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Biomedical subjects

K Hirota

Publications and source records attributed to K Hirota.

At least 145 records · Page 8Linked to original sources
PubMed1999

Prostaglandin E1 produces spasmolytic effects on histamine-induced bronchoconstriction in dogs.

OBJECTIVE: In this study, we evaluated the spasmolytic effect of intravenous prostaglandin (PG) E1 on histamine-induced bronchoconstriction with a direct visualization method using a superfine fiberoptic bronchoscope. SETTING: A university research laboratory. SUBJECTS: Mongrel dogs. INTERVENTIONS: The bronchial cross-sectional area (BCA) of mongrel dogs was measured by a direct visualization method using a superfine fiberoptic bronchoscope. Bronchoconstriction was elicited with histamine (H) infusion: 10 microg/kg iv bolus + 500 microg/kg/h continuous iv. The first protocol (n = 7) was designed to determine the effects of intravenous bolus of PGE1: 0 (saline), 0.01, 0.1, 1.0 and 10 microg/kg on H-induced bronchoconstriction. BCA was assessed before and 30 min after starting the H infusion and 5 min after each dose of intravenous PGE1. The second protocol was designed to determine whether continuous intravenous infusion of PGE1 reverses H-induced bronchoconstriction. In the PG group (n = 6), PGE1 was continuously infused at 0.1 microg/kg/min (20 mL/hr). In the control group (n = 6), saline was administered at a rate of 20 mL/hr iv. BCA was assessed before and 30 min after starting the H-infusion and at 5, 10, 30 and 60 min after commencing the PGE1 or saline infusion. Arterial blood was obtained simultaneously for measurement of plasma concentrations of epinephrine and norepinephrine by gas chromatography mass spectrometry. MEASUREMENTS AND MAIN RESULTS: In the first protocol, PGE1 produced a dose-dependent increase in the percentage of BCA and 10 microg/kg of PGE1 almost fully reversed the H-induced bronchoconstriction. Plasma catecholamines did not change significantly. In the second protocol, continuous infusion of PGE1 produced a time-dependent reversal of H-induced bronchoconstriction (percentage of BCA increased to 80.0+/-9.0% 60 min after the start of PGE1 infusion), whereas saline infusion did not reverse the bronchoconstriction. Plasma catecholamines did not change significantly in either group. CONCLUSIONS: Both intravenous bolus and continuous intravenous infusion of PGE1 reversed the H-induced bronchoconstriction. PGE1 may be used safely for patients with the hyperreactive airway and might be useful as a therapeutic agent for these patients.

Alprostadil↗
PubMed1999

Relationships between activity of daily living, and oral cavity care and the number of oral cavity microorganisms in patients with cerebrovascular diseases.

We examined the relationships among the activity of daily living (ADL), oral cavity care, and the number of oral cavity microorganisms in 40 patients with cerebrovascular diseases (CVD). The CVD patients were classified into 4 groups, I, II, III and IV based on their ADL and the method used for oral cavity care. The ADL was highest in group I and lowest in group III. Only the patients of only group III could not eat by themselves and were receiving naso-esophageal feeding. Oral cavity care was performed by the patients themselves in groups I and IV, but was performed by caregivers in groups II and III. The group IV patients had no teeth, but could eat by themselves using full dentures. The numbers of microorganisms in the pharyngeal swabs from the 4 groups were measured and expressed as colony-forming units (cfu). The numbers of both Staphylococci spp. and Candida spp. were significantly higher in group III than in the other groups. Moreover, Pseudomonas aeruginosa was isolated only from patients of group III (in about 66%). The oral cavity care by caregivers was almost the same in groups II and III, but the numbers of oral cavity microorganisms were significantly higher in group III than in group II. These results indicated that microorganisms grow more easily in the oral cavities of CVD patients with low ADL compared with CVD patients with higher ADL, and that eating is thought to be important for the prevention of an increase of microorganisms in the oral cavity.

Activities of Daily Living↗
PubMed1999

[Efficacy of combination with granisetron and methylprednisolone for nausea, vomiting and appetite loss in remission induction chemotherapy of acute myeloid leukemia--a randomized comparative trial between granisetron alone and granisetron plus methylprednisolone].

The prevention of nausea, vomiting and appetite loss induced by remission induction chemotherapy for acute myeloid leukemia was compared by randomization between granisetron alone and combination with granisetron plus methylprednisolone. Granisetron was administered at 40 micrograms/kg during chemotherapy, and methylprednisolone was administered concomitantly at 125 mg/body for 3 days or more in the combination group. The single and combination groups comprised 14 and 13 patients, respectively, and there was no significant difference between the background of both groups. To evaluate the effect they were scored according to 4 grades, and evaluated every 24 hours from the start of chemotherapy to 5 days after its completion. The complete inhibition rate of vomiting was as high as 71.4% and 92.3% in the single and combination groups, respectively, showing no significant difference. The grade of vomiting was mild in both groups. Nausea was noted in 71.4% and 46.2%, respectively, and the inhibitory effect tended to be higher in the combination group. Appetite loss developed in 92.9% and 41.7%, respectively, and the prevention effect was clearly higher in the combination group. The prevention effects on nausea 7, 8 and 10 days after the start of chemotherapy, on appetite loss 2-10 days after it, and 2-5 days after its completion, were higher in the combination group. Granisetron revealed an excellent inhibitory effect on vomiting induced by remission induction chemotherapy for acute myeloid leukemia, but combination with granisetron and methylprednisolone was considered useful for nausea in the latter half of the treatment period and for appetite loss during the whole period.

Acute Disease↗
PubMed1999

[Hereditary ataxias in Akita prefecture].

To provide a genetic survey of hereditary ataxia, we performed PCR screening of SCA1, SCA2, MJD1 (SCA 3), SCA6, DRPLA, with 71 patients in 61 families living in Akita prefecture (1,205,571 population in 1997) in Japan. Of 71 patients in 61 families, 18 MJD1, 14 SCA6, 5 DRPLA, 1 SCA1 and 1 SCA2 patients were detected. Eighty percent of autosomal dominant inherited spinocerebellar degeneration (AD-SCD) including 7 spoladic patients genetically diagnosed as AD-SCD was MJD1 (45.7%) and SCA6 (34.3%). These suggest the prevalence rate of hereditary ataxias in Akita prefecture; 1.5 and 1.2/100,000 of MJD1 and SCA6, respectively. Only one patient of SCA1 was detected, which was frequently reported in Hokkaido and Tohoku area in Japan.

Genetic Testing↗
PubMed1998

GABAergic mechanisms in the action of general anesthetics.

1. The effects of volatile and intravenous anesthetics were studied on evoked field potentials in rat hippocampal CA1 neurons in vitro to determine the role of GABAergic mechanisms in the action of general anesthetics. 2. It was observed that both volatile (halothane, isoflurane, sevoflurane) and intravenous (thiopental, pentobarbital, propofol) anesthetics decreased population spike (PS) amplitudes. 3. Using paired-pulse paradigms, it was revealed that volatile agents enhance paired-pulse facilitation (PPF), and intravenous agents reduce PPF. Use-dependent effects on PS amplitudes were observed following application of the intravenous anesthetics, whereas volatile agents did not show use-dependency. The effects of the intravenous anesthetics were blocked by the GABA(A) receptor antagonist, bicuculline. 4. It is suggested that agent specific actions of general anesthetics are a result of differential effects on GABAergic mechanisms that modulate synaptic transmission.

Anesthetics, General↗
PubMed1998

Kinesin and cytoplasmic dynein in spinal spheroids with motor neuron disease.

Kinesin and cytoplasmic dynein are two major molecular motors responsible for fast axonal transport. As visualized by immunohistochemistry with monoclonal antibodies, both motors were found to be distributed throughout the cell bodies, dendrites and axons of motor neurons in normal human spinal cords. Large axonal swellings, spheroids, in the spinal cords of patients with motor neuron disease showed massive accumulation of kinesin co-localized with highly phosphorylated neurofilaments. Of 114 spheroids in five spinal cords, 87% were stained heavily with the three anti-kinesin antibodies used in this study. Cytoplasmic dynein was scarce or absent in most of the spheroids. These findings suggest that kinesin selectively accumulates in the spheroids of motor neuron axons, causing disturbance of the machinery for anterograde fast axonal transport in motor neuron disease.

Aged↗
PubMed1998

Mature and immature myeloid cells decrease the granulocyte colony-stimulating factor level by absorption of granulocyte colony-stimulating factor.

We studied the effects of polymorphonuclear neutrophils (PMN) and immature myeloid cells on the granulocyte colony-stimulating factor (G-CSF) level in vitro to better understand the regulatory mechanisms of neutropoiesis. Intact normal PMN decreased the G-CSF level after incubation with recombinant human (rh) G-CSF in a time- and dose-dependent manner. The percent reduction decreased as the concentration of rhG-CSF increased. However, the cell-free PMN-conditioned medium (PMN-CM) did not decrease the G-CSF level. The intact PMN also decreased the granulocyte-macrophage (GM)-CSF level after culture with rhGM-CSF, but did not affect the monocyte (M)-CSF level after culture with rhM-CSF. Normal bone marrow (BM) immature neutrophilic cells and G-CSF-dependent acute myeloid leukemic cells (OCI/AML la) also decreased the G-CSF level, whereas K-562 cells, which have no detectable G-CSF receptors, did not affect it. Phenylarsine oxide (PhAsO), an inhibitor of endocytosis of ligand receptor complex, abrogated this decreasing effect of intact PMN and OCI/AML la cells. These findings suggest that mature and immature myeloid cells negatively regulate neutropoiesis by, at least in part, decreasing the G-CSF level probably through receptor-mediated continual absorption and metabolism of G-CSF.

Absorption↗
PubMed1998

Cloning and characterization of the equine F18 gene, which has a novel exon.

A genomic clone isolated from an equine genomic library probed with an oligonucleotide (CAG)10 showed high sequence similarity to the human F18 gene and was tentatively named equine F18 gene. Because the human F18 gene is expressed in many tissues, we examined whether this equine clone was also expressed in equine tissues. The cDNA encoding equine F18 was obtained by the reverse transcriptase-polymerase chain reaction (RT-PCR) from equine thymus. The nucleotide sequence of the equine F18 cDNA (1940 bp) was determined and contained both the ATG initiation codon and a poly(A) sequence. The cDNA sequence contained sequence homologous to exon 3 of human F18 gene and a new exon that is not found in the human F18 gene. The equine F18 gene contains a CAG repetitive sequence (CRS) that is translated into a polyglutamine tract. The CRS was analyzed for polymorphism by PCR: four and two different alleles were observed with unrelated east-Asian and thoroughbred horses, respectively. The equine F18 gene was mapped to Xq29.1 by fluorescence in situ hybridization. The human F18 gene is also X-linked. These data strongly supported the conclusion that the clone contains the equine homologue of the human F18 gene.

Animals↗
PubMed1998

In vitro adherence of Streptococcus constellatus to dense hydroxyapatite and titanium.

Bacterial adherence to dense hydroxyapatite (HA) and titanium (Ti) rods was examined in vitro using Streptococcus constellatus ATCC27832. Streptoccus constellatus is associated with dental abscess and was isolated from the peri-implantitis. The dense HA was etched with 5% hydrofluoric acid for 0, 10, 20, 30, 40, and 50 s Adherence to the untreated dense HA was twice as high as the adherence to the Ti. The adherence to saliva-treated Ti was 13% higher than that to untreated Ti. The adherence was increased by acid-treatment of the dense HA, following a sigmoid curve from 20 to 50 s of treatment time. The dense HA has the capacity to receive more bacterial adherence than Ti and furthermore, the etched dense HA becomes more adherent.

Abscess↗
PubMed1998

Effects of thiopental on airway calibre in dogs: direct visualization method using a superfine fibreoptic bronchoscope.

Induction of anaesthesia with thiopental sometimes causes bronchospasm. Although the mechanism by which thiopental induces bronchospasm may involve cholinergic stimulation, direct spastic effect and histamine release, the spastic effects of thiopental have not been comprehensively defined. In this study, we have assessed the effect of thiopental on in vivo airway smooth muscle tone using direct visualization method with a superfine fibreoptic bronchoscope as previously reported. Twenty-one mongrel dogs were anaesthetized with pentobarbital (30 mg kg-1) and paralysed with pancuronium (200 micrograms kg-1 h-1). The trachea was intubated with a tube that had a second lumen for insertion of the bronchoscope (od: 2.2 mm) to continuously measure bronchial cross-sectional area. The tip of the bronchoscope was placed between the second and third bronchial bifurcation of the right lung. The dogs were allocated to three groups of seven: group T, A+T, H+T. In group T, thiopental 0 (saline), 0.1, 1.0 and 10 mg kg-1 was given i.v. In group A+T, saline i.v., 5 min later atropine 0.1 mg kg-1 i.v., and 5 min later thiopental 10 mg kg-1 was administered. In group H+T, bronchoconstriction was produced with histamine 10 micrograms kg-1 i.v. followed by infusion at 500 micrograms kg-1 h-1. Thirty minutes later, thiopental 0, 1.0 and 10 mg kg-1 were given. Arterial blood sampling was performed for measurement of plasma catecholamines and histamine. In group T, thiopental significantly reduced bronchial cross-sectional area (maximally by 28.7 (5.6% at 0.5 min after thiopental 10 mg kg-1), which returned to the baseline in 3 min, while any changes in plasma concentrations of catecholamines and histamine were not observed except norepinephrine level at 1 min following thiopental 10 mg kg-1 i.v. Atropine pretreatment completely prevented thiopental-induced bronchospasm in group A+T. In group H+T, thiopental 10 mg kg-1 transiently but significantly decreases bronchial cross-sectional area. Therefore, the present study indicates that the mechanism of thiopental bronchospasm may result from cholinergic nerve stimulation.

Anesthetics, Intravenous↗
PubMed1998

The role of the N-methyl-D-aspartic acid receptor in the relaxant effect of ketamine on tracheal smooth muscle.

UNLABELLED: Ketamine and magnesium (Mg2+), well known bronchodilators, have been used to treat patients with status asthmaticus. Both can block the N-methyl-D-aspartic acid (NMDA) receptor. NMDA receptors exist in the airway, and their activation seems to be linked to the release actions of sensory neuropeptides resulting in increased airway tone. We sought to determine whether ketamine relaxes the guinea pig trachea contracted by histamine by blocking the NMDA receptor. Female guinea pigs (250-400 g) were killed with an overdose of pentobarbital. The trachea was removed and cut spirally into strips 3 mm wide and 15 mm long. The strips were mounted in a 10-mL organ bath filled with Tyrode's solution bubbled through with 95% O2/5% CO2 at 37 degrees C. Strip contractions were measured isometrically with a force displacement transducer. We then studied the effect of NMDA receptor antagonists on histamine-induced tracheal contraction. In this protocol, we examined the effect of ketamine, Mg2+, zinc (Zn2+), or MK-801 (a noncompetitive NMDA receptor blocker) on strips contracted by 10(-5) M histamine. After full contraction was attained, ketamine (0.5-1.5 mM), MgSO4 (2-8 mM), ZnCl2(0.2-0.8 mM), or MK-801 (1.5-6 x 10(-5) M) was added, and the strip tension was measured again. We also studied the effect of NMDA on the relaxation by ketamine. After full contraction by 10(-5) M histamine, 0.5-1.5 mM KET was added alone or in combination with 0.1 mM NMDA, and the strip tension was measured again. Finally, we measured the effect of MK-801 on the relaxant effect of ketamine. After full contraction by 10(-5) M histamine, 0.5-2 mM ketamine was added alone or in combination with 0.75 or 1.5 x 10(-5) M MK-801, and the strip tension was measured again. All NMDA receptor antagonists tested reversed the tracheal contraction induced by histamine in a dose-dependent manner. However, neither the agonist NMDA nor the noncompetitive receptor blocker MK-801 affected tracheal relaxation induced by ketamine. We conclude that ketamine relaxes the tracheal smooth muscle contracted by histamine through a mechanism independent of NMDA receptors. The decreased bronchomotor tone induced by ketamine is probably due to interference with a Ca2+-requiring step necessary to maintain the contraction caused by histamine. IMPLICATIONS: Stimulation of the N-methyl-D-aspartic acid (NMDA) receptor in the airway results in airway constriction. The bronchodilator ketamine blocks the NMDA receptor. However, ketamine relaxes the guinea pig trachea contracted by histamine through a mechanism independent of the NMDA receptor.

Animals↗