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Biomedical subjects

T Dohi

Publications and source records attributed to T Dohi.

At least 145 records · Page 8Linked to original sources
PubMed1988

Evidence that prostaglandins activate calcium channels to enhance basal and stimulation-evoked catecholamine release from bovine adrenal chromaffin cells in culture.

The effects of prostaglandins (PGs) on catecholamine (CA) secretion and Ca2+ fluxes were studied in a primary culture of bovine chromaffin cells. PGD2, PGF2 alpha and PGE2 induced CA release from cultured bovine chromaffin cells in a concentration dependent manner (0.03-3 microM). PGD2, PGF2 alpha and PGE2 at 3 microM elicited maximum CA release of 0.043 +/- 0.001, 0.059 +/- 0.008, 0.062 +/- 0.002 micrograms/10(6) cells, respectively. Three micromolar of PGD2, PGF2 alpha and PGE2 enhanced CA release induced by acetylcholine (ACh) in a degree of 186 +/- 10, 206 +/- 6, 150 +/- 4% of control respectively. PGs also enhanced CA release induced by 20 mM K+, veratridine and A23187. In Ca2+-free medium, PGs failed to affect basal and caffeine (50 mM)-induced CA release. PGF2 alpha increased 45Ca uptake and showed additive effect with ACh on 45Ca uptake. Nicardipine (0.1-10 microM) suppressed CA release and 45Ca uptake induced by PGF2 alpha, while diltiazem and verapamil failed to affect these responses to PGF2 alpha. BAY K 8644 (1 microM) potentiated CA release and 45Ca uptake evoked by PGF2 alpha. These results suggest that PGs enhance basal and stimulation-evoked CA release from chromaffin cells possibly through facilitation of Ca2+ influx. The mechanisms of action of PGs in adrenal medulla are discussed.

Acetylcholine↗
PubMed1988

A modulating role of prostaglandins in catecholamine release by perfused dog adrenal glands.

PGE2, PGE1, PGF2 alpha and PGD2 dose dependently potentiated the ACh-evoked catecholamine (CA) release from perfused dog adrenal glands. These prostaglandins by themselves slightly stimulated CA release. PGE2 potentiated the CA release induced by stimulation of nicotinic or muscarinic cholinergic receptors and also by stimulation with excess K+ or caffeine. However, PGE2 did not affect the release induced by caffeine in the absence of extracellular Ca2+. ACh stimulated the 45Ca efflux from adrenals prelabelled with 45Ca. PGE2 enhanced the ACh-stimulated 45Ca efflux. The CA release in response to ACh or nicotine was slightly but significantly reduced by pretreatment of the adrenals with indomethacin. SC19220, a specific prostaglandin antagonist significantly reduced the ACh-evoked CA release and blocked the enhancing action of PGE2 on the stimulation-evoked CA release. The results showed that prostaglandins stimulated the CA release evoked in perfused dog adrenals and that the effect on the Ca2+ flux across the plasma membrane could be involved in the prostaglandin mechanism of action. The possibility is suggested that prostaglandins formed endogenously in response to physiological stimulation of chromaffin cells could play a facilitating, modulatory role in CA release.

Acetylcholine↗
PubMed1988

Effects of phenolic dental medicaments on prostaglandin synthesis by microsomes of bovine tooth pulp and rabbit kidney medulla.

Prostaglandin (PG) synthesis from [1-14C]-arachidonic acid by bovine dental pulp microsomes was stimulated by 0.1-0.5 mM concentrations of p-chlorophenol (PCP) and inhibited by more than 3 mM. Dual effects (stimulation and inhibition) of phenol, PCP, o-, m-, p- and tri-cresol on PG synthesis by rabbit kidney medullary microsomes were observed. Of various compounds tested, eugenol, thymol and guaiacol were the most potent inhibitors; the inhibitory action was reversible. Phenolic compounds did not affect the activity of glucose-6-phosphatase, adenosine triphosphatase, or lactate dehydrogenase in rabbit kidney medulla within the range of concentrations that stimulated or inhibited PG synthesis. Thus the analgesic effect of phenolic medicaments in endodontic therapy may be due to inhibition of arachidonic-acid metabolism.

Animals↗
PubMed1988

Alterations of the plasma selenium concentrations and the activities of tissue peroxide metabolism enzymes in streptozotocin-induced diabetic rats.

The activity of aortic glutathione peroxidase, a selenium-dependent enzyme, significantly decreased in rats 4 and 8 months after the injection of streptozotocin (STZ). Catalase activity was shown to occur at low levels in rat aorta and was not influenced by the diabetic state. Superoxide dismutase activity was less than detectable. The activity of selenium-dependent glutathione peroxidase in kidney, but not in lung and liver, increased in diabetic rats. Catalase and superoxide dismutase activities in the kidney were not altered. The plasma lipid peroxide value increased in diabetic rats. The selenium content in plasma of diabetic rats increased markedly while the increase in plasma glutathione peroxidase activities was insignificant. The observed abnormalities in plasma of STZ rats were improved by insulin treatment. The defects in glutathione peroxidase in the diabetic rat aorta were restored by insulin treatment. These results may suggest that the capacity of the antioxidative defense system in the aorta decreased in the diabetic state, and this may help clarify the mechanism of the pathogenesis of endothelial dysfunction associated with diabetes.

Animals↗
PubMed1988

Development of motion analyzing system for implanted tilting disk valves.

A motion-analyzing system was developed to quantitatively evaluate functions of the implanted tilting disk valve, e.g., an open angle and a duration of valve open and/or shut. In this system a picture of the valve on an x-ray cinefilm is displayed on the CRT screen by the TV camera for extraction of valve position. Data extracted are stored in the computer and are used to calculate parameters for motion analysis of the valve. The reliability of this system was confirmed within 3 degrees of error using the valve model prior to the evaluation of cinefilms clinically procured. With the aid of this motion analyzing system, complicated motions of the tilting disk valve were easily quantified and the useful information as given for clinical diagnosis and further valve development.

Computer Graphics↗
PubMed1988

Development of pressure monitoring and controlling system for quantitative analysis of experimentally induced perilymph fistula.

The cause of perilymph fistula, a subgroup of sudden deafness, has not been clearly understood. To study its etiology quantitatively, the inner ear pressure monitoring system with a computer controlled pressurizing device and three types of low-pressure monitoring sensors was constructed and utilized in ex vivo experiments using white guinea pigs. Hypothesizing that cerebrospinal pressure increases cause rupture of the round window membrane, direct and indirect pressurization to cerebrospinal region and simultaneous measurement of inner ear and cerebrospinal pressures were carried out. Ruptures of the round window membranes were seen in the experiments with direct saline infusion into the cochlea when the increment of inner ear pressure exceeded 500 mmH2O. There was no sign of rupture when squeezing abdomen was employed as an indirect pressurization, although cerebrospinal pressure increased.

Animals↗
PubMed1987

Density-dependent recognition of cell surface GM3 by a certain anti-melanoma antibody, and GM3 lactone as a possible immunogen: requirements for tumor-associated antigen and immunogen.

A mouse monoclonal antibody M2590, previously established after immunization of mice (C57BL/6) with syngeneic melanoma B16 cells and showing preferential reactivity with various types of melanoma over other tumor and normal cells or tissues, was shown to be directed to GM3 ganglioside. Since GM3 is widely distributed in essentially all types of animal cells, there is a conflict with the concept of a tumor-associated antigen and immunogen. Studies on the reactivity of M2590 antibody with various cells having different GM3 density at their cell surface, including cells treated with sialidase, liposomes, and solid-phase lipid layer containing different GM3 concentrations, have indicated that 1) reactivity of the antibody M2590 depends greatly on the density of GM3 exposed at the cell surface, on liposomes, or on solid phase; and 2) there is a threshold density that is recognized by the antibody in all-or-none fashion. In addition, the antibody M2590 reacts not only with GM3 but also with GM3 lactone, and the binding affinity of the antibody to GM3 lactone is strikingly higher than to GM3; however, the antibody does not react with GM3 ethyl ester. GM3 lactone was detected in melanoma as 3H-labeled GM3 gangliosidol after melanoma cells were directly treated with NaB[3H]4. A comparative immunization of BALB/c mice with GM3 and GM3 lactone showed that GM3 lactone is a much stronger immunogen than GM3, although the antibody elicited reacts with both GM3 and its lactone. Thus, the real immunogen could be GM3 lactone, although it is a minor membrane component.

Animals↗
PubMed1987

Susceptibility of diabetic rat aorta to self-deactivation during prostacyclin synthesis.

The ability of aortic rings to produce PGI2 markedly decreased in streptozotocin-induced diabetic rats when compared with age-matched controls. Arachidonic acid dose-dependently stimulated the production of PGI2 both in normal and diabetic rat aorta during 5 min incubation. The deficiency in PGI2 production in diabetic rat aorta was temporarily corrected by the addition of 5-20 microM of arachidonic acid. However, when aortic rings were incubated over a period of 10 min in the presence of arachidonic acid, the ability of PGI2 production in diabetic rats markedly decreased. Repeated exposures of aortic rings to arachidonic acid also markedly reduced PGI2 production in diabetic rats. PGI2 production in diabetic rat aorta was inactivated more readily than in normal rat aorta by pre-incubation with t-butyl hydroperoxide. Phenol had a protective effect on incubation-induced inactivation of PGI2 generating activity in diabetic rat aorta. Serum markedly stimulated PGI2 synthesis in normal and diabetic rat aorta. The serum activity in diabetic rats was less potent than in normal rats. Melittin and dipyridamole were effective in stimulating PGI2 release from diabetic rat aorta. These results suggest that enzymes in the aorta involved in PGI2 synthesis from released arachidonic acid are susceptible to self-inactivation in diabetic rats during the metabolism of arachidonic acid. This may contribute to the defect of PGI2 synthesis in diabetic rat aorta in addition to the decreased availability of the substrate.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Enhancement of stimulation-evoked catecholamine release from cultured bovine adrenal chromaffin cells by forskolin.

Acetylcholine (ACh) increased cyclic AMP levels in cultured bovine chromaffin cells with a peak effect at 1 min after the addition. Pretreatment with forskolin (0.3 microM) enhanced the ACh-evoked cyclic AMP increase. The catecholamine (CA) release induced by ACh was enhanced by forskolin, but forskolin alone did not enhance the CA release. The effect of forskolin increased dose-dependently up to 1 microM, but decreased at higher concentrations. Dibutyryl cyclic AMP (DBcAMP) also enhanced ACh-evoked CA release, but the effect was less potent than that of forskolin. Forskolin enhanced both [3H]norepinephrine ([3H]NE) and endogenous CA release evoked by 30 mM K+ from cells that were preloaded with [3H]NE. The effects of forskolin were substantial when CA release was evoked with low concentrations of ACh or excess K+, but decreased with higher concentrations of the stimulants. Forskolin also enhanced the CA release induced by ionomycin and veratrine, or by caffeine in Ca2+-free medium. The potentiation by forskolin of the ACh-evoked CA release was manifest in low Ca2+ concentrations in the medium, but decreased when Ca2+ concentration was increased. These results suggest that cyclic AMP may play a role in the modulation of CA release from chromaffin cells.

Acetylcholine↗
PubMed1987

Stimulation-evoked Ca2+ fluxes in cultured bovine adrenal chromaffin cells are enhanced by forskolin.

Forskolin, 1 microM, increased acetylcholine (ACh)-stimulated 45Ca uptake by chromaffin cells. The stimulatory effects of forskolin decreased with increasing concentration of ACh. The attenuation of the effect of forskolin on 45Ca uptake as a function of ACh concentration correlated well with changes in the forskolin effect on ACh-evoked catecholamine (CA) release. Forskolin increased excess KCl- and veratrine-evoked CA release and 45Ca uptake. Forskolin by itself stimulated 45Ca efflux and enhanced ACh-, excess KCl-, and veratrine-stimulated 45Ca efflux. High doses of forskolin inhibited both ACh-evoked 45Ca uptake and CA release. The inhibitory action of forskolin was specific to receptor-mediated response because excess KCl- and veratrine-stimulated 45Ca uptake and CA release were not inhibited. Forskolin, 0.3-30 microM, dose-dependently increased caffeine-stimulated CA release and 45Ca efflux in the absence of Ca2+ in the medium, and the effects were mimicked by dibutyryl cyclic AMP. These results suggest that cyclic AMP increases stimulation-induced CA release by enhancing calcium uptake across the plasma membrane and/or altering calcium flux in an intracellular calcium store.

Acetylcholine↗
PubMed1986

Increase in catecholamine release and 45Ca2+ uptake induced by GABA in cultured bovine adrenal chromaffin cells.

The role of Ca2+ in GABA-evoked catecholamine (CA) release from adrenal medulla was investigated in primary cultures of bovine adrenal chromaffin cells. GABA facilitated the 45Ca2+ uptake associated with the increase of Ca release in cultured bovine adrenal chromaffin cells. The effects of GABA on both 45Ca2+ uptake and CA release were blocked by bicuculline and picrotoxin. Nifedipine reduced the 45Ca2+ uptake and CA release induced by GABA. These data support our previous suggestion that the activation of GABA receptors on adrenal chromaffin cells facilitates the Ca2+ influx through voltage-sensitive Ca2+ channels, leading to the release of CA.

Adrenal Glands↗
PubMed1986

Potassium ion is indispensable to the catecholamine releasing response of dog adrenals to gamma-aminobutyric acid.

The effect of potassium ion on the GABA-evoked catecholamine (CA) release from isolated perfused adrenal glands of the dog was investigated. When omitting the external potassium ion, the basal release of CA was increased. During this period GABA no longer caused the increase in CA release and moreover the increased basal release was diminished reversibly by GABA. 3-Amino-1-propane-sulfonic acid, a GABAA agonist, mimicked the action of GABA in K+-free solution, while baclofen, a GABAB agonist, did not cause CA release in normal solution and did not alter the basal release in K+-free solution. The inhibition by GABA of the basal CA release in K+-free solution was blocked by bicuculline. The potency of the CA releasing action of GABA was dependent on the concentration of external K+ between 1-10 mM. Reintroduction of K+ to glands which had been perfused with K+-free solution immediately reduced the basal release of CA whereas it recovered the CA releasing action of GABA. These results suggest that GABA-evoked CA release is dependent on potassium ion. The possible mechanisms by which GABA evoked CA release are discussed.

Adrenal Glands↗
PubMed1986

Forskolin enhancement of acetylcholine-evoked cyclic AMP formation and catecholamine release in perfused dog adrenals.

Unstimulated efflux of cyclic AMP from perfused dog adrenal glands was not altered by 0.1 microM of forskolin and was slightly increased by 0.3 and 1.0 microM of forskolin. ACh stimulated efflux of cyclic AMP which preceded CA release and the efflux was dose-dependently enhanced by forskolin. Forskolin did not affect the spontaneous CA release but enhanced ACh-evoked catecholamine (CA) release. There was a close correlation between the dose relationship of forskolin enhancement of stimulated-cyclic AMP efflux and that of evoked-CA release. ACh-evoked CA release in the presence of forskolin was further potentiated by R020-1724, a phosphodiesterase inhibitor. CA release evoked by excess K+, or by caffeine in the presence or absence of external Ca2+ was also potentiated by forskolin. These results suggests that cyclic AMP generation may increase in response to stimulation of adrenal chromaffin cells and that the resulting increase of the nucleotide may function as a facilitating modulator of CA release.

4-(3-Butoxy-4-methoxybenzyl)-2-imidazolidinone↗
PubMed1986

An unusual complication of a myocardial electrode--apatite mantle on the platinum-iridium spurs.

A case of a high excitation threshold that occurred 2 years 5 months after the initial implantation of pacemaker electrodes is described in a girl 4 years 3 months of age. This complication was considered to be due to calcification of the platinum-iridium electrode spurs. The calcified material was shown to be a kind of apatite using the X-ray powder diffraction method. This complication is rare, but it must be kept in mind since battery longevity has markedly improved in recent years.

Apatites↗
PubMed1986

Membrane plasma separation through small-area, hollow-fiber filters.

The filtration capabilities of small polypropylene hollow-fiber plasma filters with membrane areas ranging from 100 to 1,000 cm2 have been investigated. It is found that the filtration flux per unit membrane area is approximately proportional to the wall shear rate gamma w at least up to gamma w = 7,500 s-1. As a result, the total filtration flow rate increases very little when the number of fibers is increased as the increase in membrane area is offset by the decrease in shear rate, but it increases with the fiber length L as L 2/3. Hemolysis occurs when the transmembrane pressure exceeds a certain threshold, but this threshold is itself an increasing function of shear rate. As a result, it is possible to circulate high blood flow rates even in very small filters (100 cm2) without hemolysis, provided the fiber length is below a critical value.

Animals↗
PubMed1986

Stimulation-evoked cyclic nucleotides efflux from isolated perfused dog adrenals and possible involvement of calcium.

Nicotine and muscarine caused the transient increase in cAMP and cGMP efflux from dog adrenal glands followed by a small but lasting increase in the nucleotide efflux. The initial increase preceded catecholamine (CA) release and the latter slowly developed. Nicotine and muscarine caused the maximal increase of cAMP and cGMP levels in adrenal medulla 15 sec after the treatment, and these effects were antagonized by hexamethonium and atropine, respectively. Hexamethonium in combination with atropine, verapamil and an omission of Ca2+ in the medium prevented ACh from producing the increase in cyclic nucleotide efflux and CA release. Reintroduction of Ca2+ (1.3 mM) in fluid after perfusion with Ca2+ and Mg2+-free fluid caused the transient increase in cyclic nucleotide efflux and CA release. Adenylate cyclase activity in adrenal medulla was activated by Ca2+. These results may suggest that cAMP formation was increased by activation of adenylate cyclase as a result of increased influx of Ca2+ when adrenal medulla were stimulated.

Adenylyl Cyclases↗