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Biomedical subjects

M Fujimura

Publications and source records attributed to M Fujimura.

At least 91 records · Page 5Linked to original sources
PubMed1989

Bronchoconstrictive properties and potentiating effect on bronchial responsiveness of inhaled thromboxane A2 analogue (STA2) in guinea pigs.

Effect of subthreshold concentration of inhaled STA2, a thromboxane A2 (TXA2) analogue, on bronchial responsiveness to histamine was investigated in anesthetized and artificially ventilated guinea pigs. Percent increase in pressure of the airway opening (Pao) by aerosol histamine (50, 100 micrograms/ml) was significantly potentiated by subthreshold dose of aerosol STA2 (0.10 micrograms/ml) which was determined by dose-response curve of % increase in Pao by inhaled STA2 (0.033, 0.10, 0.33, 1.0 micrograms/ml). These results demonstrated that thromboxane A2 could contribute to bronchial hyperresponsiveness which is one of the major clinical features of bronchial asthma.

Aerosols↗
PubMed1989

[2-color analysis of lymphocyte subpopulation of bronchoalveolar lavage fluid and peripheral blood in patients with sarcoidosis].

By means of 2-color analysis, we investigated the lymphocyte subpopulation of bronchoalveolar lavage fluid (BALF) and peripheral blood (PB) of 13 patients with pulmonary sarcoidosis. The BALF-CD4+ T cells of normal subjects and patients with sarcoidosis consisted almost completely of CD4+4B4+ cells (helper inducer T cells) and BALF-CD8+ T cells were almost completely composed of CD8+CD11- cells (cytotoxic T cells). The BALF findings of sarcoidosis were characterized by increased percentages of CD4+4B4+ cells (54.9 +/- 15.7%), decreased percentage of CD8+CD11- cells (12.0 +/- 8.4%) and increased percentage of CD4+HLA-DR+ cells (27.8 +/- 13.1%). These findings suggest that activated CD4+4B4+ cells (helper inducer T cells) may primarily contribute to the pathogenesis of pulmonary sarcoidosis. The in vivo or in vitro functions of CD4+4B4+ cells in sarcoidosis need further investigation.

Adult↗
PubMed1989

[The role of cyclooxygenase products on bronchial responsiveness to methacholine in patients with sino-bronchial syndrome].

The role of cyclooxygenase products on bronchial responsiveness to methacholine was studies in 9 patients with sino-bronchial syndrome. Provocative concentrations of methacholine, producing a 20% fall in forced expiratory volume in one second (FEV1)(PC20-FEV1) and a 35% fall in inverse respiratory resistance (Grs) (PC35-Grs), were measured before and after oral administration of a thromboxane synthetase inhibitor (OKY-046) and a cyclooxygenase inhibitor (indomethacin). Baseline values of FEV1 and respiratory resistance (Rrs) were not altered by OKY-046 or indomethacin. Geometric mean values of PC20-FEV1 and PC35-Grs were significantly (p less than 0.005 and p less than 0.05) increased from 2.19 mg/ml (GSEM, 1.58) and 0.79 mg/ml (GSEM, 1.70) to 8.13 mg/ml (GSEM, 1.92) and 1.55 mg/ml (GSEM, 1.38) by indomethacin, whereas these values were not significantly increased by OKY-046. These findings indicate that not thromboxane A2 but bronchoconstricting prostaglandins may play a role in bronchial hyperresponsiveness in sino-bronchial syndrome.

Bronchi↗
PubMed1989

[Bronchoalveolar lavage fluid findings and lung function in psittacosis].

Three familial cases of psittacosis presented with fever and arthralgia. The first case was a 54-year-old man whose chest X ray film showed ground glass appearance in left S6. Ga scintigraphy revealed stronger accumulation in left lower lobe. Bronchoalveolar lavage fluid was examined in 2 of the cases and activated helper T cells were increased in both of the cases. Lung function was studied in all 3 cases in different phases. Their basic lung functions were different, but there was a similar change in courses, i.e. decrease of small airway flow and the increase of RV. These findings suggest that lung lesion of psittacosis may be related to allergic reaction and diffuse lung disease.

Adult↗
PubMed1989

[Inhibitory effect of procaterol (beta 2 agonist) on the release of cyclooxygenase products during antigen-induced bronchoconstriction in the guinea pig in vivo].

The purpose of this study was to investigate whether procaterol (beta 2 agonist) inhibits the release of cyclooxygenase products in bronchoalveolar lavage fluid (BALF) during in vivo allergic bronchoconstriction in passively sensitized guinea pigs. Antigen-induced bronchoconstriction was significantly inhibited by pretreatment with procaterol. The concentrations of 6-keto-PGF1 alpha, PGF2 alpha and TXB2 in BALF significantly decreased in guinea pigs pretreated with inhaled procaterol. The concentration of TXB2, which is the stable metabolite of TXA2, a strong bronchoconstrictor, was especially markedly decreased compared with that in the control animals. These data indicate that procaterol (beta 2 agonist) may inhibit the release of chemical mediators during allergic reactions as well as directly decrease the contractility of airway smooth muscle. Consequently, regular inhalation of procaterol may be clinically useful for prophylaxis of bronchial asthma.

Administration, Inhalation↗
PubMed1989

[Pulmonary sequestration associated with localized cystic bronchiectasis and funnel chest].

A 37-year-old woman, who presented with low grade fever and productive cough, was admitted for evaluation of an abnormal shadow on chest X-ray film. On physical examination, she had bilateral hallux valgus and funnel chest, the center of which was at the fifth rib on the right edge of the sternum. Since chest CT scan, selective bronchography, pulmonary arteriography and aortography revealed that she had pulmonary sequestration in the right cardiophrenic region associated with localized cystic bronchiectasis in the right S7b, she received right lower lobectomy. Histological examination showed the cystic change of bronchioli and a small number of emphysematous alveoli in the right S7b adjacent to the sequestered lung. The bronchopulmonary structure of right S7a was almost intact. It might be speculated that the existence of the sequestered lung constituted to the deterioration of the development of the lung and the rib cage adjacent to it.

Adult↗
PubMed1989

[Cellular localization, half-life, and secretion of peptide YY].

Tissue and plasma concentration of peptide YY (PYY) were measured by means of a radioimmunoassay (RIA) developed in our laboratory, using a specific PYY antiserum generated in New Zealand white rabbits against synthetic PYY, and dextran-coated charcoal to terminate the assay. Cellular localization of PYY was studied immunohistochemically using the peroxidase-antiperoxidase (PAP) technique. The highest tissue concentration of PYY was found in the mucosa of the terminal ileum and colon. PYY-containing secretory granules were primarily found in the basal pole of open-type endocrine cells. Basal plasma concentration of PYY was 70 +/- 9 pg/ml and rose to 357 +/- 30 pg/ml during the IV administration of PYY at 400 pmol/kg-h. A significant correlation was found (r = 0.94, p less than 0.05) between dose of PYY (12.5, 25, 50, 100, 200, 400 pmol/kg-h, IV) and plasma concentration of PYY. The calculated half-life of PYY in plasma was 8.3 +/- 1.9 minutes. Plasma concentration of PYY during the intraduodenal administration of sodium oleate (150 +/- 20 pg/ml) or long-chain triglyceride (187 +/- 37 pg/ml) was similar to plasma concentration of PYY obtained during the IV administration of PYY at 100 pmol/kg-h. Plasma concentration of PYY raised (126 +/- 10 pg/ml) after the administration of bombesin (400 pmol/kg-h, IV). Bile enhanced release of PYY. The present study suggests a hormonal role for PYY.

Amino Acids↗
PubMed1988

Surfactant replacement therapy in neonatal respiratory distress syndrome. A multi-centre, randomized clinical trial: comparison of high- versus low-dose of surfactant TA.

We conducted a prospective, randomized, controlled trial comparing the efficacy of two doses of a reconstituted bovine surfactant (Surfactant TA) in premature infants requiring mechanical ventilation shortly after birth for respiratory distress syndrome. Forty-six infants weighting 1000-1499 g were randomized into two groups: a low-dose group (23 infants given a single dose of 60 mg surfactant lipid/kg) and a high-dose group (23 infants given a single dose of 120 mg/kg). The mean (SD) age at which surfactant was given was 5.5 (+/- 1.2) h in the low-dose group and 6.0 (+/- 1.5) h in the high dose group. Both treatments improved oxygenation (increased arterial-alveolar PO2 ratio) with decreased mean airway pressure, the high-dose surfactant having a more beneficial effect in prolonging the response. Infants in the high-dose group had significantly less (P less than 0.05) incidence of both intraventricular haemorrhage and bronchopulmonary dysplasia. This prospective trial documents that a greater benefit can be obtained by increasing the dose of surfactant (120 mg/kg) beyond 60 mg/kg treatment of premature infants with severe respiratory distress syndrome (RDS).

Clinical Trials as Topic↗
PubMed1988

Effect of aging on gastric acid secretion, serum gastrin, and antral gastrin content in rats.

The purpose of this study was to characterize the effects of aging on gastric acid secretion and on serum and antral concentrations of gastrin in rats. Young and old Fischer 344 rats were prepared with gastric fistulas. Twenty-four hours after surgery, graded doses of human synthetic gastrin-17 (SHG-17) (2, 5, 10, 20, and 40 micrograms/kg) were given intravenously in random order. Gastric secretions were collected for gastric acid measurement before and at 15-min intervals after each dose of gastrin. In a separate study, blood was collected and the stomachs were removed for antral gastrin extraction from fed young and old rats. Serum and antral gastrin was measured by radioimmunoassay. The basal and gastrin-stimulated acid secretions were significantly decreased in aged rats compared to the young rats. The basal acid output was 0.4 +/- 0.2 microeq/15 min in the aged rats and 1.5 +/- 0.5 microeq/15 min in the young. The maximal acid output stimulated by gastrin was 11.1 +/- 1.8 microeq/15 min in the aged rats and 24.2 +/- 2.8 microeq/15 min in the young. Both serum and antral concentrations of gastrin were significantly decreased in aged rats. Serum gastrin concentration was 114.8 +/- 7.4 pg/ml in the aged rats and 192.0 +/- 14.4 pg/ml in the young. Antral gastrin concentration was 3.9 +/- 0.5 micrograms/g tissue in the aged rats, which was significantly less than the concentration in the young (6.5 +/- 0.4 micrograms/g tissue). Antral gastrin content did not change with aging.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1988

Peptide YY inhibits pancreatic secretion by inhibiting cholecystokinin release in the dog.

Peptide YY inhibits the pancreatic exocrine secretion (bicarbonate, water, and protein) that is stimulated by cholecystokinin, secretin, or neurotensin in the dog, but whether peptide YY inhibits the release of gut peptides that stimulate pancreatic exocrine secretion is not known. Six dogs were prepared with gastric, pancreatic, and cecal cannulas. On separate days, a single dose of sodium oleate (3, 6, 7.5, 9, 12, 15, or 18 mmol/h) was given intraduodenally for 90 min, either alone (control) or in combination with peptide YY (25, 50, 100, 200, or 400 pmol/kg.h, i.v.). We measured plasma levels of cholecystokinin-33/39, secretin, neurotensin, and peptide YY by radioimmunoassay. During infusion of peptide YY, the integrated release of cholecystokinin (3.3 +/- 0.5 ng-[0-90] min/ml) was decreased significantly (p less than 0.05) when compared with control values (5.6 +/- 0.6). Release of secretin and neurotensin was not affected. A positive correlation (p less than 0.05) was found between the release of cholecystokinin and pancreatic protein output in both control (r = 0.68) and peptide YY-treated (r = 0.67) groups. Release of peptide YY was significant after intraduodenal or intracolonic administration of sodium oleate. These studies demonstrate that inhibition of pancreatic protein secretion by peptide YY in dogs is mediated, at least in part, by an inhibition of the release of cholecystokinin.

Animals↗
PubMed1988

Peptide YY and gallbladder contraction. Studies in vivo and in vitro.

The purpose of this study was to examine the effect of peptide YY on contraction of the gallbladder in vivo and in vitro and on contraction of the sphincter of Oddi in vitro. In conscious dogs that were prepared with strain-gauge force transducers implanted in the gallbladder wall, peptide YY (400 ng/kg, bolus; 800 pmol/kg.h, infusion) did not affect the resting contractile pattern of the gallbladder, nor did it inhibit cholecystokinin-octapeptide (CCK-8)-stimulated gallbladder contraction. In contrast, the cholecystokinin antagonist proglumide (5, 10, 20, 40, or 80 mg/kg), given in vivo, inhibited CCK-8-stimulated gallbladder contraction in a dose-related manner. The highest dose of proglumide (80 mg/kg) completely abolished contraction of the gallbladder stimulated by CCK-8. In vitro studies showed that peptide YY (0.25, 0.5, or 1 microgram/ml) did not affect the resting tension of rabbit gallbladder strips, and it did not inhibit CCK-8-stimulated contraction of gallbladder strips. Proglumide (0.4, 0.8, 1.6, or 3.2 mg/ml) inhibited CCK-8-stimulated tension of gallbladder strips in a dose-related manner. Peptide YY and CCK-8 had no effect on the motility of the canine sphincter of Oddi in vitro, whereas acetylcholine caused contraction and adrenergic agonists caused relaxation. These results suggest that peptide YY and pancreatone (a peptidelike substance, extracted from ileal and colonic mucosa, that inhibits CCK-8-stimulated gallbladder contraction in vivo) do not appear to be identical.

Ampulla of Vater↗
PubMed1988

Secondary release of thromboxane A2 in aerosol leukotriene C4-induced bronchoconstriction in guinea pigs.

Effect of a thromboxane synthetase inhibitor (OKY-046) on bronchoconstriction induced by aerosol leukotriene C4 and histamine was studied in anesthetized, artificially ventilated guinea pigs in order to examine whether secondary release of thromboxane A2 is produced by aerosol leukotriene C4 or not. 0.01-1.0 micrograms/ml of leukotriene C4 and 12.5-400 micrograms/ml of histamine inhaled from ultrasonic nebulizer developed for small animals caused dose-dependent increase of pressure at airway opening (Pao) which is considered to be an index representing bronchial response. Pretreatment of the animals with intravenous OKY-046 (100mg/kg) significantly reduced the airway responses produced by inhalation of 0.1, 0.33 and 1.0 micrograms/ml of leukotriene C4, while the pretreatment did not affect the histamine dose-response curve. Based on these findings and previous reports (6,7), it is suggested that aerosol leukotriene C4 activates arachidonate cyclooxygenase pathway including thromboxane A2 synthesis and the released cyclooxygenase products have bronchodilating effect as a whole.

Aerosols↗
PubMed1988

Colocalization of calcitonin gene-related peptide and somatostatin in pancreatic islet cells and inhibition of insulin secretion by calcitonin gene-related peptide in the rat.

Calcitonin gene-related peptide (CGRP)- and somatostatin (SRIF)-containing cells were identified by immunocytochemical techniques in pancreatic islet cells of the rat. CGRP-containing cells were found primarily in the peripheral portion of the pancreatic islets. In addition, CGRP-containing cells also contained somatostatin, which identifies the islet CGRP-containing cells as D cells. In the present study, we also tested the effect of CGRP on gastrin-releasing peptide (GRP; 10(-9) M)- or cholecystokinin (CCK-8, 10(-9) M)-stimulated release of insulin from isolated rat islets in vitro. At concentrations of 10(-8)-10(-11) M, CGRP inhibited GRP- and CCK-8-stimulated release of insulin significantly when compared with GRP or CCK-8 alone. At the lowest concentration of CGRP (10(-11) M), the inhibitory effect of CGRP on CCK-8-stimulated release of insulin was statistically significant (p less than 0.05) and exceptionally potent (65-90% inhibition). We have also found that CGRP does not stimulate the release of SRIF from isolated islet cells. These findings suggest that CGRP may play a regulatory role in the release of insulin.

Animals↗