Search PubMed⌕ Search

Biomedical subjects

H Fukuda

Publications and source records attributed to H Fukuda.

At least 919 records · Page 51Linked to original sources
PubMed1987

Verapamil enhances the non-adrenergic twitch response of rat vas deferens.

Verapamil (3 X 10(-6)-3 X 10(-5) M) enhanced the twitch contractions of the epididymal and prostatic portions of vas deferens stimulated at 0.1 Hz. This verapamil effect was essentially similar to those of diltiazem, D-600 and Bay K 8644. However, when stimulation at 2 Hz was used verapamil (3 X 10(-5) M) attenuated the contractions of the epididymal portion by half but still augmented those of the prostatic portion. Verapamil enhanced the reserpine- and prazosin-resistant component of the stimulation-induced contractions of both portions of the vas deferens. Yohimbine augmented the twitch response but attenuated the verapamil-augmented response. Verapamil did not augment norepinephrine- or tyramine-induced contractions whereas it augmented ATP-induced contractions of the prostatic portion but not of the epididymal portion. Verapamil increased the stimulation-evoked 3H-efflux from the vas deferens labelled with [3H]norepinephrine. It is suggested that verapamil augments non-adrenergic responses of both portions of the vas deferens by acting as a Ca agonist on the prejunctional site to increase the release of co-transmitter, or by acting on the postjunctional site to enhance the action of the substance released. Its effect in augmenting norepinephrine release is concluded not to contribute to the potentiating action.

Animals↗
PubMed1987

Sensitivity of spinal reflexes to TRH and 5-HT in 5,6-dihydroxytryptamine-treated rats.

Destruction of descending serotonergic nerve terminals containing thyrotropin-releasing hormone (TRH) was affected in rats by the intracisternal injection of 5,6-dihydroxytryptamine (5,6-DHT) two weeks before subsequent experiments. Although the level of TRH in the lumbar enlargement was significantly reduced in 5,6-DHT-treated rats, the effects of TRH on the monosynaptic reflex (MSR) and the polysynaptic reflex (PSR) in these rats were no different from those in control rats. MSR inhibition by 5-methoxy-N,N-dimethyltryptamine (5-MeODMT) was attenuated by 5,6-DHT treatment although there was no obvious difference in the effects of 5-MeODMT on the PSR between 5,6-DHT-treated and control rats. In 5,6-DHT-treated rats, L-5-hydroxytryptophan (5-HTP) markedly decreased the MSR and increased the PSR although the same doses of 5-HTP did not produce any effects on either the MSR or the PSR in control rats. In control rats, after administration of imipramine or clorgyline, 5-HTP produced effects similar to those observed in 5,6-DHT-treated rats. These results suggest that the supersensitivity to 5-HTP in 5,6-DHT-treated rats is due to a lack of 5-hydroxytryptamine (5-HT) uptake into 5-HT-containing nerve terminals rather than to a change in 5-HT receptors.

5,6-Dihydroxytryptamine↗
PubMed1987

Effects of amino-acid composition of the medium and addition of fatty-acid derivatives on the induction of lipogenic enzymes in cultured hepatocytes.

Effects of essential and non-essential amino acids on induction of lipogenic enzymes were investigated in cultured rat hepatocytes. Glucose-6-phosphate dehydrogenase was markedly induced by the addition of essential amino acids alone to the cultured medium, but was not induced by non-essential amino acids. Fatty-acid synthetase was also markedly induced by a combination of both amino-acid types (more than by either type of amino acid alone). However, acetyl-CoA carboxylase and malic enzyme were slightly induced by the addition of essential and/or non-essential amino acids. When various kinds of fatty acids were individually added to the medium, the lipid-dependent decreases in lipogenic enzyme inductions were in the following order: 18:2 greater than 20:4 greater than 18:1 greater than 16:0. When either linoleic acid, linoleoyl-CoA or trilinolein was added to the medium, linoleic acid was more effective as an inhibitor of the induction, without impairing the viability of cells.

Acetyl-CoA Carboxylase↗
PubMed1987

Benzodiazepine receptors studied in living primates by positron emission tomography: inverse agonist interactions.

The convulsant actions of methyl 6,7-dimethoxy-4-ethyl-beta-carboline-3-carboxylate (DMCM) and of methyl beta-carboline-3-carboxylate (beta-CCM) were evaluated in the baboon (Papio papio). DMCM, 0.6-4 mg/kg, induced epileptic seizures with short latency. DMCM convulsive seizures could be blocked by i.v. administration of the benzodiazepine agonist diazepam (10 mg). Similarly, beta-CCM, 0.3-3 mg/kg i.v., provoked generalized seizures in the baboons. These seizures were also reversed by the administration of propyl beta-carboline-3-carboxylate (3 mg/kg) or of diazepam (5 mg/kg). Combining the results from Positron Emission Tomography and the EEG assessments, benzodiazepine receptor occupancy by beta-CCM and DMCM was directly correlated with their convulsant actions in the living baboon. beta-CCM exerted its convulsant action in the living baboon at 76 and 74% benzodiazepine receptor occupancy in, respectively, occipital and temporal cortices whereas DMCM displayed a similar convulsive activity when only 58 and 65% of these receptors in the above regions were occupied.

Animals↗
PubMed1987

Reversible serotoninergic neurotoxicity of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in mouse striatum studied by neurochemical and immunohistochemical approaches.

Effects of N-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) on serotonin (5-HT) were studied in mouse striatum. The 5-HT level was significantly reduced at 1 week after MPTP, though returned at 4 weeks. The level of 5-hydroxyindoleacetic acid (5-HIAA) increased at both 1 and 4 weeks. The ratio of increase in 5-HT induced by pargyline administration was larger in MPTP-pretreated mice than in vehicle-pretreated controls at 1 week, although it was identical in both groups at 4 weeks. The 5-HT immunohistochemical study confirmed the biochemical change of 5-HT. These results suggest that MPTP functionally affects the 5-HT metabolism in mouse striatum.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1987

Haemodynamics and oxygen metabolism in patients after reversible ischaemic attack or minor ischaemic stroke assessed with positron emission tomography.

Regional cerebral blood flow (CBF), blood volume (CBV) and oxygen metabolic rate (CMRO2) were evaluated and compared among normals, patients with recent reversible ischaemic attacks (RIAs) and patients with chronic minor infarction using positron emission tomography. Average CBF together with CMRO2 significantly decreased in the infarction group in the middle cerebral artery territory of the affected hemisphere while the mean values for RIAs were intermediate between the other two groups. CBV also reduced, however it was more preserved compared to flow as seen in decreased CBF/CBV values. Significant interhemispheric difference was found in CBF/CBV ratio, but it did not clearly correlate with OEF changes. Higher OEF was noted only in the restricted brain regions of RIAs where CBF showed large hemispheric asymmetry. However, in other regions, the coupled decline of blood flow and metabolism was found which suggests tissue damage or neuronal cell loss in the brain with previous RIA symptoms.

Adult↗
PubMed1987

Regional cerebral metabolic rate for glucose in subacute sclerosing panencephalitis.

Regional cerebral metabolic rates for glucose (rCMRglc) were measured in two cases of subacute sclerosing panencephalitis (SSPE) with different clinical courses. A marked decrease in rCMRglc was found in the cortical gray matter of a patient with rapidly developing SSPE (3.6-4.2 mg/100 g brain tissue per min). However, the rCMRglc was preserved in the caudate and lenticular nuclei of the patient (7.7 mg/100 g per min). The rCMRglc in a patient with slowly developing SSPE revealed patterns and values similar to those of the control. The rCMRglc correlated better with the neurological and psychological status of SSPE.

Adolescent↗
PubMed1987

Electrophysiological evidence for dreaming: human cerebral potentials associated with rapid eye movement during REM sleep.

In order to examine the relationship between rapid eye movement (REM) during REM sleep and dreaming, scalp EEGs (Fz, Cz, Pz and Oz) of 4 normal human subjects, time-locked to REM onset, to saccade onset toward fixation targets and to saccade onset in total darkness, were averaged. The results include the following: Three positive potentials were associated with REM: a sharp potential in the parieto-occipital area just before REM onset; a large, slow potential in the vertex area 140-180 msec after REM onset; and a potential in the occipital area 210-280 msec after REM onset. Three positive potentials, one being the so-called EM-antecedent potential and the others being the lambda response, were associated with the waking saccades toward targets: a sharp potential in the parieto-occipital area just before the saccade onset and two potentials in the occipital area with latencies of 140-150 and 260-310 msec from the saccade onset. Only the EM-antecedent potential appearing just before saccade onset was found in association with saccades in total darkness. The similarities between the 3 positive potentials during REM sleep and the lambda response during wakefulness, and the relationship between those potentials and dreaming, are discussed in terms of the neural processes occurring during REM sleep.

Action Potentials↗
PubMed1987

Anticonvulsant effect of intracortical, chronic infusion of GABA in kindled rats: focal seizures upon withdrawal.

The behavioral and electrographic effects of chronic (7 days), localized infusion of GABA (100 micrograms/microliter) into the somatomotor cortex of fully amygdala-kindled rats is reported. The animals were stimulated once daily until a stage 5 (generalized clonic seizure) was obtained for five consecutive days. After determination of a stable seizure triggering threshold, the rats were implanted with osmotic minipumps (1 microliter/h for 7 days) connected to previously implanted bilateral cannulae. Amygdala stimulation was continued for 14 successive days. GABA infusion reduced the motor seizure without significantly modifying the limbic afterdischarge. This effect lasted until termination of drug application, with recovery of stage 5 convulsions on the following 3 to 5 days. No effects were observed in saline-infused animals or in rats with unilateral GABA treatment. Upon cessation of GABA treatment (removal of the osmotic devices by day 7 postimplantation), spontaneous epileptic discharges localized to the infusion sites appeared. In some animals, the abnormal activity was accompanied by behavioral signs of myoclonus. This cortical hyperexcitability lasted 2 to 24 h, with complete recovery afterward. These data indicate that two types of focal epilepsy may coexist independently in the same animal and provide confirmation of previous observations in the monkey on the existence of a "GABA-withdrawal syndrome" after chronic, focal infusion of the amino acid.

Amygdala↗
PubMed1987

Role of the corpus callosum and hippocampal commissure on transfer phenomenon in amygdala-kindled cats.

Forebrain-bisected cats underwent kindling at primary and secondary amygdala sites. The behavioral effect of amygdala kindling was then examined according to the extent of the surgical lesion in the forebrain commissures. Bisection of the corpus callosum with or without lesion of the hippocampal commissure modified both kindling and kindled symmetrical generalized seizure into a lateralized and asymmetrical form. Lesion of the hippocampal commissure was correlated with the loss of the expected positive transfer effect at the secondary amygdala site. These results suggest that whereas the corpus callosum plays a major role in patterning convulsive generalization and generalized convulsion, the hippocampal commissure is involved in mediation of the transhemispheric positive transfer effect. Evidence of a callosal inhibitory influence on amygdala kindling was not obtained.

Amygdala↗
PubMed1987

In inherited porphyrias, lead intoxication is a toxogenetic disorder.

1. delta-Aminolevulinic acid dehydratase (ALA-D), blood lead and several enzymes and metabolites of the heme biosynthetic pathway were measured in a number of symptomatic porphyric patients, 22 with acute intermittent porphyria, three with hereditary hepatic coproporphyria, 10 with hereditary porphyria cutanea tarda, two with erythropoietic protoporphyria and two with congenital erythropoietic porphyria and in 84 lead intoxicated persons. 2. In the 39 individuals suffering from the inherited porphyrias and in 32 lead poisoned patients with a 30-50% reduced deaminase, blood lead content was not sufficiently increased (average 28 micrograms%) to account for the greatly decreased activity of ALA-D (average 36% of controls). 3. After a relatively trifling lead exposure they developed the signs of acute lead intoxication. 4. A second group of lead intoxicated patients showing low ALA-D activity and corresponding high concentration of lead in blood, exhibited no other physiologic deviation in the enzymes and metabolites of porphyrin biosynthesis. 5. Individuals with inherited porphyrias are ultrasensitive to low level lead exposure and that lead would also act as a triggering factor. In these patients, lead intoxication can be considered a toxogenetic disorder. 6. An inversely linear correlation between ALA-D activity and blood lead content was obtained for both groups of lead intoxicated patients, however, a different constant (k) for each was obtained, which we have taken as a measure of lead toxogeneticity: k = 10 +/- 1 for lead intoxicated individuals with otherwise normal heme metabolism and k = 5 +/- 0.5 for lead intoxicated symptomatic porphyric patients. 7. Determination of erythrocytic ALA-D, besides blood lead, will be a valuable indicator for preventive medical care for these patients, when they are expected to be exposed to lead either environmentally or in their professional life.

Heme↗
PubMed1987

5-Hydroxytryptamine agonistic action of methysergide and the absence of supersensitivity to 5-HT agonists in spinal flexor reflexes in rats.

The intravenous administration of L-5-hydroxytryptophan (5-HTP), 5-methoxy-N,N-dimethyltryptamine (5-MeODMT), p-chloroamphetamine (PCA), LSD and methysergide to acute spinal rats, transected at C1, stimulated the flexor reflexes induced by electrical stimulation applied to the skin of the toe. The enhancement produced by 5-HTP, 5-MeODMT and PCA, was not antagonized by the prior administration of a dose of LSD or methysergide, although the enhancement produced by 5-MeODMT, LSD and methysergide, but not that produced by 5-HTP and PCA, was antagonized by cyproheptadine. In rats treated with 5,6-dihydroxytryptamine (intracisternal administration, 2 weeks previously) supersensitivity was observed to the effects of 5-HTP, a precursor of 5-HT, while subsensitivity was observed for the effects of PCA, a releaser of 5-HT. However, no supersensitivity was observed for the effects of 5-MeODMT, LSD and methysergide. These results suggest that methysergide may have an agonistic action on the 5-HT receptors in spinal cord and that supersensitivity to 5-HTP in rats treated with 5,6-dihydroxytryptamine was due to the lack of uptake of 5-HT into terminals of descending 5-HT fibres or to the change in 5-HT receptors which were not sensitive to 5-MeODMT, LSD, methysergide or cyproheptadine.

5,6-Dihydroxytryptamine↗
PubMed1987

Pentylenetetrazol-induced seizure is not mediated by benzodiazepine receptors in vivo.

The selective benzodiazepine antagonist RO 15-1788, labelled with carbon 11 [11C] RO 15-1788, as a specific marker, together with positron emission tomography, allows the in vivo study of benzodiazepine receptors in primates. In addition, when coupled with recordings of electroencephalographic activity, this method offers the feasibility of studying the correlation between occupancy of benzodiazepine receptors and the convulsant action of drugs acting at the benzodiazepine-GABA receptor complex in vivo. The present study showed that convulsant doses of pentylenetetrazol (PTZ) could affect the binding of [11C] RO 15-1788 in vivo in two ways, depending on the doses tested: at concentrations of 20 and 30 mg/kg, pentylenetetrazol increased the binding of [11C] RO 15-1788 whereas larger concentrations displaced the binding of [11C] RO 15-1788. The direct correlation between the occupancy of respective benzodiazepine receptors, afforded by increasing convulsant doses of pentylenetetrazol, revealed that competitive interaction with benzodiazepine receptors was not necessary for pentylenetetrazol to induce the appearance of seizures in vivo.

Animals↗
PubMed1987

Pituitary enlargement with target organ deficiency: hypothyroidism and hypogonadism.

Three women with pituitary enlargements associated with preexisting target organ failures are reported. Two pituitary enlargements owing to primary hypothyroidism and one to primary hypogonadism were shown to be regressed on computed tomography after the replacement therapy. Clinically and pathologically, the differentiation of a pituitary hyperplasia from a pituitary adenoma is often very difficult. Moreover, the treatments for these conditions are quite different. Adequate medication can diminish a pituitary enlargement because of the feedback mechanism. Existence of the target organ deficiency should always be checked before the management of pituitary tumor.

Adult↗
PubMed1987

Diazepam restores the increased [3H]glutamate binding to hippocampal synaptic membranes in the amygdaloid-kindled rat.

[3H]Glutamic acid binding to hippocampi was increased after amygdaloid kindling in rats, and diazepam inhibited this increased binding, without any effect on the enhanced binding by CaCl2 or the binding in control rats. By inducing kindling in the same way as that used in the binding experiment, the inhibiting effects of diazepam on kindled seizures, the afterdischarge and the development of kindling were observed.

Action Potentials↗
PubMed1987

Involvement of noradrenergic systems in the effects of conditioning stimulation of the lower brain stem on the lumbar spinal reflex in rats.

The effects of conditioning stimulation at various positions in the pons and the medulla on the lumbar spinal monosynaptic reflex (MSR) were examined in rats. The conditioning stimulation facilitated the MSR. Facilitation with long latency was completely blocked by phenoxybenzamine, chlorpromazine or haloperidol. Phenoxybenzamine and chlorpromazine inhibited the MSR. Haloperidol, on the other hand, augmented the MSR, and this effect became more potent after the brain stem had been transected at the upper part of the medulla oblongata. These results suggest that pontine noradreneric systems have a facilitatory influence on the MSR via alpha-adrenoceptors, and that alpha-blockers exert an inhibitory effect on the MSR by blocking these receptors.

Adrenergic alpha-Antagonists↗
PubMed1987

Rigidity in rats due to radio frequency decerebration and effects of chlorpromazine and mephenesin.

Bilateral radio frequency (RF) lesions of the midbrain were produced in an attempt to establish a non-bleeding method of producing decerebrate rigidity in rats. Marked extensor rigidity occurred with a high reproducibility in hindlimbs without the appearance of voluntary movement. Stretch reflex tension induced by repetitive dorsiflexion of the hindfeet was employed as a measure of the intensity of rigidity. Chlorpromazine-HCl (0.1-1 mg/kg, i.v.) and mephenesin (10-50 mg/kg, i.v.) which depress intercollicular decerebrate rigidity, reduced the RF decerebrate rigidity. These results suggest that RF decerebrate rigidity can be used instead of intercollicular transection rigidity in the pharmacological and physiological studies.

Animals↗