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Biomedical subjects

M Fujimura

Publications and source records attributed to M Fujimura.

At least 73 records · Page 4Linked to original sources
PubMed1990

Effects of aerosol administration of a thromboxane synthetase inhibitor (OKY-046) on bronchial responsiveness to acetylcholine in asthmatic subjects.

Bronchial hyperresponsiveness is one of the major clinical features of bronchial asthma. We previously reported that oral administration of a selective thromboxane synthetase inhibitor, OKY-046, reduced bronchial hyperresponsiveness to acetylcholine in asthmatic subjects. In this study, the effect of aerosol administration of OKY-046 on bronchial hyperresponsiveness was evaluated in ten inpatients with intrinsic asthma. Acetylcholine inhalation tests were performed before and after four days of inhalation of OKY-046 (100 mg/day). The provocative concentration of acetylcholine producing a 20 percent fall in forced expiratory volume in 1 s (PC20-FEV1) and that causing a 35 percent fall in respiratory conductance (PC35-Grs) were measured as indexes of bronchial responsiveness. There was a significant increase in PC20-FEV1 (p less than 0.001) and PC35-Grs (p less than 0.02) after inhalation of OKY-046 from 0.79 (GSEM, 1.41) Mg/ml and 0.96 (GSEM, 1.35) mg/ml to 1.20 (GSEM, 1.41) mg/ml and 1.74 (GSEM, 1.32) mg/ml, respectively. There was no significant difference in forced vital capacity (FVC), FEV1, or respiratory resistance (Rrs) baseline values before and after inhalation of OKY-046. Platelet aggregation was not inhibited by the treatment in other five inpatients. Thus, prophylactic administration of aerosol OKY-046 may be available for treatment of asthma by reduction of bronchial hyperresponsiveness. Further studies are needed to determine the optimum dose.

Acetylcholine↗
PubMed1990

Attenuating effect of a thromboxane synthetase inhibitor (OKY-046) on bronchial responsiveness to methacholine is specific to bronchial asthma.

To determine whether the involvement of thromboxane A2 in bronchial hyperresponsiveness (BHR) is specific to asthma, we examined the effects of a selective inhibitor of thromboxane synthetase (OKY-046) and a cyclooxygenase inhibitor (indomethacin) on bronchial responsiveness to methacholine in normal subjects and patients with chronic bronchitis, diffuse bronchiectasis, and intrinsic bronchial asthma. The provocative concentration of methacholine producing a 20 percent fall in forced expiratory volume in 1 s (PC20-FEV1) was measured before and after oral administration of OKY-046 (2,600 mg over four days) and indomethacin (450 mg over three days) in ten normal, ten bronchitic, nine bronchiectatic, and eight asthmatic subjects, respectively. Baseline values of FEV1 and forced vital capacity (FVC) were not altered by OKY-046 or indomethacin. The geometric mean value of PC20-FEV1 increased significantly (p less than 0.005) from 1.78 to 4.27 mg/ml after OKY-046 in asthmatic subjects, but not in normal, bronchitic, or bronchiectatic subjects. On the other hand, PC20-FEV1 increased significantly (p less than 0.005) from 2.19 to 8.13 mg/ml after indomethacin in bronchiectatic subjects, but not in normal, bronchitic, or asthmatic subjects. We conclude that the involvement of thromboxane A2 in BHR may be specific to asthma, and bronchial responsiveness of bronchiectasis may be potentiated by inflammatory release of bronchoconstrictor prostaglandins except for thromboxane A2. Further studies using thromboxane A2 receptor antagonists are needed to confirm the conclusion.

Acrylates↗
PubMed1990

[Mucociliary transport disturbance after an asthmatic attack].

The influence of asthmatic attack on the mucociliary transport system was studied by saccharin test in 8 asthmatic patients. In stable asthmatics, the mean nasal clearance time (NCT) was 44.9 +/- 6.1 (SE) min, which was greater than in normal controls (15.1 +/- 3.4 (SE) min). Nasal clearance time in stable asthmatics correlated fairly well with the duration of asthma. There is, however, no relationship between NCT and ages, blood eosinophil counts, blood IgE, or the respiratory functions. Mean NCT during asthmatic attack was 16.9 min, but 1 week later, mean NCT was prolonged to 58.6 min and 101.1 min after 2 weeks. These results indicate that there is mucociliary transport disturbance after asthmatic attack.

Adolescent↗
PubMed1990

[Potentiating effect of spirometric maneuver on bronchial responsiveness to methacholine in asthmatic subjects--the role of deep inspiration and forced expiration].

We previously reported that spirometric maneuver (SM) had potentiating effect on bronchial responsiveness (BR) in asthmatic subjects but not in normal subjects. SM consists of deep inspiration to TLC (DI) and forced expiration to RV (FE). In this study, we examined the effect of SM, DI and FE on BR in 9 asthmatic subjects. Provocative concentration of methacholine producing a 35% fall in respiratory conductance (PC35-Grs) was significantly (p less than 0.02 and p less than 0.025) decreased from 0.34 mg/ml (GSEM, 1.51) to 0.16 mg/ml (GSEM, 1.45) and 0.14 mg/ml (GSEM, 1.51) by SM and DI, respectively but it was not altered by FE. These findings indicate that potentiating effect of SM on BR which is characteristic of asthma may be due to DI effect.

Adult↗
PubMed1990

[Thromboxane A2 could be involved in bronchial hyperresponsiveness to methacholine in asthmatic subjects but not in bronchitic subjects].

To determine whether the involvement of thromboxane A2 in bronchial hyperresponsiveness is specific to asthma, we examined the effects of a selective thromboxane synthetase inhibitor (OKY-046) and a cyclooxygenase inhibitor (indomethacin) on bronchial responsiveness to methacholine in patients with bronchial asthma and chronic bronchitis. The provocative concentration of methacholine producing a 20% fall in forced expiratory volume in one second (PC20-FEV1) was measured before and after oral administration of OKY-046 and indomethacin in eight asthmatic and 10 bronchitic subjects. Baseline FEV1 value was not altered by OKY-046 or indomethacin. The geometric mean value of PC20-FEV1 increased significantly (p less than 0.005) from 1.78 to 4.27 mg/ml after OKY-046 in asthmatic subjects, but not in bronchitic subjects. On the other hand, PC20-FEV1 was not altered by indomethacin in all subjects. It was concluded that the involvement of thromboxane A2 in bronchial hyperresponsiveness may be specific to asthma.

Asthma↗
PubMed1990

[A case of plasma cell granuloma showing rapid growth and elevation of serum CEA].

A 67-year-old man was admitted with complaints of cough and hemosputum. Chest X-ray examination revealed enlargement of a coin lesion in the right upper lobe, which had been pointed out about one year previously and had been followed up. Although the histology of TBLB specimens and the cytology of sputum and materials showed no malignancy and chest CT showed calcification at the edge of the coin lesion, the mass shadow in the right upper lobe rapidly enlarged and the serum level of CEA gradually elevated. Therefore, it seemed to be impossible to neglect the possibility of lung cancer and right upper lobectomy was performed. The dissected specimen was diagnosed as plasma cell granuloma. Because the histology of the plasma cell granuloma is multifarious, TBLB shows various results. It is therefore difficult to diagnose such inflammatory tumors by TBLB. The increase of the mass shadow in size and the elevated serum level of CEA made it difficult to diagnose this case.

Aged↗
PubMed1990

Surfactant replacement therapy with a single postventilatory dose of a reconstituted bovine surfactant in preterm neonates with respiratory distress syndrome: final analysis of a multicenter, double-blind, randomized trial and comparison with similar trials. The Surfactant-TA Study Group.

The effects of a single dose of surfactant TA were assessed in premature neonates (birth weight 750 to 1749 g) with respiratory distress syndrome (RDS) in a multicenter, double-blind, randomized clinical trial. Only neonates with surfactant deficiency and without ultrasonographic evidence of intracranial hemorrhage greater than or equal to grade II were enrolled. Fifty-four patients received surfactant (100 mg of phospholipid per kilogram of body weight) and 46 patients received an air placebo within 8 hours of life. Treatment with this surfactant resulted in a significant reduction in the severity of RDS with a concomitant increase in the proportion of neonates with mild disease. The frequency of pulmonary interstitial emphysema and of pneumothorax was significantly lower in treated neonates compared with control neonates (2% vs 26%, P = .0008, and 7% vs 39%, P = .0004, respectively). The frequency of intracranial hemorrhage was significantly lower in the surfactant group compared with the control group (20% vs 54%, P = .0008) and was also reduced for the smallest neonates in the surfactant group (13% vs 73%, P = .00008). When categorized according to severity of intracranial hemorrhage and severity of bronchopulmonary dysplasia, the surfactant group was at a significant advantage (adjusted Cochran-Mantel-Haenszel X2 = 10.72, P less than .001 and X2 = 4.43, P = .036, respectively). The proportion of neonates surviving without intracranial hemorrhage and/or bronchopulmonary dysplasia was 63% in the surfactant group vs 26% in the control group (P = .0004); as for the smallest neonates, it was 58% in the surfactant group vs 4% in the control group (P = .0002). There were no differences between the groups with respect to the frequency of patent ductus arteriosus (46% vs 37%), pulmonary hemorrhage (6% vs 7%), necrotizing enterocolitis (0% vs 2%), sepsis (4% vs 2%), retinopathy of prematurity (13% vs 22%), or death (15% vs 22%). It is concluded that treatment with the single-dose surfactant regimen used in this study reduces the severity of respiratory distress during the 48 hours after treatment and decreases the major pulmonary morbidity and intracranial hemorrhage in premature neonates with RDS. Further studies are needed to determine whether (1) treatment at birth or as soon as after RDS is diagnosed and (2) the use of multiple dose of this surfactant would result in any additional benefits.

Bronchopulmonary Dysplasia↗
PubMed1990

[Relationship between cough threshold to inhaled tartaric acid and sex, smoking and atopy in humans].

It has been reported that angiotensin converting enzyme inhibitor (ACE-I) elicits dry cough more frequently in women than in men. This study was designed to evaluate whether airway cough receptors are more sensitive in women than in men. Cough threshold to inhaled tartaric acid was measured in 33 men and 29 women. In non-atopic and non-smoking subjects, geometric mean value of cough threshold in women was 10.0 (GSEM, 1.29) %, which was significantly (p less than 0.02) lower than that in men, 22.5 (GSEM, 1.30) %. In non-atopic men, the cough threshold was significantly (p less than 0.05) lower in smokers (9.3 (GSEM, 1.57) %) than in non-smokers. In non-smoking women, the cough threshold was significantly (p less than 0.02) lower in atopic subjects (4.2 (GSEM, 1.33) %) than in non-atopic subjects. These results demonstrated that airway cough receptors may be more sensitive in women, smoking men and atopic women.

Administration, Inhalation↗
PubMed1990

[Effect of deep inspiration on maximum expiratory flow (Vmax) depends on basal bronchomotor tone in young healthy females].

The relationship between the effect of deep inspiration on Vmax and basal bronchomotor tone was studied by partial and maximum expiratory flow-volume curve in 16 young healthy females (20-21 years old). Effect of deep inspiration on Vmax (DI index; (PEF25-MEF25)/PEF25) significantly related to percent increase in PEF25 not only by inhalation of ipratropium bromide (r = 0.81, p less than 0.0002) but also by inhalation of salbutamol (r = -0.62, p less than 0.01). Furthermore, day to day variation of DI index significantly related to day to day variation of PEF25 (r = 0.68, p less than 0.005) but not to that of MEF25. These findings suggest that the bronchodilating effect of deep inspiration in young healthy females may depend on intensity of basal bronchomotor tone caused by tonic vagal nerve activity.

Adult↗
PubMed1989

Studies on neurotensin. I. Effects on gallbladder motility.

Effects of neurotensin (NT) on gallbladder contraction were examined both in vivo and in vitro. Cholecystokinin-octapeptide (CCK-8) was used to evaluate the methods used in this study and to compare the action of NT on the gallbladder. In In vivo studies, gallbladder contraction was monitored by strain-gauge force transducers implanted on the surface of the dog gallbladder. Bolus intravenous (IV) injection of NT at doses of 20 and 40 ng/kg caused gallbladder contraction of similar of magnitudes in terms of contractile force, while CCK-8 caused contraction dose-dependently. Continuous IV infusion of NT at doses of 250 and 500 ng/kg/hr, which resulted in an elevation of blood levels of NT comparable with those achieved by endogenous release, induced a transient gallbladder contraction. Both maximum contractile force and onset time of contraction were similar to both does of NT. In contrast, CCK-8 induced gallbladder contraction was sustained during infusion of CCK-8 and was dose-dependent for both maximum contractile force and onset time of contraction. NT-induced gallbladder contraction was completely abolished by atropine treatment. In In vitro studies of longitudinal rabbit gallbladder muscle strips, NT was ineffective, while CCK-8 caused a dose-dependent contraction. The present study shows that NT can stimulate gallbladder contraction in the dog via cholinergic pathways.

Animals↗
PubMed1989

Studies on neurotensin. II. Release of neurotensin.

The objective of these experiments was to confirm the localization of neurotensin (NT) in gut endocrine cells of the canine small intestine using immunohistochemistry. In addition, the release of NT from the canine small intestine in response to selective perfusion of a fatty acid (oleate), triglyceride (Lipomul) or products of fat digestion into various segments of the small intestine was studied. In the immunohistochemical study, NT was found to be primarily localized in true endocrine cells of the ileal mucosa. In addition, NT was not found or only negligible numbers of cells were seen outside the lower small intestine. This observation supports previous results based on radioimmunoassay and immunohistochemistry studies. Based on these morphological findings, NT would be released by luminal secretagogues, of which fat appears to be the most potent. In the selective perfusion studies, perfusion of oleic acid into the jejunum of the chronic dog caused NT release, whereas perfusion of the ileum in which NT cells were most abundant was ineffective. This observation suggests that a neural or endocrine message is released to the ileal NT cell from the jejunum, causing NT release. This series of studies was carried out to elucidate the mechanism of NT release and to find the direct luminal stimulants of NT by using both chronic and acute experimental models. These studies suggest that NT is not significantly released under anesthesia and that undigested fat, like triglyceride, does not release NT in either the upper or lower small intestine. Furthermore, digested fat, like oleate or digestive juices in the lower small intestine, is not a direct stimulant of NT release.

Anesthesia↗
PubMed1989

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↗
PubMed1989

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↗
PubMed1989

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↗
PubMed1989

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↗
PubMed1989

[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↗
PubMed1989

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↗