptic vesicles. The evaluations were performed either in normoxic rats or in hypoxic rats submitted to 4-week treatment with saline (controls) or a vasodilator agent (papaverine), an energy-metabolism interfering agent (theniloxazine), a calcium blocker (nicardipine), and a lipid-metabolism interfering agent (phosphatidylcholine) in order to define the plasticity and the selective changes in individual ATPases. In synaptosomes from rat cerebral cortex, the enzyme adaptation to the daily mild intermittent hypoxia for 4 weeks was characterized by an increase in the activity of Mg(2+)-ATPase, concomitant with a decrease in the activities of Na+,K(+)-ATPase, high-affinity Ca(2+)-ATPase, and Ca2+, Mg(2+)-ATPase. In hypoxic rats the enzyme adaptation to the 4-week treatment with phosphatidylcholine was characterized by an increase in Ca2+, Mg(2+)-ATPase activity and a decrease in Mg(2+)-ATPase activity. The action involves the enzymatic form located in the synaptic plasma membranes. In hypoxic rats the adaptation to the 4 week treatment with nicardipine was characterized by an increase in high-affinity Ca(2+)-ATPase activity, while the 4-week-treatment with theniloxazine induced an increase in Na+,K(+)-ATPase activity. The actions of both nicardipine and theniloxazine were related to the enzymatic forms located in the synaptic plasma membranes. The effects on the biophase induced by the sequential cycles of hypoxia/normoxia and the treatment with the various agents tested should also be related to the changes induced in the activity of some synaptosomal ATPases.

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Synaptosomal non-mitochondrial ATPase activities and drug treatment

et al. 1993

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Energy-using non-mitochondrial ATPases were assayed in rat cerebral cortex synaptosomes and synaptosomal subfractions, namely synaptosomal plasma membranes and synaptic vesicles. The following enzyme activities were evaluated: Na+, K+ -ATPase; high- and low-affinity Ca2+ -ATPase; basal Mg(2+)-ATPase; Ca2+, Mg(2+)-ATPase. The evaluations were performed after four week-treatment with saline [controls] or alpha-adrenergic agents (delta-yohimbine, clonidine), energy-metabolism interfering compound (theniloxazine), and oxygen-partial pressure increasing agent (almitrine), in order to define the plasticity and the selective changes in individual ATPases. In rat cerebral cortex, the enzyme adaptation to four-week-treatment with delta-yohimbine or clonidine was characterized by increase in both high- and low-affinity Ca2+ -ATPase activities. The action involves the enzyme form located in the synaptic plasma membranes. The enzyme adaptation to the subchronic treatments with theniloxazine or almitrine was characterized by increase in Na+, K(+)-ATPase or Mg(2+)-ATPase activities, respectively. The action involves the enzymatic forms located in the synaptic plasma membranes. Thus, the pharmacodynamic effects of the agents tested should also be related to the changes induced in the activity of some specific synaptosomal non-mitochondrial ATPases.

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Pharmacological studies on sufoxazine (Y-8894). II. Anti-anoxic effect.

Cited by 4 publications

References 0 publications

Clinical pharmacology of a new antidepressant, Y‐8894 in healthy young and elderly volunteers.

Clinical pharmacology of a new antidepressant, Y‐8894 in healthy young and elderly volunteers.

Effect of intermittent mild hypoxia and drug treatment on synaptosomal nonmitochondrial ATPase activities

Synaptosomal non-mitochondrial ATPase activities and drug treatment

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