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Biomedical subjects

J Miyamoto

Publications and source records attributed to J Miyamoto.

At least 55 records · Page 3Linked to original sources
PubMed1991

Comparison of Ca2+ channel inhibitory effects of cibenzoline with verapamil on guinea-pig heart.

1. Cibenzoline, a class 1 antiarrhythmic drug, was studied on the effects upon the myocardial slow inward Ca2+ current (ICa) and the contractile force, and was compared with verapamil. 2. In voltage-clamp experiments with guinea-pig ventricular myocytes, cibenzoline caused a concentration-related inhibition of ICa (IC50 = 30 microM), whereas verapamil exerts a stronger effect (IC50 = 0.6 microM). 3. Cibenzoline also produced a concentration-related decrease in contractile force of isolated papillary muscle preparation (IC50 = 30 microM), while IC50 of verapamil was 0.8 microM. 4. Although the myocardial Ca2+ channel blocking effect of cibenzoline is about 1/50 compared to verapamil, cibenzoline possesses an inhibitory action on Ca2+ channel as well as on Na+ channel.

Animals↗
PubMed1991

The effect of TYB-3823, a new antiarrhythmic drug, on sodium current in isolated cardiac cells.

1. Sodium current (INa) blockade by TYB-3823, a newly synthesized antiarrhythmic agent, was investigated in isolated single ventricular myocytes by use of the whole cell patch-clamp technique. 2. TYB-3823 blocked INa under steady-state conditions (Kd,rest = 500 microM, Kd,i = 4.9 microM), findings consistent with a shift in the steady state INa availability curve to more negative potentials. 3. TYB-3823 produced use-dependent block at 2 Hz in conjunction with increase in pulse duration (5-300 ms), that was markedly enhanced at less negative holding potentials. 4. The time course of the onset of block was accelerated and the degree of use-dependent block was decreased at more negative holding potential. The time course of the onset of block was accentuated with enhancing block at more positive holding potentials. 5. The time course of recovery from use-dependent block was accelerated at more negative holding potentials but was accentuated at more positive holding potentials. 6. These results suggest that both tonic block and use-dependent block of sodium channels in cardiac tissue might result from an interaction of TYB-3832 with sodium channels mainly in the inactivated channel states and the kinetics of the interaction between drug and receptor may be modulated by the inactivation gate.

Animals↗
PubMed1991

Clinical significance of hypouricemia in hospitalized patients.

Serum uric acid was measured in 586 normal subjects and 1,220 hospitalized patients. Hypouricemia was noted in 0.34% of the normal subjects and 2.54% of the hospitalized patients. Among hospitalized patients with hypouricemia, 22 were on medication, including allopurinol, anticancer drugs, antibiotics and glucocorticoids. Twenty-one patients had liver disorders and 11 of them had received transfusions. Neoplastic diseases were noted in 14 patients. Thus, hypouricemia was found to be relatively common in hospitalized patients, and seems to be caused mainly by medication, neoplastic diseases, liver disorders and transfusions.

Adolescent↗
PubMed1990

Blocking effect of 1389-S on the sodium current in isolated guinea-pig ventricular myocytes.

Under whole cell patch conditions, 1389-S blocked the INa in guinea-pig ventricular myocytes under steady state conditions (Kdrest = 30 microM, Kdi = 2.4 microM) with a shift of the inactivation curve to the hyperpolarizing direction. Both brief and long conditioning pulses could produce a use-dependent block of 1389-S. These results suggest that 1389-S had a higher affinity to the inactivated than to the rested state under steady state conditions and had a higher affinity to the activated state during train pulses as well as to the inactivated state, making channels unavailable for conduction upon activation.

Animals↗
PubMed1990

Establishment of a B-lymphoblastoid cell line infected with Epstein-Barr-related virus from a cynomolgus monkey (Macaca fascicularis).

A B-lymphoblastoid cell line (Ts-B) was established from lymph nodes of an apparently healthy cynomolgus monkey. The cells were demonstrated to contain Epstein-Barr virus-related antigens. Moreover, herpesvirus particles were found in the cells by electron microscopy. The cell-free culture medium transformed lymphocytes of cynomolgus rhesus monkeys, and of Japanese monkeys.

Animals↗
PubMed1989

Relationship between sarcolemmal damage and appearance of amorphous matrix densities in mitochondria following occlusion of coronary artery in rats.

The relationship between the progression of sarcolemmal damage and the appearance of amorphous matrix densities (AMDs) within myocardial mitochondria in the early phase of ischemia was studied in coronary-ligated rats by means of electron microscopy. The animals were divided into six groups according to the duration of ischemia (from 10 to 120 min). The severity of sarcolemmal damage was graded into four classes according to the ultrastructural ischemic changes, as follows: grade 0, normal cells; grade 1, slight ischemic changes in cellular organelles but intact sarcolemma; grade 2, formation of subsarcolemmal blebs, but overall sarcolemmal integrity; and grade 3, sarcolemmal disruption. In the experiment, grade 1 cells decreased and those of grade 3 increased with a longer period of ischemia. The appearance of grade 3 cells was distinct at 30 min of ischemia. This cellular damage proceeded from the subendocardial layer to the subepicardial layer indicating the "wavefront phenomenon." The number of AMDs within the mitochondria increased as the sarcolemmal damage became more severe. It was noteworthy that AMDs could be found in cells with an intact sarcolemma after subjection to 10 min of ischemia. Myoglobin staining of the myocardium obtained after 10 min of ischemia followed by 6 hr of reperfusion revealed no loss of myoglobin, indicating no irreversible cell damage. This finding suggests that the formation of AMDs may occur prior to the disruption of the sarcolemma or irreversible cell damage.

Animals↗
PubMed1989

Mutagenicity studies on fenitrothion in bacteria and mammalian cells.

The mutagenicity of fenitrothion was determined in strains of Salmonella typhimurium and Escherichia coli. Fenitrothion was found to be non-mutagenic in Salmonella typhimurium strains of TA98, TA1535 and TA1537 and in Escherichia coli WP2uvrA both with and without S9 mix, while weak mutagenicity was observed only in Salmonella typhimurium TA100 and enhanced by the addition of S9 mix. The mutagenicity observed in the TA100 strain was not expressed in a nitroreductase-deficient strain, TA100 NR, and decreased in a transacetylase-deficient strain, TA100 1,8-DNP6. The mutagenicity of fenitrothion was also examined by a gene mutation assay using the gene for hypoxanthine-guanine phosphoribosyltransferase (hgprt) in V79 Chinese hamster lung cells. Fenitrothion did not induce any increment of 6-thioguanine-resistant mutant cells at doses ranging from 0.01 to 0.3 mM regardless of the presence or absence of S9 mix. These results suggest that reduction of fenitrothion by a bacterial nitroreductase of TA100 to an active form is essential for the expression of the mutagenicity of fenitrothion in TA100 and that a bacterial transacetylase of TA100 also has an important role in the process of mutagenic activation.

Animals↗
PubMed1989

DNA-adduct formation in the forestomach of rats treated with 3-tert-butyl-4-hydroxyanisole and its metabolites as assessed by an enzymatic 32P-postlabeling method.

Formation of DNA-adducts by 3-BHA or its metabolites, i.e., tert-butyl-1,4-benzoquinone (TBQ) and 5-methoxy-3-tert-butyl-1,2-benzoquinone (3-TBOQ), as well as DNA-adduct formation by 4-nitroquinoline-N-oxide (4NQO), in rat forestomach were examined by an enzymatic 32P-postlabeling assay. Four DNA-adducts were clearly detected in the forestomach after treatment of rats with 4NQO. The sensitivity was 1.9 certain adducts per 10(8) normal nucleotides. On the contrary, no DNA adducts were detected in the forestomach of rats given either a single or repeated oral administration (5 days) of 3-BHA, TBQ or 3-TBOQ. The analyses were carried out under conditions which could detect the DNA-adducts produced by reaction of TBQ with calf thymus DNA in vitro. The results suggest that formation of aromatic adducts in vivo by 3-BHA, TBQ or 3-TBOQ in the rat forestomach-DNA is not evident or at least below the detection limits of the current bioassay.

4-Nitroquinoline-1-oxide↗
PubMed1989

Differences in urate metabolism between normouricemia and hyperuricemia in coronary heart disease in man.

We examined hyperuricemia in patients with coronary heart disease. In 85 patients with coronary sclerosis confirmed by coronary angiography, the serum urate level (6.08 +/- 1.60 mg/dL) was not different from that in subjects with normal coronary arteries (6.47 +/- 1.69 mg/dL). The incidence of hyperuricemia in patients with coronary sclerosis was 26%, and was significantly correlated with diuretics, obesity and hypertriglyceridemia, but not with hypertension or hypercholesterolemia. To elucidate the mechanism of urate metabolism in coronary sclerosis, we separated coronary sclerosis patients without complicating factors into hyperuricemics and normouricemics, and studied urate metabolism in comparison with subjects with normal coronary arteries. We found that normouricemics with coronary sclerosis had decreases in the filtered urate load and urate clearance with a normal urate-creatinine clearance ratio. Hyperuricemics with coronary sclerosis had decreases in urate clearance and urate-creatinine clearance ratios, but the filtered urate load was similar to that in normouricemics. It is suggested that in coronary sclerosis patients, normouricemics had a low glomerular filtration of urate with normal tubular urate transport, whereas hyperuricemics had enhanced tubular reabsorption of urate without any difference of urate filtration from normouricemics.

Coronary Disease↗
PubMed1988

Metabolism of 2- and 3-tert-butyl-4-hydroxyanisole in the rat (III): Metabolites in the urine and feces.

The urinary and fecal metabolites of orally administered 2-tert-butyl-4-hydroxyanisole (2-BHA) and 3-tert-butyl-4-hydroxyanisole (3-BHA) in rats were identified. Samples of 2-day pooled urine and feces of rats given a single intragastric dose of 1 g/kg body wt of tert[butyl-14C]3-BHA (*Bu-3-BHA). tert[butyl-14C]2-BHA (*Bu-2-BHA), [methyl-14C]3-BHA (*Me-3-BHA) or [methyl-14C]-2-BHA (*Me-2-BHA) were analyzed by comparing thin-layer chromatography (TLC) retentions with authentic standards. Conjugated metabolites were identified after enzymatic hydrolysis. Proton magnetic resonance spectroscopy and electron impact mass spectrometry were used for confirmation of the authentic standards. In rats given 3-BHA, a major metabolite in the urine was 3-BHA-glucuronide with a smaller amount of tert-butylhydroquinone (TBHQ)-sulfate, while unchanged 3-BHA and 3-BHA-glucuronide were detected in the feces. In rats given 2-BHA, the main metabolites were the sulfate conjugates of 2-BHA, 4-tert-butyl-5-methoxy-1,2-benzoquinone (2-TBOQ) and the glucuronide of 2-BHA in the urine, while unchanged 2-BHA was found in the feces.

Administration, Oral↗
PubMed1988

Electrophysiological studies on the effects of mianserin, a tetracyclic antidepressant agent, on isolated guinea-pig papillary muscle.

We studied the effects of mianserin on the action potentials of papillary muscle from the guinea-pig. Mianserin (above 10 microM) reduced the maximum rate of the rise (Vmax) of the action potential, and shifted the Vmax-Em relationship to more negative potentials. The compound also depressed the slow action potentials of K+-depolarized papillary muscles. It is concluded that relatively high concentrations of mianserin had an inhibitory action on the electrophysiological properties of both the fast- and slow-response fibers of the heart.

Action Potentials↗
PubMed1988

Comparative study of the block of Vmax by aprindine and quinidine in the guinea-pig heart muscle.

The depression of Vmax of the action potential in guinea-pig ventricular muscle by aprindine and quanidine was compared. Aprindine caused a more pronounced rate-dependent block (Kd = 10(-6) M at 3.3 Hz) than did quinidine (Kd = 1.6 X 10(-5) M at 3.3 Hz). Aprindine shifted the relationship between Vmax and resting potential to a more negative potential (mean 9.2 mV: 10 microM) than did quinidine (mean 5.7 mV: 10 microM). In addition, aprindine caused a more pronounced resting block (Kd = 1.3 X 10(-5) M) than quinidine (Kd = 8.6 X 10(-5) M). It is concluded that aprindine has a higher affinity for activated and/or inactivated and resting state channels than quinidine, making channels unavailable for conduction upon activation.

Action Potentials↗
PubMed1988

Renal hypouricemia due to an isolated renal defect of urate transport.

A 22-year-old man was found to have low serum urate concentration (1.1-1.7 mg/dl). His urate clearance was markedly increased (26.9-35.5 ml/min) and was not decreased after administration of pyrazinamide, but was even more increased after administration of benzbromarone. No other renal tubular abnormalities were detected. The young man has one sister and two brothers. His sister also has hypouricemia and hyperuricosuria. We suggest that the present case had a genetically determined renal abnormality affecting tubular presecretory reabsorption of urate.

Adult↗
PubMed1988

Substrate specificity for formation of cholesterol ester conjugates from fenvalerate analogues and for granuloma formation.

1. The substrate specificity of microsomal carboxyesterase(s) responsible for the formation of cholesteryl [2R]-2-(4-chlorophenyl) isovalerate from fenvalerate was investigated by incubating mouse kidney microsomes with 14C-cholesterol and the following substrates: fenvalerate isomers, fenvalerate analogues, other pyrethroids, methoprene and cycloprate analogues. Among the four isomers of fenvalerate, only the [2R, alpha S]-isomer yielded a cholesterol ester, being identical with the result obtained in the in vivo study. Some fenvalerate analogues produced cholesterol ester conjugates, but no other pyrethroids nor methoprene produced such conjugates. Some cycloprate analogues gave the corresponding cholesterol ester, the yields of which were dependent on their carbon-chain lengths. 2. Cholesterol ester formation in vitro from these fenvalerate analogues was well correlated with granuloma formation observed when the analogues were given to mice at 3000 ppm for a month. 3. Steroids other than cholesterol were also investigated as acceptors of the acid moiety of the [2R, alpha S]-isomer by incubating solubilized carboxyesterase(s) with the [2R, alpha S]-isomer in the presence of egg lecithin and several steroids. Dehydroisoandrosterone and pregnenolone were found to give the corresponding ester conjugates.

Animals↗
PubMed1987

Comparative metabolism of fenitrothion in aquatic organisms. I. Metabolism in the euryhaline fish, Oryzias latipes and Mugil cephalus.

[14C]Fenitrothion at 0.1 ppm in running water is more rapidly absorbed in the killifish (Oryzias latipes) at 25 than at 15 degrees C to a similar plateau level, and bioaccumulation ratios of fenitrothion are 235 and 339, respectively. Water of higher salinity (23%) resulted in slightly higher accumulation ratios of fenitrothion in both killifish (303) and mullet, Mugil cephalus (179), than fresh water (235 and 30, respectively), but the half-lives are independent of temperature and salinity, with values of 0.24-0.36 day. Fenitrothion was metabolized primarily through hydrolysis by the killifish, demethylation by the mullet, and conjugation of the liberated phenol with glucuronic acid by both species. Although metabolism of the compound was not affected by the different salinities and temperatures in both fish, the glucuronide conjugate was more directly excreted into water under lower temperature and higher salinity conditions. 14C-labeled compounds are distributed primarily in the gall bladder as shown by whole-body radioautography.

Animals↗
PubMed1987

Comparative metabolism of fenitrothion in aquatic organisms. II. Metabolism in the freshwater snails, Cipangopaludina japonica and Physa acuta.

When freshwater snails, Cipangopaludina japonica and Physa acuta, were exposed to 0.1 ppm [14C]fenitrothion in a dynamic flow system, the concentrations of fenitrothion and 14C in the body reached equilibrium on Day 1 of exposure. The maximum bioaccumulation ratios of fenitrothion were 18 and 53 in C. japonica and P. acuta, respectively. These snails metabolized the compound primarily by demethylation, hydrolysis, and reduction. The liberated phenol moiety was found to be conjugated with sulfate in C. japonica and mainly with glucose in P. acuta. When the snails were transferred to a freshwater stream, fenitrothion and its metabolites were rapidly excreted, and the half-life of the parent compound was less than 0.5 day in both snails. Fenitrothion and its decomposition products were mainly distributed in liver of P. acuta, as evidenced by whole-body radioautography.

Animals↗
PubMed1987

Comparative metabolism of fenitrothion in aquatic organisms. III. Metabolism in the crustaceans, Daphnia pulex and Palaemon paucidens.

When the waterflea Daphnia pulex and the shrimp Palaemon paucidens were exposed to 1.0 ppb [14C]fenitrothion in a flowthrough system, the concentrations of fenitrothion and 14C in the body reached equilibrium, and the maximum bioaccumulation ratios of fenitrothion were 71 and 6 in the daphnia and shrimp, respectively. These crustaceans primarily metabolized the compound by oxidation of P = S to P = O, hydrolysis of P-O-aryl linkage, and demethylation. The liberated phenol was found to be conjugated with sulfate in the daphnia and with glucose in the shrimp. When the organisms were transferred to a freshwater stream, fenitrothion and its metabolites were rapidly excreted from their bodies, and the half-life of the parent compound was less than 0.2 day in both species.

Animals↗