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M Arita

Publications and source records attributed to M Arita.

At least 199 records · Page 11Linked to original sources
PubMed1993

Heterogeneity of motilin-immunoreactive cells in the duodenum and pyloric region of several avian species.

Immunohistochemical characterizations of motilin-immunoreactive cells were examined in gastric and duodenal mucosae of nine species of birds from seven orders using five different region-specific motilin antisera. Motilin-immunoreactive cells appeared as open-type cells in the mucosal epithelium and showed varying immunoreactivities to antisera used in all the birds examined except for the cormorant and penguin, which did not show any kinds of immunoreactivity to motilin. Motilin-immunoreactive cells of the emu duodenum were detected by all the motilin-antisera used. The present results suggest that there is a wide range of heterogeneity between motilin molecules among avian species, or perhaps alternatively the existence of a family of motilin-like peptide. Furthermore, the present results should prove useful for a molecular biological study on the evolution of avian motilin.

Animals↗
PubMed1993

Intracellular Na+ activity of "diseased" human atrial muscles and its modifications by dihydro-ouabain.

In quiescent human atrial muscles obtained from patients with various cardiac diseases, the intracellular Na+ activity (aNai) and the resting membrane potential (Vm) were recorded simultaneously, using double-barreled Na(+)-selective microelectrodes. The Vm averaged -44.1 +/- 5.0 mV and the aNai, 6.9 +/- 1.7 mM under normal Tyrode's solution containing 5.4 mM [K]oi,The aiNa value was within the range of aNai reported in various cardiac tissues from intact animals. Dihydro-ouabain (10(-5) M) significantly increased the aNai and depolarized the Vm. The results suggest that even in these depolarized atrial muscles the aNai remains within physiologic levels and that the Na-K pump may not be impaired. This is the first report to measure the aNai in human atrial muscles.

Adolescent↗
PubMed1993

[Electrophysiological changes in the failing myocardium].

Contraction-excitation feedback is defined as a change in the mechanical state that precedes or alters the transmembrane electrical potential. The latter could be an important electrophysiologic disorder in patients with cardiac failure since the electrophysiological changes may be induced by alterations in ventricular size, pressure or factors common to all types of congestive heart failure, regardless of aetiology. A stretch of the ventricular myocardium caused (1) a shortening of the action potential duration (APD), (2) a decrease in the resting potential (RP) and (3) the early or delayed after-depolarization that culminated in the triggered activity. Failing myocardium without ventricular hypertrophy also showed (1) a reduction in the RP and the action potential upstroke velocity and (2) APD shortening. In contrast, the majority of investigators have found a significant lengthening of the APD in the hypertrophied myocardium. These electrophysiologic changes shown in the failing myocardium with or without hypertrophy and in the mechanically stretched myocardium may be a possible substrate for the genesis of the reentrant circuit and the early or delayed afterdepolarizations, leading to ventricular arrhythmia.

Action Potentials↗
PubMed1993

Time course of plasma histamine and tryptase following food challenges in children with suspected food allergy.

This study was undertaken to investigate the kinetics of histamine and tryptase in the circulation of patients with food allergy and to determine whether the measurements of plasma histamine and tryptase concentrations after food challenges provided additional predictive markers for the diagnosis and evaluation of food allergy. Twenty-one open food challenges were performed on 13 patients with suspected food allergy. Plasma histamine and tryptase concentrations were measured during 4 hours after challenge. In the group of patients with immediate reactions after challenges, the mean plasma histamine concentration rose significantly at 120 and 240 minutes after the challenge, and the mean plasma tryptase concentration was increased significantly at 240 minutes after challenge. Plasma histamine and tryptase concentrations were measured during 24 hours after 8 open food challenges in 7 other patients with suspected food allergy. In each patient with a nonimmediate reaction, plasma histamine concentrations were increased at the onset of symptoms after challenge, but no plasma tryptase concentrations increased. The elevation of plasma histamine and tryptase in patients with immediate reactions following food challenge indicates mast cell activation. On the other hand, the elevation of plasma histamine without elevated plasma tryptase in the patients with nonimmediate reactions following food challenge may indicate basophil activation rather than mast cell activation. Plasma histamine and tryptase measurements after food challenge may be useful in the detection and evaluation of food allergy.

Adolescent↗
PubMed1993

[Cellular electrophysiological basis of proarrhythmic and antiarrhythmic effects of ischemia-related lipid metabolites].

Lysophosphatidylcholine, an amphiphilic lipid metabolite, accumulates in the ischemic myocardium and plays a pivotal role in the production of arrhythmias. To clarify its cellular ionic mechanism(s), we investigated the effect of 1-palmitoyl-lysophosphatidylcholine (LPC) on the guinea pig ventricular myocytes, using whole cell- and patch-voltage clamp methods. In whole cell recordings, extracellular application of LPC (20-100 microM) depolarized the resting potential within several minutes and produced automatic action potential discharges from the resting and plateau potentials. Such effects were attributed mostly to the decrease in inward going rectifier K current (Ik1). Single channel recordings in the cell attached mode revealed that this decrease in Ik1 is secondary to the reduction of the single channel conductance and not due to decreased open probability. LPC (5-50 microM) also decreased the excitatory Na+ current (INa) in an all-or-nothing manner, depending upon the concentration used. Such decreases in the resting potential and peak INa could be responsible for the marked retardation of conduction velocity and therefore production of reentry. Another amphiphilic lipid metabolite, a long-chain acylcarnitine or 1-palmitoylcarnitine (PALC), had LPC-like depressant effects on INa, albeit the effect was reversible in the majority of cells tested. On the other hand, a short-chain acylcarnitine, 1-propionylcarnitine (PROC) did not affect the INa by itself even at a high concentration (50-500 microM), whereas it prevented the LPC's depressant effect on INa. Like PROC, the middle-chain acylcarnitine, e.g., 1-hexanoylcarnitine (HEXC) did not decrease the INa, but prevented the LPC's deleterious effects on INa, albeit the latter effect was much weaker than that of PROC.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Crystallization and preliminary X-ray crystallographic analysis of Mirabilis antiviral protein.

Mirabilis antiviral protein is a single-chain ribosome-inactivating protein purified from the tuberous root of Mirabilis jalapa L. We obtained several forms of crystals of the protein by the hanging drop vapor diffusion method, but most of these crystals were not suitable for X-ray crystallography. After refining the growth conditions, crystals of crystallographic quality were grown in 20-microliters droplets of an equi-volume mixture of 1.5% (w/v) protein solution and a reservoir solution containing 49 to 50% (w/v) ammonium sulfate and 50 mM-ammonium citrate (pH 5.4) at room temperature. Addition of 2 mM-adenine sulfate reduced twinning and "crystal shower". The resulting trigonal crystals diffract beyond 2.5 A resolution using a rotating anode X-ray generator. The space group was determined to be P3(1)21 or P3(2)21 (a = b = 103.9.A, c = 134.6 A, alpha = beta = 90 degrees, gamma = 120 degrees) based on their precession photography of h0l and hk0 zones. There seems to be three monomers in an asymmetric unit for VM = 2.51 A3/Da.

Antiviral Agents↗
PubMed1992

Inhibitory effects of palmitoylcarnitine and lysophosphatidylcholine on the sodium current of cardiac ventricular cells.

We investigated the effects of ischemia-related amphipathic compounds, palmitoylcarnitine (PamCar, 0.5-50 microM) and lysophosphatidylcholine (lysoPtdCho, 5-50 microM) on sodium current (INa) of guinea-pig ventricular myocytes. The cells were perfused with low-Na+ (60 mM) Tyrode's solution, and Ca2+ and K+ currents were blocked by external Co2+ (3 mM) and internal Cs+ (140 mM), respectively. INa was elicited by depolarizing voltage steps from a holding potential of -100 mV at a temperature of 33 degrees C. PamCar (5 microM) decreased the peak INa (attained at -20 mV or -30 mV) from 6.1 +/- 2.1 nA to 3.9 +/- 1.4 nA (n = 11), or by 36.1% within 2 min, and shifted the curve of steady-state INa inactivation by 5.4 mV in the positive direction (from -76.3 +/- 4.6 mV, control to -70.9 +/- 4.0 mV, in PamCar, n = 4). Partial restoration of the amplitude and the shift of the steady-state inactivation curve of INa was attained after washout of PamCar. In contrast, lysoPtdCho at concentrations over 10 microM irreversibly depressed the INa within 0.5-3 min and the reduction of INa was followed by cell contracture or cell death (n = 9). The survival time, defined as a period from the start of lysoPtdCho application to the time of the last successful recording of the INa (before evolution of sudden changes in the holding current), depended on the concentrations of lysoPtdCho. Both PamCar and lysoPtdCho retarded the time course of activation and inactivation of INa.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

A comparative study of once-a-day morning and once-a-day bedtime administration of 40 mg famotidine in treating duodenal ulcers.

A randomized controlled study comparing once-a-day morning and once-a-day bedtime administration of 40 mg famotidine in treating duodenal ulcers was carried out in 99 Japanese patients. Endoscopic examinations were performed at the baseline and repeated at 3-week intervals until healing was confirmed. Eighty-two patients fulfilled the evaluation criteria (38 in the morning group and 44 in the bedtime group). In 13 of these patients the antisecretory effects of these regimens were also assessed by 24 h intragastric pH monitoring. The healing rates were 66% after 3 weeks and 95% after 6 weeks in the morning group, and 57% after 3 weeks and 80% after 6 weeks in the bedtime group. The differences were insignificant between the two groups, but there was a higher healing rate tendency after 6 weeks in the morning group (0.05 less than P less than 0.10). Regarding pain subsidence, there were no significant differences between the two groups. Both treatments were significantly superior to the control group in increasing 24 h intragastric pH. The morning regimen was significantly superior to the bedtime regimen in suppression of daytime acidity. On the contrary, the bedtime regimen was significantly superior to the morning regimen in suppression of nocturnal acidity. These findings suggest that suppression of nocturnal acidity is important but not essential to promote duodenal ulcer healing and suppression of daytime acidity is equally important. Thus, once-a-day morning administration of 40 mg famotidine seems to be at least as effective as once-a-day bedtime administration of 40 mg famotidine in treating duodenal ulcers.

Adult↗
PubMed1992

Acute toxicity of ozone against morphology of gill and erythrocytes of Japanese charr (Salvelinus leucomaenis).

1. Acute toxicity of ozone exposure to Japanese charr (Salvelinus leucomaenis) was studied histopathologically, and hematologically on gill tissue and red blood cells (RBC) under different ozone concentrations (0-0.7 ppm). 2. Exposure of ozone above 0.7 ppm led to characteristic symptoms and all died of choking in 30 min. 3. Many swollen RBC were seen under the scanning electron microscope. 4. RBC congestion was serious in the gill where degeneration of lamellar epithelium was observed. However, injury to chloride cells was not clear.

Animals↗
PubMed1992

Blockade of 2,4-dinitrophenol induced ATP sensitive potassium current in guinea pig ventricular myocytes by class I antiarrhythmic drugs.

OBJECTIVE: The aim was to assess the effects of various antiarrhythmic drugs on 2,4-dinitrophenol (DNP) induced outward current (IDNP), presumably the ATP sensitive K+ current (IK,ATP) of isolated cardiac cells and to discuss mechanisms involved in the hypoglycaemia which occurs in patients on these drugs. METHODS: The quasi-steady state current-voltage relationship from the isolated guinea pig ventricular cells was measured using whole cell voltage clamp techniques with a ramp pulse programme. The effects of seven different antiarrhythmic drugs on IDNP were examined. Action potentials were elicited at a rate of 0.2 Hz by an intracellular current injection. RESULTS: DNP (50 mumol.litre-1) increased the quasi-steady state outward current at potentials positive to about -60 mV. This current (IDNP) was completely inhibited by the subsequent application of glibenclamide (1 mumol.litre-1), thereby suggesting that the IDNP is probably IK,ATP. Cibenzoline (10 mumol.litre-1, class Ia), disopyramide (30 mumol.litre-1, class Ia), and procainamide (100 mumol.litre-1, class Ia) significantly inhibited the IDNP by 95.5(SD 11.3)%, 77.8(21.2)%, and 76.4(23.9)% respectively. Flecainide (class 1c) inhibited the IDNP by 66.9(23.9)% at 10 mumol.litre-1 but not at 2 mumol.litre-1. Mexiletine (30 mumol.litre-1, class Ib), pilsicainide (50 mumol.litre-1, class Ic), and E4031 (10 mumol.litre-1, class III) at concentrations as high as approximately fivefold the clinically effective blood levels, did not suppress IDNP. Except for 10 mumol.litre-1 flecainide, all the concentrations listed above which blocked IDNP were within twofold of the clinical blood concentrations documented to be effective for suppression of arrhythmias. Cibenzoline, disopyramide, and procainamide, but not flecainide, belong to class Ia antiarrhythmic drugs. All these class Ia antiarrhythmic drugs "shortened" the action potential duration of guinea pig ventricular cells, an opposite change to that noted for multicellular preparations, eg, guinea pig papillary muscles. CONCLUSIONS: Class Ia antiarrhythmic drugs (cibenzoline, disopyramide, and procainamide) inhibit IDNP (presumably IK,ATP) in guinea pig ventricular cells within a range of therapeutic concentrations. This inhibitory effect of IK,ATP can probably explain the hypoglycaemia which occurs in some patients receiving these drugs, and the prolongation of the action potential duration alleged to occur in "superfused" papillary muscles.

2,4-Dinitrophenol↗
PubMed1992

Changes in cardiovascular mass, left ventricular pumping ability and aortic distensibility after calcium antagonists in Wistar-Kyoto and spontaneously hypertensive rats.

OBJECTIVES: To determine the effects of different dihydropyridine calcium antagonists on cardiovascular mass and function in normotensive Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). METHODS: The rats were treated daily for 3 weeks with nitrendipine (20 mg/kg), nifedipine (30 mg/kg), nisoldipine (6 mg/kg) or their vehicles. At the conclusion of that period left ventricular pumping ability and aortic distensibility were determined, and the aortic, cardiac and left and right ventricular masses. RESULTS: Each drug reduced arterial pressure in both rat strains; each decreased left ventricular mass in SHR but not in WKY rats. All three agents increased right ventricular mass in WKY rats; only nisoldipine did so in SHR. Each compound improved left ventricular pumping ability in WKY rats, maintaining function even when pressure was abruptly increased to pretreatment levels. In contrast, although all three calcium antagonists improved cardiac performance in SHR at the pharmacologically reduced pressures, pumping ability was not maintained when pressure was increased to pretreatment levels in nisoldipine-treated SHR. All three agents improved aortic distensibility in both strains, but only in SHR was reduced aortic mass demonstrated. CONCLUSIONS: These data not only continue to demonstrate a functional/structural dissociation associated with antihypertensive therapy, but also suggest subtle functional and structural effects that differ even within the same class of calcium antagonists.

Animals↗
PubMed1992

Effects of vagal stimulation on cesium-induced early afterdepolarizations and ventricular arrhythmias in rabbits.

BACKGROUND: Previous evidence has shown that increased sympathetic tone enhances the cesium chloride (Cs)-induced early afterdepolarizations (EADs) and ventricular tachycardias (VTs). METHODS AND RESULTS: We assessed the effects of vagal stimulation on Cs-induced EADs and ventricular arrhythmias in the rabbit heart. Monophasic action potentials (MAPs) of the left ventricular endocardium were recorded simultaneously with surface ECG. Two protocols were used: 1) While in their intrinsic sinus rhythm, 11 rabbits were given three intravenous Cs injections (1 mM/kg) 20 minutes apart, and the effects of vagal stimulation on the ventricular arrhythmias thus induced were examined. 2) Under constant atrial pacing (cycle length, 250 msec), EAD amplitude was measured after Cs injection (1 mM/kg) without (five rabbits, control group) or with (four rabbits, vagal stimulation group) vagal stimulation. We observed the following. 1) Cs produced EADs and VTs of polymorphic (PVT) and monomorphic (MVT) types. During PVT, the take-off potential of repetitive premature action potentials in MAP recordings was about the same as the peak level of EADs, and during MVT, the take-off potential was the level of full repolarization. Vagal stimulation suppressed PVT but not MVT. Vagal stimulation after spontaneous termination of MVT restarted MVT of the same morphology at a rate much slower than the preceding sinus rate. 2) EAD amplitude was significantly smaller in the vagal stimulation group than in the control group. CONCLUSIONS: The results suggest that PVT originated from triggering by EADs, whereas MVT was of different origin, and that vagal stimulation suppressed PVT by decreasing the amplitude of EADs.

Action Potentials↗
PubMed1992

Cooperative modulation of voltage-dependent sodium channels by brevetoxin and classical neurotoxins in cultured bovine adrenal medullary cells.

The effects of Ptychodiscus brevis toxin (PbTx-3) on 22Na influx, 45Ca influx and catecholamine secretion were examined in cultured bovine adrenal medullary cells and compared with the effects of classical neurotoxins. PbTx-3 alone had no effects, but greatly enhanced veratridine (30 microM)-induced Na influx, Ca influx and secretion, with a EC50 of 30, 25 and 23 nM, respectively. PbTx-3 (1 microM) reduced EC50 values of veratridine approximately 3-fold and increased the maximal responses caused by saturating concentration (300 microM) of veratridine approximately 1.3 fold. alpha- and beta-Scorpion venom shifted the concentration-response curves of veratridine to the left without altering maximal responses. PbTx-3 in combination with either alpha- or beta-scorpion venom showed only additive effects on Na influx, but augmented veratridine (30 microM)-induced Na influx to a greater extent than PbTx-3, alpha- or beta-scorpion venom alone. Na influx due to these toxins was abolished by 1 microM saxitoxin. Our results suggest that Na channels in adrenal medullary cells have neurotoxin receptors for brevetoxin that allosterically stimulate Na influx initiated by veratridine, leading to increased Ca influx and catecholamine secretion. Allosteric interactions do not exist between brevetoxin and alpha-scorpion venom, or between brevetoxin and beta-scorpion venom, but once Na channels are gated by veratridine, these toxins cooperatively augment Na influx.

Adrenal Medulla↗
PubMed1992

[A case of hypersensitivity pneumonitis presenting with copious sputum and marked obstructive impairment of lung function].

A 44-year-old male was hospitalized due to dyspnea and persistent cough with copious sputum (about 100 ml/day). Chest radiograph on admission showed hyperinflation and fine nodular shadows throughout both lungs, as well as a tram line appearance in the right lower lung field which suggested thickening of bronchial walls. Pulmonary function tests demonstrated moderate to severe reduction of %VC, FEV1.0 and PaO2. Fiberoptic bronchoscopy revealed inflammatory change in the walls of proximal bronchi. Although his dyspnea resolved rapidly, productive cough and impaired lung function were persistent and improved very slowly over the one-month-period following admission. After resolution, similar symptoms were provoked again 5 to 6 hours after returning to his home, suggesting the recurrence of hypersensitivity pneumonitis. Open lung biopsy was performed for the differential diagnosis of hypersensitivity, diffuse panbronchiolitis, and bronchial asthma, because neither transbronchial lung biopsy nor broncho-alveolar lavage was diagnostic. Histopathology of the open lung biopsy specimens revealed marked desquamation of bronchiolar epithelium in addition to bronchiolo-alveolitis with epithelial granulomas, consistent with hypersensitivity pneumonitis. Copious sputum is a very uncommon clinical feature in hypersensitivity pneumonitis. We consider that the large volume of airway fluid was caused by epithelial ulceration of bronchioles and catarrhal bronchitis associated with hypersensitivity pneumonitis.

Adult↗