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Biomedical subjects

A Hirata

Publications and source records attributed to A Hirata.

At least 235 records · Page 13Linked to original sources
PubMed1984

Electrophysiologic effects of atropine and isoproterenol on the cardiac conduction system in familial amyloid polyneuropathy.

In ten patients with familial amyloid polyneuropathy (FAP), the effects of atropine and isoproterenol on the cardiac conduction system were studied using surface electrocardiogram (ECG) and His bundle electrograms. Intravenous administration of atropine sulfate, 1 mg, prolonged the sinus cycle length ( SNCL ) in 6 of 8, sinus node recovery time (SNRT) in 3 of 6, automaticity recovery time of the atrioventricular (A-V) node in one, A-H interval in 4 of 7, effective refractory periods of the atrium and A-V node in 4 of 6 and in 3 of 7 patients, respectively. Continuous intravenous administration of isoproterenol, 0.5 micrograms/min, shortened the SNCL , SNRT, A-H interval and refractory periods of the atrium and A-V node in all patients. We conclude that the therapeutic doses of atropine may be useless or potentially detrimental for bradyarrhythmias or conduction blocks in some patients with FAP, but that isoproterenol may have beneficial effects on those arrhythmias in FAP.

Adult↗
PubMed1984

Surgical management of piriform sinus fistula.

Four cases of acute cervical abscess resulting from infection through the left piriform sinus fistula are described. The fistula seems to be related to the cause of infection in many of previously reported cases of acute suppurative thyroiditis or "recurrent lateral cervical fistula." Complete removal of the fistula is essential to a permanent cure, and the guide of a Fogarty catheter through the fistula is useful at operation for patients with repeated infection.

Abscess↗
PubMed1983

Increase of serotonin receptors in rat uterus induced by estradiol.

[3H]Spiroperidol was used to label uterine membrane-binding sites that have the characteristics expected of serotonergic receptors. The characteristics of specific [3H]spiroperidol binding to the uterine membrane of 17 beta-estradiol-3-benzoate-treated ovariectomized rats were studied. The specific [3H]spiroperidol binding was rapid and reversible, and the half-maximal saturation, taken as the apparent dissociation constant (KD) for [3H]spiroperidol, was 5.16 +/- 0.24 (n = 12) nM [3H]spiroperidol. Scatchard plots of saturation curves of the specific [3H]spiroperidol binding were convex and the Hill coefficient was 2.06 +/- 0.11 (n = 12). Cinanserin, mianserin, metergoline (which are serotonergic antagonists), and serotonin (5-HT) inhibited the [3H]spiroperidol binding with apparent Ki values of 21.2, 14.1, 14.1, and 176.5 microM, respectively. Concentrations of 1 mM sulpiride (a dopaminergic antagonist) and dopamine reduced [3H]spiroperidol binding only 26 and 23%, respectively. 1 mM GTP reduced the potency of 5-HT (10(-6) - 10(-3) M) to displace bound [3H]spiroperidol. The uterine membranes were treated with various enzymes and protein-modifying reagents, and binding studies on the treated uterine membranes showed that protein(s), phospholipids, and N-acetyl-neuraminic acid in uterine membranes were important as specific binding sites of [3H]spiroperidol. Measurement of the specific binding of [3H]spiroperidol to uterine membranes from untreated and estradiol-treated ovariectomized rats showed that estradiol significantly increased the number of specific binding sites of [3H]spiroperidol, but did not change the apparent affinity of specific [3H]spiroperidol binding. Estradiol also did not change the dissociation constant or the number of binding sites for [3H]3-quinuclidinyl benzilate, which binds to muscarinic acetylcholine receptors. These findings suggest that [3H]spiroperidol mainly binds to 5-HT receptors in the uterine membrane of estradiol-treated ovariectomized rats. The finding that administration of estradiol significantly increased the number of [3H]spiroperidol-binding sites is consistent with the specific increase in the contractile response to 5-HT observed in isolated uterus from ovariectomized rats treated with estradiol.

Animals↗
PubMed1983

Cold-sensitive nuclear division arrest mutants of the fission yeast Schizosaccharomyces pombe.

Thirteen recessive cold sensitive nuclear division arrest mutants were isolated from the fission yeast Schizosaccharomyces pombe. Twelve unlinked genes were defined; six in chromosome I, three in chromosome II and two in chromosome III. The map positions of three nuclear division arrest genes (nda1, nda2 and nda3) in chromosome II were determined precisely. Together with the previously obtained temperature-sensitive cell division cycle mutations, at least 20 genes appear to control the nuclear division of the fission yeast. Physiological studies indicated that most cold sensitive nda mutants incubated previously at 22 degrees C proceeded with a synchronously normal cell-cycle after temperature shift-up. The morphology of the nuclei and nuclear chromatin region was studied by the 4',6-diamidino-2-phenylindole staining method and by electron microscopy. Each mutant exhibited characteristic nuclear morphology at 22 degrees C, showing the specific blockages. The nda genes seem to control a pathway of structural alterations in the nuclear chromatin region with the order hemisphere, condensed ellipsoid, segregating U-form and separating hemispheres. Two genes, nda2 and nda3, pleiotropically control nuclear division, nuclear location and cell shape. The terminal phenotype of nda2-KM52 is characterized by the nuclear displacement, the absence of a spindle and abnormal locations of spindle pole bodies. The cells of nda3-KM311 were aberrant in shape and contained a partially separated chromatin region with a long spindle. Together with the results of the accompanying paper, we conclude that nda2 and nda3 genes control nuclear and cytoplasmic microtubular organization.

Alleles↗
PubMed1983

Neural regulation on the active sodium-potassium transport in hypokalaemic rat skeletal muscles.

C.N.S.-induced suppression of muscle Na-pump activity was studied in fast 'twitch' muscle, extensor digitorum longus, of hypokalaemic rats which were fed a K-deficient diet for 0-9 weeks. The results were compared with those of slow 'tonic' muscle, soleus, reported previously. K-deficient diet caused blood hypokalaemia and a considerable K+ loss and Na+ accumulation in the skeletal, heart and smooth muscles. The cellular K+ loss was in the order of soleus greater than extensor digitorum longus greater than diaphragm greater than duodenum greater than auricle greater than ventricle; C.N.S. organs such as cerebrum, cerebellum, medulla oblongata, spinal cord and liver were spared this K+ fall. Skeletal, heart and smooth muscles lost more K+ with prolongation of hypokalaemic periods, whereas plasma K+ concentration did not fall much below 1.6 mM during hypokalaemia. Peripheral nerve section, cervical and brain-stem transection, decerebration and cortical spreading depression with 20% KCl, which activated the active Na+ and K+ transport in soleus muscles during hypokalaemia, could not enhance the pump activity in extensor digitorum longus muscles. Alpha-adrenoreceptor antagonists such as phenoxybenzamine, phentolamine and dibenamine and a specific blocker of post-synaptic alpha 1-adrenoreceptor, prazosin, did not stimulate Na+ and K+ transport in the extensor digitorum longus muscles during hypokalaemia while the beta-adrenoreceptor antagonist, propranolol, also had no effect. The sensitivity of the active Na+ and K+ transport system in rat muscles to ouabain applied intraperitoneally was greater in extensor digitorum longus muscles than in soleus muscles. The binding experiment with a radiolabelled ligand of alpha 1 adrenoreceptor antagonist, [3H]prazosin, demonstrated the presence of alpha 1-adrenergic receptors on the soleus muscle membranes of hypokalaemic rats, but not of normal rats. alpha 1 Adrenergic receptors were not detected on the extensor digitorum longus muscle membranes prepared from either hypokalaemic or normal rats. The correlation between the C.N.S.-induced inhibition on the Na pump in soleus muscle during hypokalaemia and the occurrence of alpha 1 adrenergic receptors on the muscle was discussed.

Adrenergic alpha-Antagonists↗
PubMed1983

Mechanism of action of habekacin, a novel amino acid-containing aminoglycoside antibiotic.

The molecular basis for activity of habekacin was studied by using Escherichia coli Q-13. Electron microscopic studies revealed that numerous blebs, derived from the outer membrane, were formed on cells treated with habekacin. Cytoplasmic contents leaked into the lumina of blebs, and the membrane of some enlarged blebs was disrupted. In a cell-free system, habekacin interfered with polypeptide synthesis, caused codon misreading, and inhibited translocation of N-acetylphenylalanyl-tRNA from the acceptor site to the donor site on ribosomes. [3H]habekacin bound to both 50S and 30S ribosomal subunits. The current experiments indicated that the mechanism of action of habekacin is similar to that of 2-deoxystreptamine-containing aminoglycoside antibiotics such as dibekacin, kanamycin, gentamicin, and related substances. The relationship of membrane damage to inhibition of ribosomal functions remains to be determined.

Aminoglycosides↗
PubMed1982

Multiple postsynaptic dopamine receptors and behavioral manifestation.

Previously we demonstrated the existence of non- and positive-cooperative dopamine receptors in rat striatum in [3H] apomorphine binding experiments. Non-cooperative sites were sensitive to the inhibition of sulpiride while cooperative sites were not. In the present study results dealing with the involvement of those two types of postsynaptic dopamine receptors in different behavior manifestations is shown employing lisuride hydrogen maleate (LHM). LHM elicited contralateral turnings in 6-hydroxydopamine lesioned rats unilaterally in the striatum whereas it caused ipsilateral turnings in kainic acid lesioned rats as was observed following the administration of apomorphine. Furthermore, the effect of LHM on rotating behavior was abolished by the pretreatment with sulpiride. On the other hand, LHM inhibited apomorphine induced stereotyped behavior whereas the sulpiride failed to block it. These results suggested the dual action of LHM on multiple postsynaptic dopamine receptors. The results also indicated that non-cooperative postsynaptic dopamine receptors are involved in rotating behavior while cooperative receptors participate in the elicitation of stereotypy.

Animals↗
PubMed1982

Ascospore development in the fission yeasts Schizosaccharomyces pombe and S. japonicus.

The fine structure of ascospore formation in the fission yeasts Schizosaccharomyces pombe and Schizosaccharomyces japonicus var. japonicus was studied by serial thin-sectioning and electron microscopy. The morphogenetic events were almost the same in both species. Ascospore development was initiated by the formation of the forespore membrane on the cytoplasmic side of the differentiated nucleus-associated organelle (NAO) in the interval between meiosis I and II in S. pombe, or during the post-meiotic nuclear division in S. japonicus, and the process proceeded almost synchronously through the two or four nuclei in the ascus. The forespore membrane developed by fusion of the cytoplasmic vesicles and this was clearly demonstrated in S. japonicus where the behaviour of vesicles involved in the forespore membrane development could be traced as they were marked by the presence of electron-dense granules. The staining technique, by phosphotungustic acid--chromic acid (PTA-CA) after treatment with periodic acid, was used to attempt to elucidate the origin and the nature of the forespore membrane. The method specific to plasmalemma-type membranes stained both ascus and ascospore plasmalemmas; the forespore membrane was not stained at first but developed the same affinity for stain as the plasma membrane in the course of ascospore development. The results suggest that the forespore membrane did not come directly from the ascus plasma membrane, but from another membrane system such as the endoplasmic reticulum. Spore wall material was deposited in the space between the inner and outer leaflets of the forespore membrane.

Ascomycota↗
PubMed1982

[Toxicological study of amikacin following intravenous drip infusion. 1. Acute toxicity in rats, rabbits and dogs, and subacute toxicity in rabbits].

Acute toxicity of amikacin sulfate (AMK) was studied in rats, rabbits and dogs following 1 hour drip intravenous infusion (1 hour d.i.v.), and compared with those after intravenous injection (i.v.). Subacute toxicity was studied in rabbits following 1 hour d.i.v. of AMK at doses of 400, 200, 100 and 25 mg/kg for 36 days. Acute toxicity: Acute toxicity of AMK by 1 hour d.i.v. was extremely diminished as compared with that by i.v. judging from LD50, the toxicity was approximately 1/6 in rats and approximately 1/2 in rabbits and dogs. No difference was observed between males and females. Subacute toxicity: 1. No death was found in all rabbits. 2. At the doses of 25 mg/kg and 100 mg/kg, there were no significant changes or signs recognized as toxicological effects of AMK. 3. At the dose of 200 mg/kg, very slight renal damages were observed histopathologically in all the 5 rabbits. 4. At the dose of 400 mg/kg, slight or moderate renal damages were observed in all the rabbits. Those were mainly dilatation of renal proximal tubules, hydropic swelling and degeneration of renal proximal tubular epithelium. No significant impairment effect of AMK was found in heart, lung, liver and other organs. 5. From these results, it is considered that the maximum no effect dose from a view point of safety is about 100 mg/kg in this study.

Amikacin↗
PubMed1981

A further study on constrictor responses of dog coronary arterial strips to acetylcholine under potassium-contracture.

Experiments were designed to clarify what mechanisms are involved in the contraction of dog coronary artery induced by acetylcholine. Helical strips cut from the left circumflex coronary artery were suspended in a bath filled with oxygenated Krebs-Ringer solution at 37 degrees C, and tension developments were recorded isometrically. During potassium-contracture acetylcholine produced further contractions of the strips, which were significantly depressed by atropine together with phentolamine or atropine together with d-tubocurarine. In the strips prepared from dogs in which 6-hydroxydopamine was administered 2 hrs before isolation of hearts, acetylcholine-induced contraction was suppressed by atropine alone. Norepinephrine produced contractions in these strips, which were blocked by phentolamine. Results indicate that acetylcholine may directly constrict the artery through a muscarinic action and simultaneously produce norepinephrine release from sympathetic nerve endings by acting on presynaptic nicotinic receptors resulting in the contraction of the artery.

Acetylcholine↗
PubMed1980

Effects of dopaminergic agonists and antagonists on [3H]apomorphine binding to striatal membranes: sulpiride lack of interactions with positive cooperative [3H]apomorphine binding.

Effects of dopaminergic agonists and antagonists on [3H]apomorphine binding to striatal membranes of rat brain was examined. Haloperidol and spiroperidol exhibited biphasic inhibition of [3H]apomorphine binding; one of which had the Hill coefficient of 0.9, whereas the other had that of 0.4. The former accounted for 65% of [3H]apomorphine binding while the latter consisted of 35% of the binding. Furthermore, the latter disappeared after kainic acid lesions. On the other hand, sulpiride and metoclopramide reduced [3H]apomorphine binding to 31% with the Hill coefficient of 0.9. The inhibition of [3H]apomorphine binding with the Hill coefficient of 0.4 which was shown by haloperidol and spiroperidol was not observed for sulpiride and metoclopramide. Previously, we demonstrated non- and positive-cooperative [3H]apomorphine binding to stiatal membranes. In the present study, it has been also shown that sulpiride inhibits non-cooperative [3H]apomorphine binding leaving that with allosteric properties unaffected. No inhibition of dopamine-sensitive adenylate cyclase was observed by 10(-4) M sulpiride while 90% inhibition was obtained with 10(-5) M haloperidol. From those results, it is suggested that non-cooperative [3H]spomorphine binding is not coupled with dopamine-sensitive adenylate cyclase.

Adenylyl Cyclases↗