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Biomedical subjects

M Fujimura

Publications and source records attributed to M Fujimura.

At least 271 records · Page 15Linked to original sources

Possible role of cholecystokinin in the development of acute pancreatitis in rats.

The aim of this study was to elucidate whether cholecystokinin (CCK) had a role in the occurrence and/or in the development of experimental acute pancreatitis in rats, and furthermore to find the possibility for the treatment of acute pancreatitis with a CCK antagonist, proglumide. The administration of CCK-8 significantly increased serum levels of amylase, lipase and pancreatic wet weight. The administration of proglumide significantly reduced the blood levels of trypsin, pancreatic wet weight, water content and improved survival rate. These findings were supported by microscopic examination. The results of this study demonstrate that CCK has an important role in the development of acute pancreatitis and that proglumide might have prophylactic and therapeutic effects in acute pancreatitis.

Acute Disease

Release of neurotensin by selective perfusion of the jejunum with oleic acid in dogs.

Plasma neurotensin concentrations are rapidly elevated after oral ingestion or intraduodenal infusion of fat, apparently before fat reaches the ileum where neurotensin is highly concentrated. The purpose of this study was to investigate the site of neurotensin release and to determine whether neurotensin is released by direct luminal stimulation by fat in conscious dogs. Dogs were prepared with isolated jejunal or ileal segments and portal vein catheters. Release of neurotensin into the portal venous blood was examined by selective perfusion of each intestinal segment with sodium oleáte. The results of this study show that selective perfusion of the jejunum, but not the ileum, with sodium oleate, caused a significant release of neurotensin. We speculate that release of ileal neurotensin is not due to direct luminal stimulation, but is mediated by local neural or humoral intermediates.

Animals

Pancreatic juice enhances fat-stimulated release of enteric hormones in dogs.

The presence of pancreatic juice in the intestinal lumen results in the hydrolysis of dietary fat. The hydrolytic products of dietary fat are potent stimulants of pancreatic exocrine secretion and potent inhibitors of gastric acid secretion. In this study, residual pancreatic enzyme activity in the intestinal lumen may account for the observed increase of triglyceride-stimulated pancreatic exocrine secretion and the release of peptides during diversion of pancreatic juice. The presence of pancreatic juice enhanced the pancreatic protein output that was stimulated by the intraduodenal administration of a triglyceride (corn oil, 2 g/kg/h) by 240% (p less than .05). The presence of pancreatic juice during the intraduodenal administration of a triglyceride nearly abolished the output of gastric acid as well as the release of gastrin (p less than .05) that had been stimulated by the intragastric placement of a 10% peptone meal. Pancreatic juice in the duodenum significantly enhanced the triglyceride-stimulated release of cholecystokinin-33/39, secretin, neurotensin, peptide YY, pancreatic polypeptide, and insulin (p less than .05) when compared with the release of these enteropancreatic hormones during the diversion of pancreatic juice. This study shows that the presence of pancreatic juice in the duodenal lumen enhances the fat-stimulated release of enteric hormones that have a stimulatory action on the enteroacinar and enteroinsular axis as well as an inhibitory action (enterogastrone-like activity) on the postprandial regulation of gastric function.

Animals

Application of the trimethylsilyl trifluoromethanesulfonate deprotecting procedure for the synthesis of porcine peptide YY (PYY).

A 36-residue peptide amide corresponding to the entire amino acid sequence of porcine peptide YY (PYY) was synthesized by assembling eight peptide fragments of established purity, followed by hard acid deprotection with 1M trimethylsilyl trifluoromethanesulfonate in trifluoroacetic acid. beta-Cycloheptylaspartate, Asp(OChp), was employed to minimize the base-catalyzed succinimide formation. When administered to dogs, synthetic PYY was active as natural peptide in its effects on exocrine pancreatic secretion and pancreatic tissue blood flow.

Amino Acid Sequence

[The effect of erythromycin treatment on natural killer (NK) cell activity in patients with chronic lower respiratory tract infections].

We measured NK activity before and after administration of erythromycin in 7 cases of chronic respiratory infection, and investigated the relationship between NK activity and improvement of the clinical syndrome. 1) We saw a significant rise in NK activity after treatment of erythromycin. Values before and after ranged from 40.0 +/- 21/2% to 62.0 +/- 32.7%. 2) There was no correlation between treatment period of erythromycin and the rate of rise in NK activity in the various cases such as rapidly rising cases or slowly rising cases, etc. 3) We saw a rise in NK activity before improvement of the clinical syndrome. Therefore it is suggested that treatment of erythromycin affects a rise in NK activity.

Adult

Chorioamnionitis and serum IgM in Wilson-Mikity syndrome.

A total of 753 infants weighing less than 1800 g at birth were studied prospectively and their serum IgM concentrations measured within 72 hours of age. Placentas from 584 of these infants were examined histologically for chorioamnionitis. The results were correlated with chronic respiratory insufficiency. Altogether 101 infants developed chronic respiratory insufficiency of which 22 had bronchopulmonary dysplasia and 35 Wilson-Mikity syndrome. The remaining 44 infants were classified as 'unexplained chronic lung disease'. Mean serum IgM concentration for Wilson-Mikity syndrome was 1.02 g/l whereas it was 0.14 g/l for bronchopulmonary dysplasia and 0.32 g/l for unexplained chronic lung disease. The incidence of chorioamnionitis was significantly higher in Wilson-Mikity syndrome (30/35) compared with bronchopulmonary dysplasia (4/16) and with infants without chronic respiratory insufficiency (145/490). Wilson-Mikity syndrome was shown to be significantly correlated with the evidences of intrauterine inflammation.

Chorioamnionitis

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

[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

[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

[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

[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

[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

[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

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

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