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Biomedical subjects

S Ameshima

Publications and source records attributed to S Ameshima.

7 recordsLinked to original sources
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↗
PubMed1992

[A case of pulmonary tuberculosis associated with severe respiratory failure, DIC and intractable bilateral pneumothoraces].

We had a sixty-five year old male patient who suddenly complained of dyspnea and fever with pulmonary tuberculosis, severe respiratory failure, disseminated intravascular coagulation (DIC) and intractable bilateral pneumothoraces. From the first hospital day severe hypoxemia which did not respond to conventional oxygen therapy developed with a diffuse ill-defined reticulo-nodular shadow in the plain chest x-ray film. On the 2nd hospital day mechanical ventilation with 2cmH2O PEEP was introduced. Antituberculous agents as well as corticosteroids were started suspecting acute interstitial pneumonia with pulmonary tuberculosis and adult respiratory distress syndrome (ARDS). Medication was followed by the treatment of Gabexate mesilate and heparin against DIC on laboratory data. Though clinical findings and pulmonary infiltrate on chest x-ray film transiently improved, right pneumothorax occurred suddenly on the 6th day followed with left pneumothorax on the 36th day. Tube drainage of both pleural spaces and repeated instillation of thrombin-rich oxycel cotton via bronchofiberscope failed to stop air leakage. He ultimately expired on 49th hospital day. At postmortem lung had multiple bilateral bulla several of which ruptured to the pleural site and caseating necrotic area containing bacilli positively stained with Ziehl-Nielsen stain in the bilateral upper lobe. No typical caseating necrotic lesion, however, was found in the other lung tissue. Therefore, it seemed to show a chronic phase of diffuse alveolar damage (DAD).

Aged↗
PubMed1992

[Leukotoxin, 9,10-epoxy-12-octadecenoate, causes vasodilation in isolated pulmonary artery rings preconstricted with endothelin 1].

Leukotoxin, a cytochrome P450-dependent metabolite of linoleate synthesized by neutrophils, caused dose dependent vasodilation (10(15)-5 x 10(-4) M) of isolated rat pulmonary arterial rings preconstricted with endothelin 1 (10(-8) M), although similar doses of linoleate had no effect. The relaxing effect of leukotoxin was largely ablated by mechanical denudation of the endothelium and by treatment with L-NMMA (1 mM) and methylene blue (5 x 10(-6) M), but not indomethacin (10(-5) M). Endothelium-independent relaxation of leukotoxin was not inhibited by pretreatment with nicardipine (10(-6) M) in both pulmonary arterial rings and aortic rings. In A7r5 cultured rat aortic smooth muscle cells, leukotoxin markedly inhibited Ca2+ uptake in the basal nonstimulated state, and in the stimulated state with endothelin 1. We conclude that leukotoxin causes vascular tone-dependent vasodilation via augmentation of EDRF production, and causes decrease of intracellular calcium concentration that is not related to the dihydropyridine-sensitive calcium channel, which may be a mechanism of the endothelium-independent relaxation caused by leukotoxin.

Animals↗
PubMed1992

[Inhibitory effects of alpha 1 protease inhibitor on the production of IL-1 and TNF alpha by alveolar macrophages in patients with lung cancer].

In the present study, we investigated the effect of alpha 1 protease inhibitor (alpha 1PI) on the production of interleukin-1 alpha (IL-1 alpha, ELISA), IL-1 beta (ELISA), and tumor necrosis factor alpha (TNF alpha, ELISA) by alveolar macrophages (AM) recruited by bronchoalveolar lavage (BAL) from patients with lung cancer and benign pulmonary diseases. Levels of BALF alpha 1PI were significantly increased in patients with lung cancer compared with benign pulmonary diseases. When BALF AM were cultured and stimulated by LPS (20 micrograms/ml) for 48 hours, production of IL-1 alpha and IL-1 beta was less marked in patients with lung production showed a similar tendency, but the difference between patients with lung cancer and benign pulmonary diseases was not significant. Addition of alpha 1PI to the LPS-stimulated AM culture system inhibited production of these cytokines dose-dependently. Thus, the local increase of alpha 1PI in lung cancer may act as a humoral inhibitor against the production of IL-1 and TNF by AM.

Adult↗
PubMedDate not supplied

Reappraisal of OP-1206, a prostaglandin E1 derivative in combination with low-flow oxygen inhalation therapy in chronic lung disease.

For the purpose of alleviating pulmonary hypertension and maintaining cardiac output, which tended to be decreased to acute low-flow oxygen therapy in chronic lung diseases, we evaluated combined low-flow oxygen therapy and oral administration of OP-1206, a prostaglandin E1 derivative, in 7 patients with obstructive lung disease and 3 with restrictive one. Low flow oxygen inhalation (1 l/min. 30 minutes) increased PaO2 from 67.2 +/- 12.8 mmHg to 91.0 +/- 18.2 mmHg (p less than 0.001), PVO2 from 36.4 +/- 3.1 mmHg to 41.7 +/- 7.0 mmHg (p less than 0.01) and decreased cardiac index from 3.38 +/- 0.39 l/min/m2 to 3.07 +/- 0.32 l/min/m2 (p less than 0.01), RVSWI from 18.7 +/- 2.6 g.m/m2 to 6.1 +/- 2.0 g.m/m2 (p less than 0.01), transpulmonary driving pressure from 13.0 +/- 5.4 mmHg to 9.8 +/- 5.5 mmHg (p less than 0.01) and mean PA from 21.6 +/- 7.7 mmHg to 18.3 +/- 6.9 mmHg (p less than 0.05) with a trend of increase in COD and no change at oxygen delivery. OP-1206, on the contrary, decreased mPA from 21.6 +/- 7.7 to 18.2 +/- 5.6 mmHg (p less than 0.05), RVSWI from 8.7 +/- 2.6 g.m/m2 to 6.9 +/- 2.3 g.m/m2 (p less than 0.01) with trend of decrease in transpulmonary driving pressure, TPVR and PAR with no substantial changes in gasometric parameters. The decrease rates of PA by low-flow oxygen therapy and OP-1206 administration correlated significantly.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗