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T Dohi

Publications and source records attributed to T Dohi.

At least 163 records · Page 9Linked to original sources
PubMed1986

Facilitation of acetylcholine-evoked catecholamine release by cyclic AMP on isolated perfused dog adrenal glands.

The effects of cyclic nucleotides on catecholamine (CA) release and Ca2+ efflux were determined on isolated dog adrenals perfused with 1.3 mM Ca2+ containing fluid except indicated. Dibutyryl cyclic AMP (DBcAMP, 50 microM--1 mM) substantially enhanced CA release evoked by acetylcholine (ACh) and slightly increased the spontaneous CA release. Dibutyryl cyclic GMP (100-500 microM) narrowly increased the basal CA release. DBcAMP, 200 microM also significantly facilitated CA release caused by nicotine, bethanechol and excess K+, and by caffeine in the absence of extracellular Ca2+. 45Ca efflux evoked by ACh and by caffeine in the absence of extracellular Ca2+ from prelabelled adrenals with 45Ca was enhanced significantly by DBcAMP, 200 microM. These results suggest that cAMP may function as a facilitatory modulator in CA release from the adrenal medulla via in part the effect on Ca2+ flux including alterations in the function of systems for intracellular Ca2+ homeostasis.

Acetylcholine↗
PubMed1985

Enhancement of acetylcholine-evoked catecholamine release from perfused dog adrenals by elevating cyclic AMP levels.

Guanylyl-imidodiphosphate, guanosine 5'-tetraphosphate and phosphodiesterase inhibitors, 3-isobutyl-1-methylxanthine and RO 20-1724 significantly increased the basal cAMP output and caused a slight catecholamine (CA) release. These agents accelerated ACh-induced increase in cAMP output followed by a markedly enhanced CA release. Cholera toxin did not cause CA release but markedly enhanced ACh-evoked CA release. These results may suggest that cAMP plays a modulating role in CA release from chromaffin cells.

1-Methyl-3-isobutylxanthine↗
PubMed1984

The nature of the stimulatory action of gamma-aminobutyric acid in the isolated perfused dog adrenals.

The effect of gamma-aminobutyric acid (GABA) on catecholamine (CA) release from adrenal medulla was investigated. GABA and GABA agonists, 3-amino-1-propane-sulfonic acid and imidazole-4-acetic acid caused CA release from isolated perfused dog adrenals in a dose-dependent manner, and no tachyphylaxis to GABA was observed. CA release elicited by GABA was antagonized by bicuculline and picrotoxin. This antagonism was specific for GABA- and GABA agonist-induced responses, response to acetylcholine being unaffected. Pretreatment with atropine plus hexamethonium did not affect the response to GABA. GABA-induced CA release was abolished by the removal of Ca2+ from perfusion medium, but not by the removal of Na+ or Cl-. Verapamil, CoCl2 and dibucaine blocked the effect of GABA. A Na+ channel blocker, tetrodotoxin did not reduce GABA-evoked CA release. These results suggest that GABA may interact with its receptor to evoke CA release from adrenal medulla in a fashion of Ca2+-dependence and independence on external Na+ or Cl-.

Acetylcholine↗
PubMed1983

Effect of sodium azide on catecholamine release from isolated adrenal gland and on guanylate cyclase.

Sodium azide and other compounds which activate guanylate cyclase could stimulate catecholamine (CA) release from perfused dog adrenals. Verapamil reduced the secretory effect of sodium azide, but atropine and hexamethonium did not affect it while isobutyl methylxanthine potentiated it. Ca2+ deprivation abolished the stimulating effect of sodium azide on CA release and cyclic AMP output but the increased output of cyclic GMP remained. These results suggest the involvement of the Ca2+ influx mechanism in the secretory action of sodium azide.

Adrenal Glands↗
PubMed1983

Labelled-calcium release from rat mandibles exposed to prostaglandins in vitro.

Bone resorptive effects of prostaglandins (PGs) in cultured mandibular bone tissue of rat fetus prelabelled with 45Ca were examined in comparison with those in radius-ulna. PGE1 (3 X 10(-6)-10(-4) M) and PGE2 (3 X 10(-8)-10(-4) M) could significantly stimulate the release of 45Ca from mandible with a peak effect at 3 X 10(-6) M. The effects of PGEs were more marked in mandible than in radius-ulna. Salmon calcitonin (SCT) inhibited the stimulating effect of PGE2. PGF 2 alpha did not cause the significant increase of 45Ca-release. Parathyroid hormone (PTH) at concentrations of 0.01-1.0 IU/ml dose-dependently stimulated 45Ca-release and the effects were greater in mandible than in radius-ulna. Dibutyryl cyclic (DBc)-AMP stimulated the release of 45Ca in mandible with a sharp peak effect at 5 X 10(-4) M. The results indicate that mandible is more susceptible to these bone resorptive agents than radius-ulna.

Alprostadil↗
PubMed1983

Inhibition of gamma-aminobutyric acid release from synaptosomes by local anesthetics.

The effects of local anesthetics on the synthesis, release, and degradation of gamma-aminobutyric acid (GABA) in rat brains were investigated. The addition of procaine, lidocaine, cocaine, or tetracaine did not alter either glutamic acid decarboxylase (GAD) activity or GABA transaminase (GABA-T) activity in vitro. Neither did the enzyme activities in rats with local anesthetic-induced convulsions differ from control values. Tetracaine inhibited high K+-evoked [2,3-3H]GABA release from synaptosomes of rat brain in a dose-dependent manner with a minimal effective concentration of 10(-4) M. Cocaine, lidocaine, and procaine also reduced the release, although they were less potent than tetracaine. The GABA release inhibitors in order of potency are tetracaine, cocaine, lidocaine, and procaine which correlates well with their relative toxicity as convulsants. These results suggest that local anesthetics reduce GABAergic activities by inhibiting the release of the neurotransmitter from the nerve terminals, and that inhibition of the GABA system may be involved in the mechanism of local anesthetic-induced convulsions.

4-Aminobutyrate Transaminase↗
PubMed1982

Protection from local anesthetic-induced convulsions by gamma-aminobutyric acid.

The effects of gamma-aminobutyric acid (GABA) on the induction of convulsions by local anesthetics were investigated in mice and rats. Intraventricular administration of 0.8-1.6 mg GABA protected rats against convulsions induced by procaine, lidocaine, cocaine, and tetracaine in a dose-related manner. Intraperitoneal gamma-acetylenic GABA was also effective against procaine-induced convulsions in mice, but the metabolites of GABA, gamma-hydroxybutyrate, and gamma-butyrolactone were without effect. Intraventricular GABA, 1.6 mg, delayed the onset of convulsions induced by hydrazine, but had no influence on the incidence of convulsions induced by nicotine, pentylenetetrazol, picrotoxin, or strychnine. These results suggest that the GABA system may be involved in the mechanisms of local anesthetic-induced convulsions.

Anesthetics, Local↗
PubMed1982

Development and clinical application of a new membrane oxygenator using a microporous polysulfone membrane.

We have developed a new plate-type membrane oxygenator (MO) using a microporous polysulfone membrane. The MO is compact, handy and very easy to set up, and has easy defoaming. The MO is primed with crystalloid; through the cardiotomy reservoir, air exits across the porous membrane and is removed through ports in the membrane oxygenator. Performance and clinical use have shown that the PS oxygenator has a better gas exchange than conventional silicone oxygenators, with appropriate O2/CO2 balance and a capability for controlling oxygen and carbon dioxide separate exchange. The advantage of the MPS membrane is improved blood compatibility, and TABLE 1. BLOOD GAS ANALYSIS DURING PERFUSION Mean +/- SD Range Blood Flow (L/min) 1.56 +/- 0.29 1.04-2.12 Gas Flow (L/min) 1.89 +/- 0.73 0.5-3.0 Gas/Blood Flow Ratio 1.19 +/- 0.38 0.45-1.95 pH venous 7.340 +/- 0.083 7.220-7.443 arterial 7.390 +/- 0.080 7.272-7.507 pCO2 (mm Hg) venous 44.8 +/- 10.8 29.6-65.2 arterial 35.7 +/- 7.1 23.8-51.1 pO2 (mm Hg) venous 46.4 +/- 17.2 26.1-98.8 arterial 276.3 +/- 135.6 66.1-533.4 SO2 (%) venous 71.9 +/- 14.7 35.7-95.6 arterial 98.7 +/- 2.3 91.5-99.9 a larger number of small pores than the MPP membrane. Vapor loss, thought to be typical of microporous membranes, was found to be negligibly small. Use of the PS oxygenator for open heart surgery on 15 pediatric patients proved satisfactory, and in the future the oxygenator may prove useful for prolonged perfusions.

Animals↗
PubMed1981

Effects of pyruvate and other metabolites on cyclic GMP levels in incubations of rat hepatocytes and kidney cortex.

Pyruvate increased cyclic GMP levels in rat hepatocytes. The effects were observed without or with 1-methyl-3-isobutylxanthine. Lactate, acetate, oxaloacetate, alpha-ketoglutarate, succinate, acetoacetate and beta-hydroxybutyrate also increased cyclic GMP levels. Some compounds increased cyclic GMP in kidney cortex slices. The effects were dependent upon Ca2+ in the medium. Cyclic AMP was increased 30-50% by some of these substances with 2.6 mM Ca2+. Rotenone, oligomycin, antimycin, dinitrophenol, KCN, and arsenate decreased GTP and ATP, basal cyclic GMP and the pyruvate effect, but did not alter cyclic AMP. Although fluoroacetate alone had no effect on cyclic nucleotides, GTP, or ATP, it potentiated the pyruvate effect on cyclic GMP. Adenosine and guanosine increased cyclic GMP and GTP to a similar extent of 30-50%. Aminooxyacetate, cycloserine, pentenoic acid and mepacrine decreased the pyruvate effect while cycloserine or mepacrine alone increased cyclic GMP. Citrate and mepacrine inhibited soluble and particulate guanylate cyclase from rat liver while cycloserine and acetoacetate increased guanylate cyclase activity. None of the other compounds altered guanylate cyclase activity. These results indicate that various metabolites and inhibitors can alter cyclic GMP accumulation in hepatocytes and renal cortex slices. Several mechanisms may be involved in these effects.

1-Methyl-3-isobutylxanthine↗
PubMed1980

Handy type haemofiltration-plasma exchange apparatus.

A simple, compact and light weight design for a machine to perform plasma exchange or haemofiltration at a desired place is required. Based on these considerations, we have designed and fabricated a portable machine having a unique volume balancing mechanism and evaluated the in vitro and in vivo fluid balancing performances. We have obtained fully acceptable results during the evaluations and have performed clinical tests with favourable results.

Blood↗