Biomedical subjects
Publications and source records attributed to M Fujimura.
Congenital bronchobiliary fistula is a rare malformation. We have presented a case that was diagnosed and treated successfully in an adult. The diagnosis was made by bronchoscopy and bronchography. After excision of the fistula the patient recovered completely. For each patient in whom this anomaly is suspected, bronchoscopy and bronchography are useful for diagnosis.
The clinical and pathological findings in a patient with monocytic aleukemic leukemia presenting initially as multiple monoblastic tumors of the skin is described. The patient was a 35-year-old Japanese woman, who had first noticed multiple, asymptomatic, reddish-brown papules on her trunk. Asymptomatic enlargements of several lymph nodes were present in the bilateral cervical and axillary areas. There was no hepatosplenomegaly, sternal tenderness, bruising, or bleeding. The skin and lymph node biopsies were originally interpreted as malignant lymphoma. The diagnosis of acute monocytic leukemia was established when bone marrow involvement was detected. Immunohistochemical observation of the skin eruptions revealed the following: Positive staining with lysozyme was noted in almost half of the infiltrating atypical cells. Most of the infiltrating cells reacted positively with antisera to Leu-M5 and some of them reacted to Leu-M1. The helper T cell antibody, Leu-3a+3b, showed weak positive staining of most infiltrating cells. However, there were no reactions with antisera to Leu-6, Leu-7, Leu-14, CALLA, OKT 6, OKT 8, OKT 16, OKB 19, OKM 14, beta F1, or delta TCS1. OKM 5-positive keratinocytes were observed in some parts of the upper epidermis, although no OKM 5 expression could be detected on any tumor cells. Cytochemistry, immunohistochemistry, and electron microscopy can aid in the diagnosis of monocytic leukemia. This case illustrates the importance of using an expanded panel of monoclonal antisera in certain hematopoietic tumors.
Slow-reacting substance of anaphylaxis (SRS-A) is an important factor mediating bronchoconstriction in asthma. We developed a guinea pig model for SRS-A mediated bronchoconstriction induced by antigen inhalation. Using this model, we investigated the effect of inhaled WP871, a new anti-allergic drug, on bronchoconstriction. Aerosol WP871 (0.01 and 0.033%) to some extent inhibited the antigen-induced bronchoconstriction in a dose-dependent fashion, but high-dose WP871 (0.1%) inhalation itself produced a non-specific bronchoconstriction. However, aerosol WP871 (0.033%) showed no inhibitory effect on bronchoconstriction caused by direct inhalation of leukotriene C4, a component of SRS-A. These findings indicate that aerosol WP871 does not antagonize SRS-A, but inhibits synthesis and/or release of SRS-A and has some non-specific bronchoconstrictive effect in high concentration.
The threshold for cough induced by inhaled tartaric acid was measured in 71 non-atopic healthy volunteers. The cough threshold was lower in women than in men, which may be relevant to previous reports that angiotensin converting enzyme inhibitors induce cough more frequently in women than in men.
To investigate the relationship between pulmonary congestion and bronchial responsiveness, we measured bronchial responsiveness to acetylcholine in 51 patients with left heart disorders. The measurement of bronchial responsiveness was performed by inhaling doses of acetylcholine chloride (0.08 to 20 mg/ml) and calculating the PC20-FEV1. The median value for PC20-FEV1 was above 20 mg/ml in the subjects without history of congestive heart failure (n = 18), was 5.29 mg/ml in the subjects with clinical evidence of congestive heart failure in the past days (n = 18; p less than 0.01), and was 5.74 mg/ml in the subjects with clinical evidence of congestive heart failure at the time of study (n = 15; p less than 0.01). The hemodynamic variables by cardiac catheterization and the clinical symptoms were not correlated with the grade of bronchial responsiveness. These results suggest that the bronchial responsiveness was increased in most of the patients with chronic congestive heart failure. We concluded that continuous pulmonary congestion may contribute to the pathogenesis of bronchial hyperresponsiveness.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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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.