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Biomedical subjects

T Satoh

Publications and source records attributed to T Satoh.

At least 1,315 records · Page 73Linked to original sources

Convergence of sleep-wakefulness subsystems onto single neurons in the region of cat's solitary tract nucleus.

Neurons in the region of cat's solitary tract nucleus were classified into three groups on the basis of their spontaneous discharge rate during slow wave sleep (SS) as compared with wakefulness (W): group I: SS greater than W; group II: SS less than W; and group III: SS divided by W. These three groups were further examined with regard to the modulation of discharge rate i) during motor activity in W, ii) at the transitional phase from SS to paradoxical sleep (PS), iii) during rapid eye movements (REMs) in PS, and iv) following electrical stimulation of the midbrain reticular formation (MRF). During motor activity in W, increase in unit discharge was frequently observed in group II, while group I and III were often associated with suppression. At the transitional phase from SS to PS many neurons showed a reduction in discharge rate. During REMs in PS, about a half of the neurons of each group responded with burst discharge. The responsiveness to electrical stimulation of the MFR was highest for the group I neurons and the lowest for the group III. The inhibitory responses tended to be smaller in magnitude during SS than during W. During PS, both excitatory and inhibitory responses were, in general, markedly diminished. The analysis of the results has suggested that groups I and II neurons may be involved in more multiple functions than group III neurons which have a tendency to maintain steady discharge rate.

Animals↗

Tryptic hydrolysis of omega-amidino alpha-amino acid (indospecine) esters.

Several esters of a series of omega-amidino alpha-amino acids were synthesized. Some of them were shown to be efficiently hydrolyzed by bovine trypsin [EC 3.4.21.4]. The kinetics of hydrolysis of the esters were compared with those of the omega-guanidino series. The relationships between the length of the side chain and the susceptibility to hydrolysis by trypsin were somewhat different in the two series. These slight differences are discussed in terms of the molecular structures and their relation to the structural requirements of the trypsin active site.

Amino Acids, Diamino↗

Partial purification and immunological aspects of carboxylesterase from rat liver microsomes.

Carboxylesterase (CEase) was solubilized from rat liver microsomes by autolysis followed by cholate treatment and then purified by the combination of ammonium sulfate fractionation, gel filtration, chromatography on DEAE Sephadex A-50 and hydroxyapatite and preparative Disc electrophoresis. The overall purification was 25-fold with a yield of 6% of the original enzyme activity. Analytical Disc electrophoresis of the final enzyme preparation showed a single band. However, SDS polyacrylamide gel electrophoresis revealed one main band of 93% and three other minor bands. To investigate the interaction between CEases of rat, monkey, pig and rabbit liver microsomes, rabbit antibody to the above enzyme preparation was prepared and immunological analyses, i.e., Ouchterlony's test and immunoelectrophoresis, were performed. In the comparative double diffusion test, the partial fusion of precipitation line between anti-rat CEase and the enzymes of other species was observed. In the second analysis, sharp arc precipitation lines also could be seen in all specimens and, furthermore, mobilities of each enzyme were different. These observations suggest that rat liver CEase seems to be immunologically related in part but not completely identical with the CEases of other species and the charge difference may exist in these specimens.

Animals↗

Potentiation of ethyl para-nitrophenyl phenyl-phosphonothioate (EPN)-induced inhibition of liver microsomal carboxylesterase by NAD in vitro in rats.

The higher inhibition of liver microsomal carboxylesterase (CEase) by EPN, as compared to that of acetylcholinesterase (AchE) may be, at least in part, explained by the present findings that NAD potentiated the anti-CEase, but not anti-AchE, action of EPN. This phenomenon was referred to as "NAD-effect" in this paper. NAD-effect was not due to the increased formation of oxygen analog of EPN (EPN=O) by NAD addition through liver microsomal cytochrome P-450 catalyzed monoxygenase, because the amounts of EPN=O formed during incubation in the presence and absence of NAD were not significantly changed as shown by gaschromatography-mass spectrometric estimations. In addition, HAD-effect could be observed in the experiments even under carbon monoxide atmosphere. Such NAD-effect was observed only when NAD, EPN and an unidentified component bound to liver microsomal membrane were co-existent in the incubation mixture.

Anaerobiosis↗

Induction of NADH-dependent aldehyde reductase by successive administration of barbiturates in rat brain.

The effect of long-term administration of phenobarbital (PB) or barbital for five weeks on brain aldehyde reductase (A1R) and aldehyde dehydrogenase (A1DH) activities in the rat was studied. Mitochondrial (m)-A1DH and NADH-dependent A1R activities were significantly increased over control values after five-week treatment with PB or barbital, while no significant alteration of supernatant (s)-A1DH and NADPH-dependent A1R activities was observed under the same condition. Increase in m-A1DH activity by the treatment with barbiturates was recovered to the control level, however, increased activity of NADH-dependent A1R was maintained even after the cessation of the treatment. In groups of rats pretreated with barbiturates for five weeks, no animals were induced to sleep after intracerebroventricular injection of PB, and this finding strongly suggests the decrease in sensitivity of rats to barbiturates.

Aldehyde Oxidoreductases↗

Changes in serotonin turnover and the brain sensitivity to barbiturates by disulfiram treatment in rats.

The influence of intraperitoneal administration of disulfiram on the serotonin (5HT) turnover and the brain sensitivity to barbiturates were investigated in rats. Treatment of the animals with 200 mg/kg disulfiram resulted in the prolongation of duration of barbiturate-induced hypnosis. This indication and increment of the brain sensitivity to barbiturates after disulfiram treatment. Under the identical condition, disulfiram caused both the reduction of turnover of 5HT and the elevation of 5HT levels, although this effect was less potent than that of phenobarbital. Furthermore, simultaneous administration of disulfiram and phenobarbital resulted in the severe retardation of 5HT metabolism. These results strongly suggest that disulfiram potentiates the hypnotic action of barbiturates by altering 5HT metabolism in rat brain.

Animals↗

Effects of barbital and disulfiram on the metabolism of intracerebroventricularly administered [14C]-5-hydroxytryptamine in rats.

Effects of barbital and disulfiram on the metabolism of serotonin (5-HT) in vivo were studied. One hr after intracerebroventricular injection of [14C]-5-HT (3 nmoles, 0.5 muCi), the levels of the total and deaminated radioactive materials were increased in rats receiving either barbital or disulfiram, as compared to those of control rats. In addition, an additive effect was observed by a combined administration of these two drugs. The results in this paper strongly suggest that barbital and disulfiram inhibit the metabolism of 5-hydroxyindoleacetaldehyde (5-HIAAld), a first deaminated metabolite in 5-HT metabolism.

Animals↗

The effects of diltiazem hydrochloride on the cardiac conduction: a clinical study of His bundle electrogram.

The effects of diltiazem hydrochloride, a new Ca++ antagonistic antianginal drug, on the cardiac conductivity were evaluted in 10 patients with atherosclerotic heart disease. His bundle electrograms were obtained by catheter technique. R-R, A-H and H-V intervals were measured before and after intravenous administration of diltiazem. Diltiazem acted towards significant prolongation in A-H interval. R-R and H-V intervals were insensitive to diltiazem. Diltiazem did not interrupt the cardiac effects of atropine when A-H prolongation was still observed in the subject pretreated with atropine. In short, diltiazem depresses the conductivity of the atrioventricular node selectively and this is not mediated through vagus tone change. This Ca++ antagonist induced A-H prolongation strongly suggests the contribution of Ca++ current on the generation of atrioventricular nodal action potential in humans.

Action Potentials↗