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Biomedical subjects

H Ono

Publications and source records attributed to H Ono.

At least 613 records · Page 34Linked to original sources
PubMed1982

Demonstration of slow channel activation in skeletal muscle of the dog.

The effects of verapamil, MnCl2, CaCl2 and tetrodotoxin on the contracture induced by KCl infusion were studied on the isolated, blood-perfused canine diaphragm preparation. Continuous intra-arterial infusion of KCl (30-100 mg/min) produced a biphasic contracture; initially a fast and large contracture was induced which soon declined and was replaced by a second smaller contracture which was sustained throughout the KCl infusion. Verapamil (3 micrograms-10 mg, i.a.) and MnCl2 (0.1-10 mg, i.a.) produced a dose-dependent relaxation in the sustained contracture. Intra-arterial injection of CaCl2 produced a dose-dependent contractile response which was inhibited by treatment with verapamil and MnCl2. On the other hand tetrodotoxin, even in high doses, did not show a significant inhibitory effect on the sustained potassium-induced contracture. Therefore, the present results indicate that the slow calcium channel of skeletal muscle of the dog was activated with depolarization induced by potassium infusion.

Animals↗
PubMed1982

Determination of captopril and its disulphide in biological fluids.

A gas chromatographic-mass spectrometric method for the simultaneous determination of captopril (SQ 14,255) and its disulphide (SQ 14,551) in biological fluids by means of selected ion monitoring is described. In order to prevent oxidative degradation, captopril was treated with N-ethylmaleimide (NEM). The captopril-NEM adduct and the disulphide were converted into the hexafluoroisopropyl esters, which were separated on a 10% Dexsil 300 GC column and determined by employing the captopril-N-butylmaleimide adducts as an internal standard. The blood and urine levels of captopril and its disulphide in dogs to which captopril had been administered orally were measured by the proposed method. The urinary excretion of these two substances in rats was also determined in a similar manner.

Animals↗
PubMed1982

Fine structural studies of ciliary processes after treatment with cholera toxin or its B subunit.

Delivery of 2 micrograms of cholera toxin (CT), a specific, irreversible activator of adenyl cyclase, via the blood causes dilation of capillaries and stromal edema of the ciliary processes. These morphologic changes occur within 3 h, are maximal at 12 to 24 h, then gradually return to normal by 72 h. In the late phase of hypotony, ultrastructural changes in the ciliary epithelia, similar to Greeff vesicles, are due to a "paracentesis effect" from hypotony, caused by decreased aqueous flow through the eye. Delivery of 2 micrograms of the B subunit of CT (Sub-B) causes very mild capillary dilation and stromal edema of ciliary processes. These changes reach their peak at 3 h, then return to normal at 24 h. No significant damage occurred to the pigmented or non-pigmented epithelium with either agent. No hemorrhage, invasion of inflammatory cells or appearance of fibrin exudates in the ciliary processes could be detected.

Animals↗
PubMed1982

Ventral root depolarization and spinal reflex augmentation by a TRH analog in rat spinal cord.

The experiments were performed on spinal rats transected at the C 1 level. Intravenous administrations of TRH and its analog DN-1417 (gamma-butyrolactone-gamma-carbonyl-L-histidyl-L-prolinamide), which has less endocrine activity, produced a marked increase in the monosynaptic reflex (MSR) and depolarization of the ventral root, without affecting the dorsal root reflex (DRR) and the resting potential of the dorsal root. Excitation of the monosynaptic reflex was not antagonized by chlorpromazine, haloperidol, atropine or cyproheptadine, and was not influenced by pretreatment with reserpine. The depolarization of the ventral root persisted in the presence of baclofen or tetrodotoxin. These findings suggest that depolarization of the ventral root induced by TRH and DN-1417 is due to a direct action on motoneuronal membranes, and that an increase in the monosynaptic reflex is in part due to a depolarization of motoneurones. The effect of DN-1417 were longer lasting than those of TRH.

Animals↗
PubMed1982

Effect of gonadotropins, steroids and culture media on bovine oocyte maturation in vitro.

The present experiment was to investigate the effect of gonadotropins (LH and hCG), steroids (estradiol and progesterone) and culture media (TCM 199, Ham-F-12, BMOC-3 and modified KRB) on in vitro maturation of cumulus-enclosed bovine oocytes. Oocytes isolated from follicles of </=5 mm in diameter were cultured for 27 to 30 hours. Dosages of gonadotropins were 10 mug/ml and 2 i.u./ml for LH and hCG, respectively, and that of steroids was 1 mug/ml for both estradiol and progesterone. The study showed that the proportion of matured (metaphase II and a polar body formation) oocytes was significantly affected by the presence or absence of steroids (P < 0.01), but not by the gonadotropins and the media. Estradiol, but not progesterone, significantly increased the rate of oocyte maturation when compared with that of no steroid treatment (47.8%, 61.7% and 55.2% for none, estradiol and progesterone, respectively). These results indicate that steroids, especially estradiol, were the most important factor for bovine oocyte maturation rather than gonadotropins and culture media, and that the effect of the hormones differed in the media tested.

Journal Article↗
PubMed1982

Biosynthesis of sulfite oxidase in rat liver-determination of the site of synthesis.

The site of biosynthesis of sulfite oxidase in rat liver was determined by immunoprecipitation of nascent peptides released from ribosomes and in vitro translation products of isolated polysomes. The specificity of the immunoprecipitation of sulfite oxidase nascent peptides was confirmed by examination of the size distribution of immunoprecipitated peptides and by the competition with purified enzyme in the immunoprecipitation. Both nascent peptides analysis and the in vitro translation experiment indicated that this enzyme was mainly synthesized by free ribosomes in the cytoplasm, although bound ribosomes also contributed to the synthesis of this enzyme to some extent. When the discharge of sulfite oxidase peptides from bound ribosomes was examined with rough microsomes, however, about two thirds of the enzyme peptides synthetized by bound ribosomes were discharged to the outside of microsomal vesicles.

Animals↗
PubMed1982

Biosynthesis of sulfite oxidase in rat liver - presence of a large precursor form of the enzyme in cytosol.

The time courses of in vivo incorporation of [3H]leucine into mitochondrial, microsomal, and cytosolic sulfite oxidase were examined and it was found that the cytosol contained a precursor pool of newly synthesized sulfite oxidase which was rapidly transport into mitochondria. At 10 min after the injection of the radioactive leucine, most of the radioactivity of cytosolic sulfite oxidase was associated with the precursor whose molecular size was about 3,000 daltons larger than the authentic sulfite oxidase subunit. We concluded that sulfite oxidase was synthesized as a larger precursor in the cytosol, and transported into mitochondria to be converted to the mature enzyme. The turnover rate of the sulfite oxidase in rat liver was also determined by measuring the decay of enzyme radioactivity after the injection of [14C]leucine. Mitochondrial, microsomal, and cytosolic sulfite oxidase had an almost identical half-life of 3-4 days.

Animals↗