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Biomedical subjects

S Ameshima

Publications and source records attributed to S Ameshima.

At least 37 records · Page 2Linked to original sources
PubMed1998

The activation of nitric oxide synthase by copper ion is mediated by intracellular Ca2+ mobilization in human pulmonary arterial endothelial cells.

The aim of the study was to elucidate the vasodilatory mechanism due to Cu2+ by assessing nitric oxide (NO) production as determined by NOx (NO, NO2-, and NO3-) that is released from human pulmonary arterial endothelial cell (HPAEC) monolayers using a NO chemiluminescence analyzer, and also to assess Ca2+ movement using 45Ca and fura 2 in HPAEC. Cu2+ (10(-6)-10(-4) M) significantly increased NO production in a dose-dependent manner when extracellular Ca2+ was present. 45Ca influx into the adherent cells was dose-dependently enhanced by Cu(2+) (10(-6)-10(-4) M), but not by Mn(2+), Zn(2+) or Fe(2+). [Ca2+]i, measured by monitoring the fluorescence changes of fura 2, was significantly elevated in the presence of Cu2+. The increase in [Ca2+]i induced by Cu2+ was inhibited by either diethyldithiocarbamate (DDC) or the depletion of extracellular Ca2+. The dihydropyridine receptor agonist, BayK8644, significantly attenuated the Cu2+-induced increase in [Ca2+]i in a dose dependent manner and nitrendipine or nifedipine, the dihydropyridine receptor antagonists, dose-dependently inhibited a Cu2+-induced increase in [Ca2+]i. These results suggest that Cu2+ activates eNOS through the mechanism of [Ca2+]i elevation due to Ca2+ influx into HPAEC and that the Cu2+-induced [Ca2+]i elevation in HPAEC is likely due to activation of the dihydropyridine-like receptors.

6-Ketoprostaglandin F1 alpha↗
PubMed1998

[Lung abscess resulting from esophageal carcinoma successfully treated with intraesophageal covered self-expandable metallic stent].

An 82-year-old man was admitted to our hospital with high fever and back pain. He already suffered from esophageal carcinoma and expandable metallic stent had been inserted because of esophageal stenosis. A chest x-ray film obtained on admission showed infiltrative shadows in the right lower lung filled. The diagnosis of lung abscess was made on the basis of aspirate findings. Despite closed drainage, antibiotic treatment, and fasting therapy, progressive pulmonary infiltrates developed. Esophagography and esophagoscopy revealed that an esophageal fistula due to an advanced esophageal carcinoma had caused the lung abscess. An additional covered self-expandable metallic stent (EMS) was placed on the surface of the esophageal carcinoma, close to the esophageal fistula. This promptly resolved the lung abscess. Our conclusion was that the covered-EMS can be effective for the palliation of esophagorespiratory fistulas.

Aged↗
PubMed1997

The effect of Cu2+ on rat pulmonary arterial rings.

In the current study, Cu2+ was tested for its ability to relax vessels and to accumulate cyclic GMP (cGMP) in rat pulmonary artery employing rat extrapulmonary arterial rings. Cu(2+)-induced relaxation was endothelium and concentration (in the range from 10(-7) to 10(-4) M) dependent. The content of cGMP in the rings was increased 1.7-fold with 10(-4) M Cu2+. NG-Monomethyl-L-arginine abolished both the copper-induced relaxation and the increase in cGMP of rings. Cu2+ and zaprinast, which inhibits phosphodiesterase activity, caused a synergistic increase in cGMP level in the rings, suggesting that Cu2+ enhanced cGMP level through a mechanism different from that of zaprinast, probably as a consequence of elevated accumulation of nitric oxide (NO). The magnitude of vasorelaxation observed due to simultaneous addition of Cu2+ and acetylcholine was additive, not synergistic. Cu2+ did not augment relaxation induced by exogenously added NO donor. These results suggest that Cu2+ elevates NO level in the rings not by prolonging the half-life of NO, but by activation of endothelial nitric oxide synthase and subsequently potentiating the action of NO on vascular tone.

Acetylcholine↗
PubMed1996

Effect of probucol, an oral hypocholesterolaemic agent, on acute tobacco smoke inhalation in rats.

1. We hypothesized that probucol, an oral hypocholesterolaemic agent, can suppress the oxidant stress induced by acute tobacco smoke inhalation in rats. We determined lung tissue glutathione (reduced and oxidized), lipid peroxide, tocopherol and plasma elastase inhibitory capacity, ferroxidase activity and lipid peroxide in rats after inhalation of tobacco smoke. 2. Rats treated with the probucol diet for 3 days or 4 weeks equally showed no suppression of plasma elastase inhibitory capacity and ferroxidase activity compared with control rats after acute tobacco smoke inhalation, although both animals treated with probucol for 3 days or 4 weeks had pharmacologically effective concentrations of probucol to lower plasma cholesterol but plasma cholesterol in rats treated with probucol for 3 days was still in the normal range. 3. Probucol treatment for 4 weeks lessened tobacco smoke-induced suppression of lung tissue glutathione, attenuated tobacco smoke-induced increases in lung tissue lipid peroxide and did not alter lung tissue tocopherol compared with control (lungs). 4. These findings demonstrate that probucol, via its antioxidant ability, confers a protective effect on lung exposed to acute tobacco smoke inhalation.

Animals↗
PubMed1996

Protective effects of BQ-123, an ETA receptor antagonist, against leukotoxin-induced injury in rat lungs.

We tested the hypothesis that BQ-123, a novel endothelin type A (ETA) receptor antagonist, protects the lung against leukotoxin 9,10-epoxy-12-octadecenoate (Lx), which causes acute lung injury in animals. In isolated rat lungs perfused with Earle's balanced salt solution, BQ-123 suppressed the Lx-induced increase in wet lung weight, wet lung weight/dry lung weight, the effluent perfusate lactic dehydrogenase activity, and effluent perfusate and lung tissue ET-1 levels. BQ-123 also significantly attenuated the Lx-induced increase of the pulmonary capillary filtration coefficient. Thus our experimental results indicate that the ETA receptor antagonist, BQ-123, protects against Lx-induced experimental lung vascular injury.

Animals↗
PubMed1996

Pneumonitis during interferon and/or herbal drug therapy in patients with chronic active hepatitis.

We report four cases of acute pneumonitis due either to interferon, or a herbal drug, "Sho-saiko-to", or both in combination, in patients with chronic active hepatitis, focusing on its pathogenesis and response to prednisolone therapy. These cases shared common clinical features: fever, dry cough, dyspnoea, hypoxaemia, diffuse infiltrates both on chest radiography and chest computed tomography, restrictive pulmonary functional impairment, and alveolitis on examination of transbronchial lung biopsy, all of which suggest acute interstitial pneumonia. Furthermore, lymphocytosis was observed in association with the dominant CD8+ T-cell subset in bronchoalveolar lavage fluid. A lymphocyte stimulation test using peripheral blood was positive to interferon in one case and to Sho-saiko-to in another. All patients responded to oral prednisolone therapy. Peripheral soluble interleukin-2 receptor levels decreased in parallel with improvement in the clinical course. All patients were free of symptoms with a follow-up of 1-3 yrs. We conclude that interferon- and/or Sho-saiko-to-induced acute pneumonitis may be due to allergic-immunological mechanisms rather than toxicity, and that peripheral levels of soluble interleukin-2 receptor appear to be good markers of disease activity.

Adult↗
PubMed1996

[Immunodeficiency with thymoma (Good's syndrome) similar to sino-bronchial syndrome].

A 58-year-old man was admitted to our hospital because of recurrent pulmonary infections that began three years previously. Laboratory data showed hypogammaglobulinemia and a chest computed tomogram showed diffuse bilateral micronodular shadows and an anterior mediastinal tumor. Immunodeficiency with thymoma (Good's syndrome) was diagnosed. After undergoing a thymectomy, he received intravenous gamma-globulin injections once a month for prophylaxis. Good's syndrome occurs rarely in Japan. A solid tumor-like shadow is not necessarily observed in routine chest X-ray studies, and hypogammaglobulinemia is one sign of this syndrome. The hypogammaglobulinemia of Good's syndrome should be carefully differentiated from that of other immunodeficiency diseases such as common variable immunodeficiency, the acquired immunodeficiency syndrome, chronic lymphocytic leukemia, non-Hodgkin's lymphoma, and multiple myeloma (non-secretory type).

Agammaglobulinemia↗
PubMed1995

Leukotoxin, 9,10-epoxy-12-octadecenoate inhibits mitochondrial respiration of isolated perfused rat lung.

To investigate how mitochondrial function was affected in leukotoxin (Lx)-,9,10-epoxy-12-octadecenoate-induced lung injury, lung mitochondria were extracted from isolated perfused rat lung with or without Lx-induced edematous injury. In the lung treated with 30 mumol of Lx, the mitochondrial respiration rate in states 3 and 4 significantly decreased (without mitochondrial uncoupling) concomitantly with increased release of lactate dehydrogenase (LDH), a parameter for cellular damage, into the perfusate and decreased ATP content in the lung tissue compared with those of untreated lung. Moreover, 30 mumol of Lx resulted in significant inhibition of cytochrome-c oxidase activity (vs. vehicle control). In contrast, lower doses of Lx (10 mumol) caused lung edema and cellular damage without evidence for mitochondrial dysfunction. We also examined cellular and mitochondrial damage in hydrostatic lung edema. Such edema showed neither suppressed mitochondrial respiration nor elevated LDH activity in perfusate, although lung wet weight increased as much as it did after 30 mumol Lx treatment. Our results suggest that the ex vivo mitochondrial dysfunction is one of the secondary (vs. initial augmented permeability) but specific manifestations of toxicity of Lx, and together with the previous reports, the ex vivo damaging effect of Lx against mitochondria may be ascribed not to its direct action on mitochondria but to Lx-derived cellular mechanism(s).

Adenine Nucleotides↗
PubMed1995

[The clinical study on secretory leukoprotease inhibitor (SLPI) in sera of patients with various pulmonary diseases].

It has been reported that secretory leukoprotease inhibitor (SLPI) can be a useful indicator for acute respiratory tract inflammation. In the present study, we attempted to measure automatically the serum concentration of SLPI by enzyme immunoassay (EIA) in patients with various pulmonary diseases. In this automatic measurement of SLPI, by which the results basically well-correlate with the manual method, we could measure many samples easily. Serum levels of SLPI in patients with various pulmonary diseases were significantly higher than those in healthy controls (50.5 +/- 9.8ng/ml). The serum concentration of SLPI in patients with inflammatory lung diseases correlated with that of C-reactive protein (CRP) or interleukin 6 (IL-6) significantly but not strongly. These results suggest that SLPI may be a useful indicator for local inflammation in respiratory tract. The serum concentration of SLPI in patients with lung cancer (71.1 +/- 10.8ng/ml), in particular adenocarcinoma, was significantly higher than that in healthy controls, but not correlated with other inflammatory markers.

Adult↗
PubMed1995

[Lung injury and pulmonary vascular endothelial cell injury].

Pulmonary vascular endothelial cells are an important barrier that helps keep lung tissue intact. These cells are exposed to potentially injurious cells and to harmful mediators that are produced in or released into the blood. The endothelial cells may then be stimulated and injured. Stimulated and injured pulmonary vascular endothelial cells can themselves produce and release injury-promoting mediators. Using isolated perfused rat lungs and cultured human pulmonary endothelial cells, we assessed the effect of neutrophil-derived injurious mediators, leukotoxin, and neutrophil elastase on the pulmonary endothelium. Both mediators caused high-permeability pulmonary edema in the isolated lungs and caused dose-dependent and time-dependent damage in the cell cultures. Injury due to leukotoxin was suppressed in the presence of LNMMA or superoxide dismutase and injury due to neutrophil elastase was suppressed by neutrophil elastase inhibitors. These data indicate that these mediators cause lung injury via different mechanisms and that they may synergistically evoke clinical lung injury.

Acute Disease↗
PubMed1993

[Adult case of bronchial asthma induced by chironomid midges].

A 48-year-old woman who was diagnosed to have bronchial asthma induced by chironomid midges is reported. In spring of 1985, massive growth of chironomid midges occurred in the river beside her house. Since then, moderate growth has occurred in every spring or summer. She had wheezing attacks every May or June since June 1986. On May 2, 1991, she was hospitalized because of exacerbation of wheezing and dyspnea. Wheezing attacks were improved by appropriate medical treatment during hospitalization. Examination was performed during the state of stable clinical symptoms. RAST scores to Chironomus thummi thummi (CTT) and Chironomus plumosus (CP) were 4 and 3, respectively. Allergic skin reaction showed the threshold dilution of CP of 10(-6). CP skin test concomitantly provoked a mild acute asthma attack. The midges found swarming around her house were identified as Chironomus nippodorsalis. According to her clinical history and allergic skin reactions followed by acute asthmatic attack, this patient was diagnosed to have bronchial asthma induced by chironomid midges. Chironomid midge can be one of the inhalant allergens in adults.

Adult↗
PubMed1993

[Effects of cilostazol, a cyclic AMP phosphodiesterase inhibitor, on pulmonary vascular tone].

We examined the effect of Cilostazol, a cyclic AMP phosphodiesterase inhibitor, rat isolated pulmonary arterial ring tone. Cilostazol dilated pulmonary arterial rings pre-contracted with 10(-6) M phenylephrine in a dose-dependent manner (ED50 3.00 x 10(-6) M). This vasodilatory effect of Cilostazol was not affected by pretreatment with meclofenamate (10(-5) M), mechanical endothelium denudation, methylene blue (10(-5) M) or nitro-L-arginine (2 x 10(-4) M). The vasodilatory effect of Cilostazol on rat thoracic aortic rings was stronger than that on rat pulmonary arterial ring (ED50 1.89 x 10(-6) M). Cilostazol (10(-6) M-10(-4) M) inhibited hypoxic contraction of rat pulmonary rings in a dose-dependent manner. Our experimental data indicated that Cilostazol caused vasodilation regardless of vascular endothelium function and inhibited hypoxic contraction due to inhibition of cyclic AMP phosphodiesterase.

3',5'-Cyclic-AMP Phosphodiesterases↗
PubMed1993

[Home intermittent negative pressure ventilation in a case of chronic respiratory failure due to old tuberculous pleuritis].

A 64-year-old male with a history of tuberculous pleuritis at age 29 had received home oxygen therapy since age 58 because of chronic respiratory failure. He was admitted with symptoms of dyspnea at rest and myoclonus at age 62. Because CO2 narcosis occurred twice, we performed intermittent negative pressure ventilation (INPV) after short-term positive pressure ventilation with transnasal intubation. He has received INPV for 7 hours every day at his home for 20 months without acute exacerbation of respiratory failure, and his activity of daily life subsequently improved. In conclusion, INPV seems to be useful for patients with chronic hypercapnic respiratory failure due to lung disease.

Chronic Disease↗
PubMed1992

[Bronchial hyperresponsiveness to acetylcholine during acute pulmonary congestion in guinea pigs].

To understand the precise mechanism of bronchial hyperresponsiveness in patients with congestive heart failure, we studied the effect of mild pulmonary congestion on bronchial responsiveness to inhaled acetylcholine (ACh) in guinea pigs. We induced mild pulmonary congestion by inflation of a balloon placed in the left atrium, and maintained the left atrial pressure (Pla) at 10 mmHg for 30 minutes with continuous monitoring of lung resistance (RL) and dynamic compliance (Cdyn). Furthermore, we determined the provocative concentration of ACh producing 100% increase in RL (PC100-ACh), before and during balloon inflation. In animals with propranolol pretreatment, but not in animals without propranolol pretreatment, mild pulmonary congestion caused slight increase in RL (N.S.) and significant decrease in Cdyn (p less than 0.01) and PC 100-ACh (p less than 0.01). Cutting of bilateral vagal nerves partially inhibited the decrease of PC100-ACh, but pretreatment with either phenoxybenzamine, indomethacin, AA-861 or OKY-046 had not effect. These results suggest that blockade of beta-adrenergic receptors and the vagal reflex, but not of alpha-adrenergic receptors or arachidonates, contributes to bronchial hyperresponsiveness during acute pulmonary congestion.

Acetylcholine↗
PubMed1992

[Probucol inhibits tobacco smoke-induced decrease in plasma anti-elastase activity and ferroxidase activity in rats].

Elastolytic enzymes and active oxygen species derived from leukocytes and alveolar macrophages during exposure to tobacco smoke, together with active oxygen species directly derived from tobacco smoke, are thought to play a crucial role in the pathogenesis of pulmonary emphysema by inactivating alpha 1 protease inhibitor (alpha 1 PI), a novel anti-elastase. We studied the inhibitory effect of probucol, an oral hypocholesterolemic agent, on tobacco smoke-induced decrease in plasma anti-elastase activity (EIA) and ferroxidase activity (FA) in conscious venous catheter instrumented rats. Rats exposed to the smoke of 5 cigarettes (nicotine 11 mg, tar 115 mg) in a plastic chamber showed a prompt increase in plasma COHb to 17.9 +/- 2.7%, and a prompt decrease in plasma EIA by -17.9% (p less than 0.05) and FA by -14.8% (p less than 0.01), which lasted for 6 hours after exposure. Rats administered probucol (1% probucol in food) for 3 days showed normal cholesterol plasma levels, and rats administered probucol for 4 weeks showed hypocholesterolemic plasma levels. EIA and FA were not depressed after smoking, and lipid peroxide product (TBA reactive substance) in lung tissue (p less than 0.05) and serum (p less than 0.1) showed a smaller increase in association with a smaller decrease in the ratio of lung tissue GSH/GSSG (p less than 0.01) compared with control rats. These results indicate that probucol, via its antioxidant action rather than its cholesterol lowering effect, has a protective effect on lung exposed to tobacco smoke in terms of protease-antiprotease balance and oxidant-antioxidant balance.

Animals↗