Biomedical subjects

T Miyamae

Publications and source records attributed to T Miyamae.

At least 73 records · Page 4Linked to original sources

PubMed1994

Species and age-dependent differences of functional coupling between opioid delta-receptor and G-proteins and possible involvement of protein kinase C in striatal membranes.

[D-Ser2,Leu5]-enkephalin-Thr6 (DSLET) and [D-Pen2,5]-enkephalin (DPDPE), both delta-agonists, stimulated the high affinity GTPase in the rat striatal membranes in a naltrindole-reversible manner. Similar stimulation was also observed in the striatal membrane preparations of 16-week-old guinea pigs, while not in those preparations of 4-week-old ones. When calphostin C, a protein kinase C inhibitor, was added to the reaction mixture, DSLET showed a marked stimulation in this activity in 4-week guinea pig striatal membranes. There was no effect of KT5720, a cyclic AMP-dependent protein kinase inhibitor, on such delta-opioid-mediated responses. These findings suggest that protein kinase C is locally involved in the functional uncoupling of delta-receptors to G-proteins in the striatum of young guinea pigs.

Aging↗

PubMed1994

Non-effective dose of exogenously applied L-dopa itself stereoselectively potentiates postsynaptic D2 receptor-mediated locomotor activities of conscious rats.

We attempted to clarify whether or not under inhibition of central dopa decarboxylase non-effective i.p. doses of L-dopa potentiate D2 receptor-mediated locomotor activities without conversion to dopamine in normal and i.v.t. 6-hydroxydopamine-treated rats. In normal rats, only the highest dose of quinpirole, a selective D2 agonist, at ranges used (0.01-1 mg/kg, s.c.) slightly increased the total counts of locomotor activities for 140 min after injection. A simultaneously injected non-effective dose of L-DOPA (30 mg/kg) potentiated locomotor activities by quinpirole (0.1 and 1 mg/kg). L-dopa potentiated quinpirole (1 mg/kg)-induced locomotor activities 90 to 140 min after the injection with marked increase in basal release of L-DOPA without increase in dopamine release simultaneously monitored during striatal microdialysis, compared to quinpirole alone. D-dopa (30 mg/kg) produced no potentiation. In 6-hydroxydopamine-treated rats, a non-effective dose of L-dopa (10 mg/kg) also potentiated quinpirole (0.3 mg/kg)-induced locomotor activities. L-dopa acting on a recognition site for itself stereoselectively potentiates postsynaptic D2 receptor-mediated locomotor activities of rats.

Animals↗

PubMed1994

Hot spots on liver scans associated with superior or inferior vena caval obstruction.

Although hot spots on hepatic scintigrams have been reported in association with superior and inferior vena caval obstruction, these studies were not clinically correlated, and are hampered by the poor resolution of earlier scintillation cameras. In this report, a modern scintillation camera was used to study the formation of hot spots associated with superior and inferior vena caval obstruction. Moreover, radionuclide cavography was performed in 70 patients with superior vena caval (SVC) obstruction and in 95 patients with inferior vena caval (IVC) obstruction. As a result, 13 cases of hot spots in the liver were observed. In cases of SVC obstruction, hot spots were seen in the quadrate lobe, the medial segment, and the bare area of the liver. In IVC obstruction, a hot spot was seen in the quadrate lobe in all cases. In rare instances, in cases of both SVC and IVC obstruction, a hot spot was seen in the wide area. For these hot spots to develop, it appears necessary to have systemic-portal venous blood flow through the internal thoracic vein and the paraumbilical vein.

Adult↗

PubMed1994

Inducement of respiratory mucosal immunogenicity for nasal vaccine due to amine- and amide-inactivation of parainfluenza virus type 1, Sendai.

The protective effects in mice by nasal vaccination of amine- and amide-inactivated Sendai viruses were investigated by a contact exposure experiment, immunofluorescent examination of the entire respiratory tract, and checking the serum HI antibody development. Of 10 monoamines, ethanolamine and 2-methoxyethylamine vaccines induced complete protection, and methylamine, ethylamine, n-propylamine, n-butylamine, 2-ethoxyethylamine, diethylamine and triethylamine vaccines brought about almost complete protection or lower respiratory infection. The methoxyamine-treated mouse conferred the least protection. Of 5 diamines, 1,3-diaminopropane vaccine inhibited completely the infection, but hydrazine, ethylenediamine, putrescine, and cadaverine vaccines produced regional infection. Two polyamines, spermine and spermidine, did not inactivate the virus. Of 4 amides, only semicarbazide vaccine conferred complete mucosal defense, while acetamide, propionamide, and isonicotinic acid hydrazide vaccines lead to regional infection. Serum HI titers developed by vaccination were low on the whole, following their slight rise, fall or maintenance postexposure. In effect, the 4 vaccines inactivated by a best-suited interstrand cross-link between phosphate groups in helix of viral RNA brought about the strongest protection, and showed the necessity of a definite length of molecules for inactivants.

Administration, Intranasal↗

PubMed1994

[The effect of stellate ganglion block on the local and global cardiac uptake of 123I-metaiodobenzylguanidine].

To investigate the effect of stellate ganglion block (SGB) on the cardiac uptake of 123I-metaiodobenzylguanidine (MIBG), four patients without heart disease underwent SGB. Studies were done twice: once with SGB and once without SGB. Anterior planar images and myocardial SPECT images were taken at 10 minutes and 60 minutes after MIBG injection both with and without SGB. Cardiac uptake of MIBG on planar images estimated by heart/liver ratio was significantly higher with SGB at both imaging times (p < 0.01, p < 0.05) than without SGB. SGB had no effect on the local uptake of MIBG on SPECT images. In conclusion, SGB did not change the local cardiac uptake of MIBG, but it appeared to increase the global myocardial uptake of MIBG.

3-Iodobenzylguanidine↗

PubMed1993

Evidence for L-dopa relevant to modulation of sympathetic activity in the rostral ventrolateral medulla of rats.

By microdialysis in the rostral ventrolateral medulla (RVLM) of anesthetized rats, the spontaneous L-3,4-dihydroxyphenylalanine (DOPA) release was partially Ca(2+)-dependent and tetrodotoxin-sensitive and was markedly reduced by alpha-methyl-p-tyrosine (alpha-MPT; 200 mg/kg, i.p.). K+ (50 mM) Ca(2+)-dependently evoked L-DOPA. By microinjections into unilateral RVLM, L-DOPA (30-300 ng) produced dose-dependent hypertension and tachycardia similarly in rats untreated, treated with i.p. 3-hydroxybenzylhydrazine, a central DOPA decarboxylase inhibitor, or with i.v.t. 6-hydroxydopamine. These responses were antagonized by L-DOPA methyl ester (1.5 micrograms), a competitive L-DOPA antagonist. D-DOPA, dopamine, noradrenaline or adrenaline (300 ng) produced no effect. Furthermore, L-DOPA methyl ester alone microinjected into bilateral RVLM (2 micrograms x 2) produced prolonged hypotension and bradycardia, which were abolished by alpha-MPT. These data suggest that L-DOPA is relevant to modulation of sympathetic activity in the rat RVLM.

Animals↗

PubMed1993

Delta opioid receptor mediates phospholipase C activation via Gi in Xenopus oocytes.

Cloned mouse delta-subtype opioid receptor (DOR1) was expressed in Xenopus oocytes to study the signal transduction. Opioid delta-agonists evoked a calcium-dependent chloride current in oocytes injected with mRNA derived from DOR1, together with that from the alpha subunit of Gi1. The delta-agonist-induced current was blocked by naltrindol, a delta-specific antagonist. The delta-agonist evoked no or very weak currents in oocytes with the alpha subunit of Gq or G(o). These findings indicate the functional coupling between the opioid delta-receptor and phospholipase C through an activation of Gi.

Analgesics↗

PubMed1993

L-dopa induces Ca(2+)-dependent and tetrodotoxin-sensitive release of endogenous glutamate from rat striatal slices.

L-DOPA (10-1000 microM) concentration-dependently released glutamate (Glu) from superfused rat striatal slices. D-DOPA and dopamine (300 microM) produced no effects. The L-DOPA-induced release of Glu was not affected by 3-hydroxybenzylhydrazine (20 microM), an L-aromatic amino acid decarboxylase inhibitor. L-DOPA methyl ester (200 microM), a selective L-DOPA antagonist, antagonized the effect of L-DOPA in a competitive manner. Ca2+ deprivation and tetrodotoxin decreased L-DOPA (300 microM)-induced release of Glu. These findings indicate that L-DOPA induces a transmitter-like release of Glu via activation of a recognition site for itself.

Animals↗

PubMed1993

Functional differences of dyes in inducing respiratory immunogenicity by azo-, thiazole-, quinoline-, reactive-, and naphthol-dye-inactivated Sendai viruses.

The prophylactic effects by mouse nasal inoculation of 31 kinds of organic dye-inactivated Sendai viruses were investigated by contact exposure experiment that used mouse nasally infected with 10(5.8) EID50, immunofluorescent examination of the entire respiratory tract, and check of rise of serum HI titer postexposure. The relative merits of the dye-structures for inciting nasal immunogenicity were determined. Of 14 azo-dye-inactivated vaccines, only azo blue- and amido black 10B treated ones brought about nearly complete protection, while the other 5 dye-groups provided partial protection and the remaining 7 dye-groups the least protection. Of 6 thiazole dye-vaccines, primuline-, thioflavine S-, and thioflavine T-vaccines induced complete or almost complete protection, and the others moderate or the least protection. With 3 quinoline-vaccines, both pinacyanol- and quinaldine red-inactivated ones provided complete protection, but not with quinoline blue-vaccine. Of 4 reactive dye-vaccines, both cibacron brilliant yellow 3G-P- and reactive blue 4-treated ones brought about nearly complete protection, but the remaining 2 vaccines induced regional infection. Nevertheless, all 4 naphthol group (AS, AS-BS, AS-BI, and AS-MX)-treated vaccines yielded complete or almost complete protection. The thirteen most effective vaccine groups suppressed marked rise of high or low serum HI titers developed through nasal vaccination postexposure. In short, specified dyestuffs having a great affinity for cellulosic fibers, evidently incited mucosal immunogenicity, probably by major union of the dyes to viral core ribose.

Animals↗

PubMed1993

Endogenously released DOPA is probably relevant to nicotine-induced increases in locomotor activities of rats.

The relevance of endogenously released DOPA to the (+/-)-nicotine-induced increase in locomotor activities was explored in rats. This increase was dose (0.1-1.0 mg/kg, s.c.)-dependent, stereo-selective and mecamylamine (1.0 mg/kg, s.c.)-sensitive, but was not antagonized by L-dopa methyl ester (200 micrograms, i.v.t.), a competitive L-dopa antagonist. Then, by microdialysis, low doses of alpha-methyl-p-tyrosine (alpha-MPT, i.p.) at 1-10 mg/kg, were tested to find a dose that selectively inhibits the basal DOPA release in the striata: the release was consistently inhibited by 3 mg/kg without any tendency to inhibit the basal dopamine release. Pretreatment with this dose did inhibit the nicotine-induced increases in locomotor activities. This suggests that endogeneously released DOPA is in part relevant to the nicotine-induced behavior in rats.

Animals↗

PubMed1993

L-dopa potentiates presynaptic inhibitory alpha 2-adrenoceptor- but not facilitatory angiotensin II receptor-mediated modulation of noradrenaline release from rat hypothalamic slices.

L-dopa is a potentiator for presynaptic beta-adrenoceptors. We studied whether L-dopa potentiates the activities of other presynaptic receptors to modulate the evoked noradrenaline (NA) release in rat hypothalamic slices. UK14304 (0.1-1 microM), a selective alpha 2-agonist, concentration-dependently inhibited NA release. Noneffective 10 pM L-dopa potentiated the UK14304-induced inhibition. This potentiation was selectively antagonized by 1 nM L-dopa methyl ester, a competitive L-dopa antagonist, while yohimbine antagonized both the inhibition by UK14304 alone and its potentiation by L-dopa. However, 10 pM L-dopa produced no effect on angiotensin II (0.1-1 nM)-induced facilitation. L-dopa potentiates activities of presynaptic beta- and alpha 2-adrenoceptors but not those of angiotensin II receptors on rat hypothalamic NA neurons.

Adrenergic alpha-Agonists↗

PubMed1993

Review on the relationship between nicotinic acetylcholine receptors and dopaminergic neurotransmission in the central nervous system--dopa is an endogenous neuroactive substance.

L-3,4-Dihydroxyphenylalanine (DOPA) is believed to be an inert precursor for dopamine (DA). Contrary, transmitter-like endogenous DOPA is released from in vitro and in vivo striata: DOPA is released by neuronal activities under physiological conditions from striata of conscious rats. Furthermore, exogenous nanomolar DOPA itself produces an in vitro presynaptic response to facilitate the catecholamine release. An in vivo postsynaptic depressor response is elicited by DOPA microinjected into the nucleus tractus solitarii. These responses are antagonized by L-DOPA methyl ester, a competitive DOPA antagonist. In striata, DOPA is an endogenous potentiator for presynaptic beta-adrenoceptors to facilitate the DA release and also probably for postsynaptic D2-receptors to increase locomotor activities. Nicotine releases DA and transmitter-like DOPA in vitro and in vivo striata. Nicotine (0.1-1.0 mg/kg, sc) dose-dependently increases locomotor activities. This increase is stereoselective and mecamylamine (1.0 mg/kg, sc)-sensitive but not antagonized by L-DOPA methyl ester (200 micrograms, ivt). Then, a selective low ip dose of alpha-methyl-p-tyrosine (alpha-MPT) to inhibit the basal release of DOPA without decreasing the basal release of DA was explored in vivo striata: it was 3 mg/kg. Pretreatment with this dose did inhibit the nicotine-induced increases in locomotor activities. This result suggests that endogenously released DOPA is in part relevant to nicotine-induced behavior in rats.

Animals↗

PubMed1992

Transmitter-like 3,4-dihydroxyphenylalanine is tonically released by nicotine in striata of conscious rats.

Microdialysis and high performance liquid chromatography with an electrochemical detector were applied to compare the characteristics of nicotine-evoked release of endogenous 3,4-dihydroxyphenylalanine (DOPA) from striata of conscious rats and those of the release of dopamine (DA). Dialysates were collected every 20 min 3-8 h after the start of perfusion. Nicotine was perfused for 20 min through a probe. (+/-)-Nicotine (100-300 microM) constantly and repeatedly released DOPA and DA over a similar time course in a dose-dependent manner. The ratio of the DOPA and DA release evoked was approximately 1:3. The (+/-)-nicotine (200 microM)-induced DOPA release was mecamylamine (500 microM)-sensitive, tetrodotoxin (100 nM)-sensitive and Ca2+ (removal plus 12.5 mM Mg2+ addition)-dependent. The (+)-isomer produced no DOPA release. These characteristics of DOPA release were almost the same as those of DA release. Furthermore, mecamylamine alone inhibited the basal release of DOPA but not of DA. Nicotine released stereoselectively endogenous DOPA via nicotinic acetylcholine receptors from striata of freely moving rats in a manner similar to transmitter DA. These acetylcholine receptors function tonically for the release of DOPA. These findings are further support for our proposal that DOPA is an endogenous neuroactive substance.

Animals↗

PubMed1992

Effects of phenylalaninol on centrally induced gastric acid secretion.

The effects of phenylalaninol (D-isomer) on gastric acid secretion and gastric ulcer were studied in rats. The compound reduced the gastric acid secretion stimulated by intracisternal thyrotropin releasing hormone and intravenous 2-deoxy-D-glucose, but not that stimulated by subcutaneous carbachol or histamine. Phenylalaninol prevented stress- and indomethacin-induced gastric ulcers. We conclude that phenylalaninol inhibits ulcer formation mainly by central inhibition of gastric acid secretion.

Animals↗

PubMed1992

[Right ventricular volume determination by continuous 81mKr infusion and 99mTc blood pool imaging].

Our newly developed radionuclide method for the calculation of right ventricular (RV) volume was examined in this study. Using a semi-geometric count-based method, volume can be measured by the following equation: Cv = Cm/(L/d). V = (Ct/Cv) x d3 = (Ct/Cm) x L x d2. (V = volume, Cv = voxel count, Cm = the maximum count of a container, Ct = the total count of the container, L = maximum length of the image of the container obtained from a direction perpendicular to the direction where the count data were collected, and d = pixel size.) A phantom study was performed by setting a cylindrical container in a system which circulated 5 liters of water per minute. 81mKr solution was infused continuously into the container, and images of the container were collected for one minute. Cm and Ct were obtained and, because the container was cylindrical, the maximum width of the image of the container was measured as L. The volume of the container was calculated using the above equation. The container's true volume and the volume measured by this method showed a good correlation with r = 0.997 (n = 13, p < 0.001). This theorem was applied to RV images obtained in the 30 degree right anterior oblique position by continuous infusion of the 81mKr solution. Multiple gated acquisition was performed and RV end-diastolic maximum counts and total counts were obtained. The RV maximum width was measured as L on the end-diastolic cardiac pool image with 99mTc-D-HSA collected in the 40 degree left anterior oblique position.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1992

[Left ventricular volume determination by first-pass radionuclide angiocardiography using a semi-geometric count-based method].

A new radionuclide technique for the calculation of left ventricular (LV) volume by the first-pass (FP) method was developed and examined. Using a semi-geometric count-based method, the LV volume can be measured by the following equation: CV = CM/(L/d). V = (CT/CV) x d3 = (CT/CM) x L x d2. (V = LV volume, CV = voxel count, CM = the maximum LV count, CT = the total LV count, L = LV depth where the maximum count was obtained, and d = pixel size.) This theorem was applied to FP LV images obtained in the 30-degree right anterior oblique position. Frame-mode acquisition was performed and the LV end-diastolic maximum count and total count were obtained. The maximum LV depth was obtained as the maximum width of the LV on the FP end-diastolic image, using the assumption that the LV cross-section is circular. These values were substituted in the above equation and the LV end-diastolic volume (FP-EDV) was calculated. A routine equilibrium (EQ) study was done, and the end-diastolic maximum count and total count were obtained. The LV maximum depth was measured on the FP end-diastolic frame, as the maximum length of the LV image. Using these values, the EQ-EDV was calculated and the FP-EDV was compared to the EQ-EDV. The correlation coefficient for these two values was r = 0.96 (n = 23, p less than 0.001), and the standard error of the estimated volume was 10 ml.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Volume↗

PubMed1991

Collateral pathways observed by radionuclide superior cavography in 70 patients with superior vena caval obstruction.

Schematic representations of collateral pathways that have developed in association with superior vena caval obstruction have been established in studies using radionuclide superior cavography (RNSC). However, these were hampered by the poor resolution of earlier scintillation cameras. Using a modern scintillation camera, we performed RNSC in 70 patients with obstruction of the superior vena caval system, and examined the differences in collateral pathways in the presence or absence of obstruction of the azygos vein. RNSC visualized the site of obstruction and collateral pathways far more readily than in prior studies. When the orifice of the azygos vein was not obstructed, collateral flow drained into the azygos system. When it was obstructed, however, the collaterals drained into the inferior vena caval system. An important collateral pathway comprising the contralateral brachiocephalic vein and the jugular venous arch was also found, which has not previously been reported. Our diagrams of collateral circulation may provide a means of determining the site of obstruction in the superior vena caval system by RNSC.

Adult↗

PubMed1991

[Thallium-201 myocardial scintigraphy after intravenous infusion of adenosine triphosphate disodium: a preliminary study in the diagnosis of coronary artery disease].

The feasibility and safety of thallium-201 myocardial scintigraphy after the intravenous infusion of adenosine triphosphate disodium (ATP) (Adetphos, Kowa) were studied in eight patients with angina pectoris and/or old myocardial infarction. Coronary arteriography (CAG) was performed by the conventional method in all patients. ATP was infused for 5 min and thallium was injected at 3 min after the start of ATP infusion. ATP was given at 0.12 mg/min/kg in two patients (group A), 0.16 mg/min/kg in three patients (group B), 0.20 mg/min/kg in one patient (group C) and 0.28 mg/min/kg in two patients (group D). SPECT images were obtained at 10 min and 180 min after thallium injection. No significant hemodynamic changes were observed in group A and B. Severe hypotension was observed in group C and one member of group D. Chest pain was experienced by one patient in group A, two in group B, one in group C, and both of the two in group D. ST depression on the electrocardiogram (ECG) was documented in one patient each of groups B and C. In one group D patient, the study was discontinued because of complete atrioventricular block persistent for 5 beats. The correlation between thallium imaging and CAG was unclear in group A, reasonable in groups B and C, and obscure in group D because of side effects. None of the patients who developed side effects of ATP were administered sublingual nitroglycerin or intravenous aminophylline. Their symptoms or ECG changes improved spontaneously within 2 min and disappeared within 5 min after termination of infusion. In conclusion, the optimal ATP regimen for this purpose was considered to be a 5 min infusion at 0.16 mg/kg/min and this method was found to be feasible and safe.

Adenosine Triphosphate↗