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Biomedical subjects

M Hirata

Publications and source records attributed to M Hirata.

At least 649 records · Page 36Linked to original sources
PubMed1982

Effects of arachidonic acid and bradykinin on the coronary flow, release of PGI2 and cardiac functions in the perfused guinea-pig heart.

The contribution of prostacyclin (PGI2) to the coronary vasodilating action of arachidonic acid (AA) and bradykinin (BK) was examined in isolated perfused guinea-pig hearts. The injection of Aa (100 to 1,000 ng) and BK (1 to 100 ng) into the heart resulted in a dose-dependent increase in the total amount of coronary flow and a release of 6-keto-prostaglandin F1alpha, a stable metabolite of PGI2. Both AA and BK showed weak positive chronotropic effects. In addition, higher doses (300 and 1,000 ng) of AA caused a transient reduction in the coronary flow rate, left ventricular systolic pressure, and left ventricular dp/dt. The changes in coronary flow, release of PGI2, and all cardiodynamic parameters induced by AA were abolished by pretreatment of the preparation with diclofenac-Na. On the other hand, the BK-induced increase in coronary flow rate was only partially reduced by diclofenac-Na when the release of 6-keto-prostaglandin F1alpha was completely inhibited. It is concluded that in isolated perfused guinea-pig hearts, BK has both PGI2-independent and PGI-2-dependent coronary vasodilating actions; the latter action is less than 25%, and the coronary vasodilating action of AA is mainly mediated via PGI2.

Animals↗
PubMed1982

[Determination of bromine contents in the blood and hair of workers exposed to methyl bromide by radioactivation analysis method].

The bromine contained in blood and hair samples obtained from workers exposed to methyl bromide was analyzed by non-destructive activation analysis. The samples were irradiated for 1 min in pneumatic irradiation facility of Kyoto University research reactor with an estimated thermal neutron flux density at 2 X 10(13)n X cm-2 X sec-1. The irradiation was counted with Ge(Li) detector. The duration of measurement of radionuclide bromine in blood and hair was 200 sec within 2-10 min after irradiation. The bromine content of serum sample obtained from a worker suspected of methyl bromide poisoning was found to be 412 micrograms/g on 13 days apart from exposure to methyl bromide. The biological half-life of bromine in this case was found to be about 16 days. Then bromine contents in serum and hair samples obtained from workers exposed to methyl bromide were found to be 1.7 and 2.6 times higher respectively than those of nonexposed workers. Any correlations of bromine contents were not observed between serum and hair samples obtained from workers exposed to methyl bromide, nor between bromine amount in the serum of workers exposed to methyl bromide, and the terms exposed to it, but statistically significant positive correlation was observed between bromine amount in the hair of workers exposed to methyl bromide and the terms exposed to it.

Adult↗
PubMed1982

[Effects of 2,3-dimethoxy-5-methyl-6-(10'-hydroxydecyl)-1,4-benzoquinone (CV-2619) on myocardial energy metabolism in the hypertrophied heart of spontaneously hypertensive rats].

Effects of CV-2619 (10 and 30 mg/kg/day, p.o.) or ubiquinone-10 (Q-10, 10 mg/kg/day, p.o.) treatment for 5 weeks on systolic blood pressure (SBP) and myocardial energy metabolism were studied in spontaneously hypertensive rats of 20 weeks of age. The systolic blood pressure was about 205 mmHg at the start of the experiment, and a slight increase was noted thereafter in the control (vehicle) group. CV-2619, but not Q-10, inhibited the increase in the blood pressure. At 25 weeks of age, cardiac hypertrophy was noted to the same extent in either treated group. Myocardial contents of glycolytic intermediates (glycogen, glucose, pyruvate and lactate) and creatine phosphate (Cr-P), ATP, ADP, and AMP were not significantly influenced by CV-2619 or Q-10 treatment. CV-2619, however, significantly increased the energy charge, an index of myocardial energy state, with higher dose and lowered the lactate/pyruvate ratio with either dose. These results suggest that CV-2619 has a mild antihypertensive effect and improves the myocardial energy state in the hypertrophied heart during the sustained phase of hypertension in SHR rats.

Animals↗
PubMed1982

Biochemical evidence for the coexistence of monomorphic and polymorphic N-acetyltransferase activities on a common protein in rabbit liver.

New Zealand White rabbits were classified as rapid or slow acetylators by measuring the N-acetylation half-life of i.v. administered sulfadiazine, by pedigree analysis and by determination of liver N-acetyltransferase (NAT) activity in vitro. Slow acetylator rabbits were found to have significantly lower levels of p-aminobenzoic acid NAT activity in vitro than did rapid acetylator rabbits, demonstrating genetic covariation of p-aminobenzoic acid (monomorphic) and isoniazid (polymorphic) NAT activity. Monomorphic and polymorphic NAT activities could not be separated by two extensive purification procedures involving sequential centrifugation, fractional precipitation with ammonium sulfate, ion-exchange chromatography on DEAE-cellulose, gel filtration on Sephadex or Sephacryl and isoelectric focusing or electrophoresis on polyacrylamide gels. In addition, indistinguishable heat inactivation patterns were demonstrated for the two NAT activities utilizing highly purified NAT preparations at two different temperatures. Each of these findings support the coexistence of monomorphic and polymorphic NAT activities on a common protein.

Acetylation↗
PubMed1982

[Effects of 2,3-dimethoxy-5-methyl-6-(10'-hydroxydecyl)-1,4-benzoquinone (CV-2619) on adriamycin-induced ECG abnormalities and myocardial energy metabolism in spontaneously hypertensive rats].

Antidote actions of CV-2619 and ubiquinone-10 (Q-10) against adriamycin (ADM) cardiotoxicity were studied in spontaneously hypertensive rats. ADM (1 mg/kg/day, i.p.) elicited widening of the QRS complex in the ECG. The widening of the QRS complex was counteracted by a 10-day treatment with CV-2619 (10 and 30 mg/kg/day, p.o.) or Q-10 (10 mg/kg/day, p.o.), which was started on the 15th day of the ADM treatment. CV-2619 or Q-10, however, did not influence ADM-induced decrease in body and heart ventricular weights. Systemic hypotension caused by adriamycin was accelerated by CV-2619 or Q-10. The ADM treatment significantly decreased myocardial glycogen and glucose contents, while it did not affect the lactate content. Furthermore, ADM did not affect the myocardial content of adenine nucleotides, but significantly increased that of creatine phosphate. CV-2619 or Q-10 medication did not counteract changes in these contents by ADM. On the contrary, both agents decreased the lactate content and increased the phosphorylation potential, an index of myocardial energy state. In conclusion, CV-2619 might be as effective as Q-10 to protect the heart against ADM cardiotoxicity, and both test agents improved the myocardial energy state.

Animals↗
PubMed1982

[Effects of 2,3-dimethoxy-5-methyl-6-(10'-hydroxydecyl)-1,4-benzoquinone (CV-2619) on the energy metabolism of red blood cells of rats].

Effects of CV-2619 and ubiquinone-10 (Q-10) on the energy metabolism of red blood cells (RBC) of Sprague Dawley rats were studied in the presence or absence of NaF. NaF (0.3--10 mM) dose-dependently decreased the ATP and lactate contents of the RBC. In the presence of NaF (1.5 mM), ATP content decreased to about 30% of the control. Phosphofructokinase (PFK) was markedly activated, while glyceraldehydephosphate dehydrogenase (GAPDH) and enolase were inhibited by NaF. Thus, the decrease in ATP by NaF might be attributed to retarded glycolysis due to inhibition of the latter two enzymes. The decrease in ATP by NaF (1.5 mM) was dose-dependently inhibited by CV-2619 (0.3--30 microM). Inhibition of enolase and activation of PFK by NaF were still noted even in the presence of CV-2619. Inhibition of GAPDH by NaF, however, was released by CV-2619. Q-10 (1--100 microM) did not affect the ATP levels decreased by NaF. It could be concluded that CV-2619 counteracted the NaF-induced decrease in the ATP level by accelerating the glycolytic flux through the GAPDH step, which was a rate-limiting one in the presence of NaF. Q-10, however, had no effect on the glycolytic flux.

Adenosine Triphosphate↗
PubMed1981

Sulfoconjugation and glucuronidation of salicylamide in isolated rat hepatocytes.

Sulfoconjugation and glucuronidation of salicylamide by isolated hepatocytes were examined with various concentrations of salicylamide and sodium sulfate. The ratio of sulfate to glucuronide formed changed markedly, depending on the concentrations of salicylamide and inorganic sulfate in the medium. The apparent Km value of sulfoconjugation for salicylamide was 0.006 mM, while its Vmax value varied depending on the concentration of inorganic sulfate (e.g., 2.1 and 0.5 nmoles/min/10(6) cells at 1.2 and 0.5 mM inorganic sulfate, respectively). The Km and Vmax values of glucuronidation for salicylamide were 0.19 mM and 1.28 nmoles/min/10(6) cells, respectively, in the absence of sodium sulfate. Glucuronidation was suppressed in the presence of inorganic sulfate. The suppression could be attributable to the competitive consumption of salicylamide by sulfotransferase. Additional in vivo experiments revealed that an extra amount of salicylamide markedly lowered the blood inorganic sulfate levels of rats. The significance of the finding is discussed in conjunction with the variation of the Vmax value of sulfoconjugation with the inorganic sulfate concentration.

Animals↗
PubMed1981

Effects of external cations on calcium efflux from single cells of the guinea-pig taenia coli and porcine coronary artery.

1. Single smooth muscle cells were prepared from the guinea-pig taenia coli and the porcine coronary artery by treatment with collagenase, in order to measure the 45Ca flux with special reference to the effects of external cations. 2. In excess [K]o solution, cell suspensions prepared from both tissues showed an increased 45Ca uptake within 3-5 min. In Na-free solution, the cells prepared from taenia coli, but not from coronary artery showed an increased 45Ca uptake. The Ca uptake of the cells paralleled with the tension increase recorded from tissues of both species. 3. The efflux of 45Ca into Ca-free EGTA containing solution was markedly increased by [Na]o in cells from the taenia coli, but not in cells from the coronary artery. 4. The [Na]o-activated 45Ca efflux from cells of the taenia coli was slightly larger in Ca-free solution than in the Ca-containing (10)-4) M) solution. Depolarization of membranes produced by excess [K]o did not effect the [Na]o-activated 45Ca efflux. 5. Increase in [Na]i by treatment with K-free solution suppressed the [Na]o-activated 45Ca efflux in the taenia coli. Re-addition of [K]o reactivated the [Na]o-activated 45Ca efflux. This re-activation was blocked by ouabain. 6. The efflux of 45Ca was slightly activated by [Ca]o in cells from the taenia coli. This [ca]o-activated 45Ca efflux was larger in Na-free solution than in Na-containing solution, thus suggesting interactions between [Na]o and [Ca]o on the Ca efflux. 7. In cells from the taenia coli, 45Ca efflux could still be observed in nominally Na-and Ca-free solution. This residual 45Ca efflux made a large contribution to the total 45Ca efflux. 8. When 45Ca uptake was measured in Na-free (Tris) solution, the [Na]o-activated, [Ca]o-activated and residual 45Ca effluxes of cells from the taenia coli were accelerated, non-selectively. 9. These results obtained with cells prepared from the guinea-pig taenia coli are comparable to the Ca2+ efflux mechanism seen in the squid axon. However, maintenance of low concentrations of [Ca]i seems to require not only the above three 45Ca efflux mechanisms, but also Ca sequestering mechanisms in the cell.

Animals↗
PubMed1981

An enzyme marker to ensure reliable determinations of human isoniazid acetylator phenotype in vitro.

Human liver N-acetyltransferase (NAT) activity undergoes rapid inactivation after death. Thus, in vitro determination of acetylator phenotype in liver autopsies may be unreliable. In the present investigation, the relative stabilities of monomorphic and polymorphic NAT activity were compared in situ in human and rabbit liver of rapid and slow acetylator phenotype. In both phenotypes, the monomorphic NAT activity was considerably less stable than the polymorphic, enabling it to be utilized as an enzyme marker to assure reliable in vitro phenotype classification.

4-Aminobenzoic Acid↗
PubMed1981

Metabolism of isoniazid and free hydrazine formation in isolated rat hepatocytes.

Isoniazid (INH) was incubated with isolated rat hepatocytes, and the amounts of acetyl-INH, monoacetylhydrazine, diacetylhydrazine and hydrazine formed were determined by gas chromatography-mass spectrometry (GC-MS). Subsequent analyses of kinetic parameters of metabolic pathways and enzymological study of rat liver homogenate revealed that hydrazine was formed preferentially from INH, catalyzed by soluble hydrolytic enzymes.

Animals↗
PubMed1981

Distribution study of a synthetic ACTH analogue in rat tissue.

Tissue distribution of (Aib1, Lys17, 18, 19)-corticotrophin-(1-19)-nonadecapeptide amide (690024-S), iv injected to hypophysectomized rats, were surveyed by bioassay. Among the tissues examined. the largest amount of 690024-S was found in the liver during 3 h of search for the injection, while a higher concentration of the peptide per tissue weight was found in kidney. Though a small amount of 690024-S was detected in spleen, heart and lung at an early stage, it was not detectable in other tissues such as brain, stomach, small intestine, thigh muscle, fat or foetus. The peptide was found to be excreted into bile for the duration of about 2 h. It was also found that the elimination of 690024-S in blood followed biphasic first order kinetics.

Adrenocorticotropic Hormone↗