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Biomedical subjects

J Ishigooka

Publications and source records attributed to J Ishigooka.

23 records · Page 2Linked to original sources
PubMed1988

Phase 1 study of a new antipsychotic drug, OPC-4392.

1. A phase I study of OPC-4392 (OPC), a quinolinone derivative recently developed in Japan and recognized to have an agonistic effect on dopamine autoreceptors, was performed in 7 male healthy volunteers in comparison with chlorpromazine (CPZ). 2. Clinical pharmacology The main clinical symptoms of OPC were sleepiness, weakness, fatigability, heavy headedness, disturbance of concentration, nausea, etc. The severity of these symptoms increased dose-dependently, and the upper limit dosage of OPC was considered to be 5 mg for the healthy volunteers. 3. Endocrinological research The serum prolactin level decreased dose-dependently in the OPC group, whereas it rose in the CPZ group. A significant negative correlation was recognized between the OPC-plasma level and serum prolactin level as well. 4. Psychological tests In the Kraepelin test, a decrease in the average work quantity was observed in both groups, but it was less in the OPC group. 5. Pharmacokinetic study From the pharmacokinetic parameters measured, two features were recognized: one was the slowness of Tmax (4-6 hours) and the other was the length of its biological half-life (56-88 hours). It was estimated that the plasma level of OPC-4392 would take 2 weeks to reach a steady state.

Adult↗
PubMed1986

A sporadic case of benign myoclonus epilepsy of adult onset: its clinical aspects and electroencephalographic, polygraphic study.

A sporadic case of myoclonus epilepsy of adult onset with a benign course is presented. Its clinical implications were discussed symptomatologically and nosologically. EEG findings consisted of the slowing of basic activity, characteristic polyspike and wave discharges or other paroxysmal patterns and photomyoclonic response (PMR). The PMR was well evoked by flashes of 6-21 Hz and of yellow or red color. Clinical similarities of this case to those of hereditary myoclonus epilepsy without progressive dementia and cerebellar ataxia, and pathognomonic characteristics of electrophysiological findings indicated that the myoclonic epilepsy syndrome might share basic properties, which are state-dependent, but independent of underlying neuropathology or heredity. During sleep, paroxysmal discharges with spike(s) significantly decreased in slow-wave sleep and almost recovered in REM sleep. This finding suggests that the brain stem may be responsible for the epileptogeneity in this case.

Adult↗
PubMed1985

Different effects of centrally acting drugs on rabbit platelet aggregation: with special reference to selective inhibitory effects of antipsychotics and antidepressants.

Twenty-four drugs, consisting of antipsychotics, tricyclic antidepressants, other centrally acting drugs, and related compounds, were studied for their effects on aggregation of rabbit platelets. Phenothiazine neuroleptics, haloperidol, sultopride, tricyclic antidepressants, sulpiride, atropine, and propranolol showed a selective inhibitory effect on the collagen-induced aggregation, but not on aggregations induced by arachidonic acid (AA) or adenosine diphosphate (ADP). These drugs are thought to inhibit the liberation of AA from phospholipids in platelet membranes, suggesting that they might inhibit phospholipases. Mepyramine, promethazine, phentolamine, and clozapine inhibited the aggregations evoked by collagen and AA, but failed to inhibit the ADP-induced aggregation. These drugs might inhibit the generation of prostaglandin endoperoxides or thromboxanes. Phenobarbital, phenytoin, procaine, lidocaine, flurazepam, trihexyphenydil, and lithium carbonate did not inhibit any kind of aggregation at the concentrations used. The clinical and pharmacological significance of these findings is discussed; it seems that the inhibitory effects of antipsychotics and antidepressants on platelet aggregation are closely related to the specific clinical and psychotropic effects of these drugs, but not to other actions.

Animals↗
PubMed1980

Selective inhibitory effects of chlorpromazine and imipramine on platelet aggregation.

The effects of chlorpromazine (CPZ) and imipramine (IMP) on platelet aggregation in vitro were investigated. Both CPZ and IMP inhibited epinephrine-induced secondary aggregation in a dose-dependent fashion and changed adenosine diphosphate (ADP)-induced irreversible aggregation into a reversible response in human platelets. With rabbit platelets, CPZ (0.6-20 microM) and IMP (6-60 microM) showed a selective inhibitory effect on the aggregation by collagen, whereas, even at 200 microM, this effect was found neither in arachidonic acid (AA)-induced aggregation nor in ADP-induced one. CPZ and IMP also inhibited human platelet aggregations induced by collagen, but not by AA. The antiaggregating action of CPZ and IMP was thought to be due to their inhibitory effects on AA liberation from platelet membranes, suggesting that they might inhibit participating enzymes (phospholipase A2, C or lipase) or the process of the activation of the enzymes.

Acetophenones↗