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Biomedical subjects

Y Oyama

Publications and source records attributed to Y Oyama.

At least 127 records · Page 7Linked to original sources
PubMed1992

Voltage-dependent modification of Vmax recovery from use-dependent block by pirmenol in guinea pig papillary muscles: comparison with other class I drugs.

Voltage-dependent modification of Vmax (the maximum upstroke velocity of the action potential) recovery from use-dependent block (UDB) by pirmenol was examined and compared with those observed with other Class I drugs using standard microelectrode techniques. A partial depolarization of the resting membrane by increasing extracellular potassium concentration ([K+]o) from 4 to 8 mM potentiated UDB at 2 Hz stimulation by any of the following drugs: pirmenol (10 microM), disopyramide (20 microM), pentisomide (50 microM), quinidine (20 microM), mexiletine (30 microM), and flecainide (5 microM). The recovery time constants from UDB of quinidine and mexiletine were prolonged and that of flecainide was unchanged in 8 mM [K+]o. However, the recovery time constant from UDB of pirmenol was shortened in high K+ solution, as observed with disopyramide and pentisomide. Thus, disopyramide and its analogues, including pirmenol, show a voltage dependency of recovery process, which is different from those of other class Ia, Ib, and Ic drugs. The main unblocking pathway of disopyramide and its analogues from sodium channels during diastolic interval may be different from that of other Class I drugs.

Action Potentials↗
PubMed1992

Tri-n-butyltin increases intracellular Ca2+ in mouse thymocytes: a flow-cytometric study using fluorescent dyes for membrane potential and intracellular Ca2+.

Effects of tri-n-butyltin (TBT) on mouse thymocytes were examined using a flow-cytometer and fluorescent dyes for membrane potential and intracellular Ca2+ ([Ca2+]i). TBT at concentrations from 1 x 10(-7) M to 3 x 10(-7) M caused hyperpolarization in thymocytes during 30 min. after drug application in a time- and dose-dependent manner. Further increase in TBT concentration (to 1 x 10(-6) M) made hyperpolarization of thymocytes more profound within 5 min. after application, thereafter gradually depolarized them during the next 25 min. TBT at 3 x 10(-8) M or more (up to 1 x 10(-6) M) increased the [Ca2+]i of thymocytes. After reaching maximum [Ca2+]i at the various TBT concentrations used within 5 min. after drug application, the [Ca2+]i slightly decreased in a time-dependent manner. Effects of TBT on membrane potential and the [Ca2+]i were greatly reduced under nominal external Ca(2+)-free condition. Results suggest that TBT can promote Ca(2+)-influx to thymocytes, resulting in hyperpolarization by activation of Ca(2+)-dependent K+ current. The increase in [Ca2+]i by TBT may be related to its cytotoxic action on thymocytes.

Animals↗
PubMed1992

Accelerating action of quinidine on the decay phase of transient outward current in dissociated hippocampal pyramidal neurons of rats.

The effect of quinidine on the transient outward current (IA) in rat hippocampal neurons was studied. Quinidine at 1 x 10(-6) M or more dose-dependently decreased the IA without affecting the current-voltage relationship. Quinidine accelerated the decay phase of the IA, suggesting the blockade of open channels. This result may have an implication on the side effects of quinidine in the central nervous system, since the IA is involved in the control of rhythmic electrical activity of the neurons.

Animals↗
PubMed1992

Triphenyltin-induced increase in the intracellular Ca2+ of dissociated mammalian CNS neuron: its independence from voltage-dependent Ca2+ channels.

To test the possibility that triphenyltin (TPT) increases the intracellular Ca2+ ([Ca2+]i) in neurons as found previously in thymocytes, the effect of TPT on [Ca2+]i was examined in rat cerebellar neurons by a flow-cytometer with fluorescent dyes. TPT at concentrations ranging from 3 x 10(-7) M to 1 x 10(-5) M dose-dependently increased the [Ca2+]i. The TPT-induced increase in [Ca2+]i was not attenuated by a Ca2+ channel blocker, suggesting that it was not dependent on voltage-dependent Ca2+ channels. As the concentration of external Ca2+ ([Ca2+]e) increased, TPT produced a more profound increase in the [Ca2+]i. However, the increase in the [Ca2+]i by TPT was observed even in nominally [Ca2+]e-free solution. These results suggest two possibilities. First, TPT may promote Ca(2+)-influx to the neuron. Secondly, TPT may affect the intracellular Ca-store sites. This study is relevant to the neurotoxicity of organotins because it has become progressively clear that sustained increases in the [Ca2+]i can activate various Ca(2+)-dependent degradative processes.

Animals↗
PubMed1992

Characterization of the triphenyltin-induced increase in intracellular Ca2+ of mouse thymocytes: comparison with the action of A23187.

The properties of triphenyltin (TPT) in increasing intracellular Ca2+ ([Ca2+]i) of thymocytes was studied, in comparison with those of A23187, by the use of fluorescent dyes to monitor membrane potential and [Ca2+]i. Both 1 microM TPT and 30 nM A23187 increased the [Ca2+]i associated with the hyperpolarization mediated by Ca(2+)-dependent K+ conductance. The time course for the TPT-induced increase in the [Ca2+]i was much slower than that of A23187. When the external Ca2+ ([Ca2+]o) was removed, TPT produced a slight, but persistent, increase in the [Ca2+]i while A23187 caused only a transient increase in the [Ca2+]i. Reintroduction of Ca2+ to the external solution produced an increase in [Ca2+]i in both cases. Therefore, these results suggested that the increase in the [Ca2+]i of thymocytes induced by TPT and A23187 was dependent on the presence of [Ca2+]o and an intracellular Ca store. The potency of TPT in increasing the [Ca2+]i was greater than those of diphenyltin and monophenyltin, suggesting an involvement of the lipophilic property of organotins in increasing [Ca2+]i. The TPT-induced increase in the [Ca2+]i may be partly responsible for the toxicity of TPT on organs and/or organ systems.

Animals↗
PubMed1992

Flow cytometric estimation of the effect of Ginkgo biloba extract on the content of hydrogen peroxide in dissociated mammalian brain neurons.

The effect of Ginkgo biloba extract (GBE) on the content of hydrogen peroxide was estimated in cerebellar neurons dissociated from rats, by means of a flow-cytometer and 2',7'-dichlorofluorescein (DCF) diacetate, a fluorescent dye for intracellular hydrogen peroxide. The GBE started to reduce the DCF fluorescence of the neuron at 0.1 microgram/ml to 0.3 microgram/ml. Further increases in the GBE concentration (up to 3 micrograms/ml) produced a dose-dependent decrease in the DCF fluorescence, suggesting that GBE reduces the content of hydrogen peroxide or suppresses the reactive oxygen species (ROS) formation of cerebellar neurons. The present technique may be useful for preliminary evaluations of agents affecting the ROS formation in mammalian brain neurons.

Animals↗
PubMed1992

What is the clinical disadvantage of discarding old radiographs? Survey of patients not re-examined for a long time.

The clinical disadvantage of discarding old radiographs was evaluated in patients who had not been re-examined for more than 8 years after their last radiological examination, 38,772 in total. During the 1 year survey, 158 (0.41%) of them underwent re-examination after a long interval. Retrospective evaluation revealed that in only 12 patients (0.032%) were the old films useful. This survey suggested that the clinical risk of not referring to films more than 8 years old would be less than 0.049%. We consider this acceptable, and have formulated new guidelines of storage of films.

Evaluation Studies as Topic↗
PubMed1991

Delayed potassium current and non-specific outward current in pyramidal neurones acutely dissociated from rat hippocampus.

The electrical property of delayed K+ currents (IKD) was studied in pyramidal neurones freshly isolated from the rat hippocampal CA1 region. The IKD was separated pharmacologically from other membrane currents. Activation and inactivation processes of the IKD were highly voltage-dependent in the potential range between -30 and +20 mV. The steady-state inactivation of IKD was observed at -100 mV or more positive potentials. The potential for half steady-state inactivation was -65 mV. The IKD was fully inactivated around -20 mV. Reactivation of IKD consisted of two exponential components. After pharmacological suppression of IKD, the small amount of residual voltage-dependent outward current (one-fifteenth to one-twentieth of IKD amplitude) was observed. The current kinetics was similar to that of IKD and greatly reduced by substitution of internal K+ with N-methyl-D-glucamine+. It was concluded that the properties of IKD was basically similar to those of IKD in other excitable tissues and that the residual current might be non-specific outward current.

4-Aminopyridine↗
PubMed1991

Rapid interaction of tetraethylammonium with delayed K+ channel in mammalian brain neuron.

In order to study the rapidity of interaction between tetraethylammonium (TEA) and the delayed K+ channel of the mammalian brain neuron, TEA was applied to isolated rat hippocampal pyramidal neurons in a time-controlled sequence with a voltage step using a concentration clamp technique. TEA at a concentration of 30 mM, externally applied, started to decrease the delayed K+ current (IKD) without any detectable delay after the onset of the drug application. The inhibitory action of TEA reached a steady state within 10 ms while the full recovery from the inhibition required 20-30 ms after removing TEA from the external solution. Ba2+ at a concentration of 30 mM also reduced the IKD without any detectable delay. However, it took 40-60 s to reach the steady state of inhibition. Full recovery from the inhibition by Ba2+ was obtained around 60 s after removal of Ba2+ from the external solution. It is suggested that the interaction of TEA with the delayed K+ channel is much faster than that of Ba2+.

Animals↗
PubMed1991

[How many years should we keep films?].

In our university hospital, all of the radiographs have been stored since the hospital opening in 1974, and they can be retrieved easily. The total number of jackets is about 230,000. Access rates to them were surveyed, and it became clear that inactive jackets were increasing with the age of the hospital. On the contrary, fraction of active jackets increased slightly. Five radiologists evaluated the usefulness of referring to the previous films in the film reading processes. Subjects were 158 patients who were examined after the interval of 8 years or more. Assuming to discard their previous radiographs, the simple inaccessibility risk was 0.41% and the risk decreased to 0.0026% taking the clinical disadvantage into consideration. Risk to research works was estimated as 0.97%. Based on these surveys and evaluations, our university decided to discard radiographs of patients who had not revisited these 10 years with the exception of important cases for researches.

Humans↗
PubMed1991

Cytotoxic action of triphenyltin on mouse thymocytes: a flow-cytometric study using fluorescent dyes for membrane potential and intracellular Ca2+.

Effects of triphenyltin on mouse thymocytes were examined using fluorescent dyes to monitor membrane potential and intracellular Ca2+. Triphenyltin at 3 x 10(-7) M to 1 x 10(-6) M hyperpolarized thymocytes and depolarized them at 3 x 10(-6) M or more, associated with increasing intracellular Ca2+. Hyperpolarization was suppressed by quinine, but not by tetraethylammonium and 4-aminopyridine, suggesting the involvement of Ca(2+)-activated K+ current. Triphentyltin failed to hyperpolarize thymocytes in Ca(2+)-free solution. Results indicate that triphenyltin promotes Ca(2+)-influx to thymocytes. Such an action of triphenyltin may be related to the immunotoxicity of organotins.

4-Aminopyridine↗