Vanishing bile duct syndrome in canine liver allotransplants.
Explore the source record for details and available documents.
Animals↗
Biomedical subjects
T Takishima
Publications and source records attributed to T Takishima.
Control of the larynx in patients with obstructive and restrictive pulmonary impairment.
To study changes in glottic movements associated with pulmonary functional abnormalities, we measured changes in glottic resistance (Rgl) during quiet tidal breathing in normal subjects (N), patients with chronic obstructive pulmonary disease (COPD) and patients with idiopathic pulmonary fibrosis (IPF). Changes in Rgl were measured with a non-invasive method using low frequency sound. Changes in Rgl were tightly coupled to changes in tidal volume and were reproducible in all subjects. Rgl was higher during expiration than during inspiration in N and COPD. COPD showed greater changes in Rgl between inspiration and expiration than did N. However, Rgl did not differ between inspiration and expiration in three of six IPF, and was lower during expiration than during inspiration in two of six IPF. We suggest that glottic movements during quiet tidal breathing change in association with the functional abnormalities of pulmonary diseases.
Air Pressure↗
[Respiratory function during sleep].
Explore the source record for details and available documents.
Airway Resistance↗
Breathing 30 per cent oxygen attenuates bronchial responsiveness to methacholine in asthmatic patients.
The effect of breathing 30% oxygen on bronchial responsiveness to inhaled methacholine was studied in 30 asthmatic patients using a direct graphical recording method. An aerosol of methacholine solution was inhaled during tidal breathing by measuring respiratory resistance (Rrs) continuously, and dose-response curves were obtained on two separate days during air and 30% oxygen inhalation. Oxygen inhalations for 20 min caused no change in baseline Rrs. The threshold dose of methacholine, the dose which increased Rrs from the baseline value while breathing 30% oxygen, increased significantly compared with that while breathing air (p less than 0.01). No significant difference was found between the mean values of the slopes of the dose-response curves of the two groups. End-expiratory oxygen concentration (FETO2) during air breathing decreased significantly from 13.7% to 12.0% at the point where methacholine dosage reached threshold. This study suggests that hyperoxia attenuates the bronchial responsiveness to methacholine in asthmatic patients.
Adolescent↗
[Pulmonary hemodynamics during exercise in anesthetized dogs with inspiratory loading and in patients with chronic obstructive pulmonary disease].
We studied 1) the effects of inspiratory elastic loading on pulmonary hemodynamics and pulmonary gas exchange with and without electrically induced hindlimb exercise in 8 anesthetized dogs, 2) pulmonary hemodynamics at rest and during single stage exercise on a supine cycle ergometer in 6 patients with chronic obstructive pulmonary disease (COPD) and 3) changes in P wave height in lead II of electrocardiogram during progressive exercise on a treadmill in 9 COPD patients. The pulmonary arterial pressure-flow relationship from resting to exercise was not affected by inspiratory elastic loading, but elastic loading accompanied by exercise increased alveolar-arterial O2 tension difference (AaDO2). The pulmonary arterial pressure-flow relationship in COPD from rest to exercise showed higher pulmonary vascular resistance than that in control group. Moreover, we found a greater increase in P wave height during exercise in COPD with decrease in PaO2 during exercise than in COPD without decrease in PaO2 during exercise. This increase in P wave height during exercise was inhibited by oxygen inhalation. We speculated that 1) increased AaDO2 during exercise with elastic loading may be due to increased shunt effects with low ventilation-perfusion ratio and 2) increased P wave height during exercise in COPD may be correlated with hypoxia during exercise and may be useful to detect latent cor pulmonale in COPD.
Aged↗
[Clinical assessment of uneven ventilation by factor analysis of Xe-133 washout scintigram].
Factor analysis (FA) was applied to 50 consecutive Xe-133 washout lung scintigrams, and its findings were compared with dynamic scintigrams of Xe-133 washout (DSW). Mean transit time (MTT) of radioactive xenon measured by FA also was compared with that measured by height/area (H/A) or two-compartment analysis (2CA). In 12 patients with normal DSW, FA separated and located two factors: one represented background activity, and the other uniform washout from the lung. In 31 out of 38 patients (82%) with abnormal DSW, FA separated the same areas where the washout was delayed on DSW. In 5 (13%) patients, FA diagnosed more areas of delayed washout than DSW. FA failed in 2 (5%) patients, but this failure was due to small number of counts of pixels. Diagnosis by FA was seemed easier than diagnosis by DSW in 95% of all patients by the authors' impression. MTT by FA (y) correlated with MTT by 2CA (x) in small groups of patients: in 9 patients in whom only one MTT was obtainable by FA (r = 0.75, p = 0.02, y = 4.2x + 1.9), and in 8 patients of normal DSW in whom two MTT's were obtainable by FA (r = 0.77, p = 0.02, y = 0.69x + 6.2, y; shorter MTT by FA between the two). MTT by FA did not correlate with MTT by H/A. In conclusion, FA is useful for diagnosing uneven Xe-133 washout from the lung.
Adolescent↗
Effects of N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate on the ventriculo-atrial conductivity of accessory pathways.
The purpose of this study was to examine the effects of N-(2,6-dimethylphenyl)-8-pyrrolizidineacetamide hydrochloride hemihydrate (SUN 1165), a newly developed antiarrhythmic agent belonging to class Ic, on the ventriculoatrial (VA) conductivity of accessory pathways and paroxysmal supra-ventricular tachycardia (PSVT). Twelve patients with accessory pathways were examined by standard electrophysiologic technique before and after a single oral dose of SUN 1165 (100 mg). 1 h after administration, SUN 1165 blocked VA conduction of the accessory pathway in six of twelve patients and prevented the induction of PSVT in six of seven cases. In the cases in which VA block did not occur, the VA interval prolonged (from 178 +/- 7 to 190 +/- 11 ms, p less than 0.05), and the effective refractory period of VA conduction was also increased (from 273 +/- 10 to 318 +/- 15 ms. p less than 0.05). SUN 1165 also prolonged the conduction time in normal conduction systems (AH and HV intervals and QRS duration), but the degree of the prolongation was moderate and not dangerous. There was no adverse effect. These results indicate that SUN 1165 is a potent and safe antiarrhythmic agent, and useful for preventing or stopping PSVT by blocking or depressing VA conduction through accessory pathways.
Administration, Oral↗
The use of the dose-response curve in the assessment of normal and asymptomatic asthmatic patients.
We studied bronchial reactivity, the slope of the dose-response curve to inhaled methacholine, in normal subjects (N), young asthmatics with normal respiratory resistance (Rrs) (YAL), young asthmatics with high Rrs (YAH), and old asthmatics with high Rrs (OAH) by three different methods: linear reactivity (slope of the linear cumulative dose-conductance (Grs = 1/Rrs) curve), timed reactivity (slope of the log concentration-Grs or time-Grs curve), and log reactivity (slope of the log cumulative dose-Grs curve). There were significant differences in linear reactivity between the N and the three asthmatics but no difference among the three asthmatic groups. On the other hand, both timed and log reactivities showed significant differences between the three asthmatic groups. Log and timed reactivities corrected by baseline Grs did not differentiate the YAL from the YAH but showed a significant difference between the YAH and OAH. This study suggests that timed and log reactivities may be better indices of bronchial reactivity than linear reactivity because they differentiate asthmatics, and that bronchial reactivity in asthmatics may be dependent on not only baseline airway caliber in asthmatics but also other factors such as atopic status or age.
Adult↗
The unfolded map using 201T1 myocardial SPECT.
The unfolded map is a new method to show the 201T1 distribution of left ventricle using SPECT. In 52 cases these maps were obtained at the stress study and 4 h later. The maximal count profiles of the perimeters for each short axis image were unfolded and were arranged from the apex to base of the left ventricle into a two dimensional map. All patients had chest pain and were suspected of coronary artery disease. The unfolded map had significant correlations between coronary arteriogram and exercise ECG findings. In conclusion, this method reflects the ischemic area of left ventricular myocardium, closer to the real left ventricular myocardium than Bull's eye display and is useful in the diagnosis of coronary heart disease.
Adult↗
Possible site of bronchodilation due to inhaled procaterol aerosol in asthmatic patients.
We studied the effective site of an inhaled aerosol of procaterol, a beta 2-selective adrenergic bronchodilator, in 8 asthmatic patients whose basal lung functions are almost within the normal range in both slow vital capacity (VC) and forced expiratory volume in one second (FEV1.0), and are free from asthmatic attack. In patients who had received procaterol 30 min after inhalation of aerosol, there was no significant change in VC, although FEV1.0, maximal expiratory flow at 50% VC (V50), maximal expiratory flow at 25% VC (V25) and maximal expiratory flow at 30% VC of partial maximal expiratory flow volume curve (V30p) improved significantly. On the other hand, in those who had received placebo, none of the parameters changed. Furthermore, R1 decreased and C0.5 increased significantly during the first 5 min after inhalation of procaterol aerosol. After an interval of 5 min, R1 did not change any further, while C0.5 continued to improve until 30 min after inhalation of procaterol. These results suggest that procaterol may first dilate the large airway and then may gradually dilate the small airway in bronchial asthma.
Adult↗
K channels of human alveolar macrophages.
The activation of macrophages has been reported to be associated with Ca-activated K permeability change. In order to study this permeability change in human alveolar macrophages, we examined alveolar macrophages electrophysiologically at a single channel level. We observed two types of Ca-activated K channel currents having conductances of 218 +/- 2 and 32 +/- 0.6 picosiemens in symmetrical 154 mmol/L KCl solutions. The characteristics, such as voltage dependency and Ca sensitivity, as well as channel conductance, were different between these two types of channel currents. Quinine (a blocker of Ca-activated K conductance), 0.5 mmol/L, reduced these channel currents by 45 +/- 8% and 31 +/- 8%. Quinine, 0.5 mmol/L, also inhibited chemiluminescence and leukotriene B4 release by 82 +/- 6 to 88 +/- 3% and 88 +/- 2%, respectively. These results suggest the presence of two types of Ca-activated K channels, which may be related to the release of inflammatory mediators from human alveolar macrophages.
Calcium↗
Effect of ketotifen on human alveolar macrophages.
In order to examine the possibility of human alveolar macrophages being an effector site of an antiasthmatic drug, we studied the effect of ketotifen on chemiluminescence and Ca-activated K conductance at single channel level because they are associated with the activation of macrophages. Peak chemiluminescence response, induced by a single concentration of phorbol myristate acetate (0.5 micrograms/ml), was inhibited by 28 +/- 3, 51 +/- 8, and 76 +/- 7% by ketotifen concentrations of 0.02, 0.12, and 0.24 mmol/L, respectively. The inhibition of chemiluminescence by ketotifen concentrations of 0.12 and 0.24 mmol/L was also observed in macrophages stimulated with zymosan activated serum (54 +/- 7 and 80 +/- 6%, respectively). Moreover, ketotifen, 0.24 mmol/L, inhibited Ca-activated K channel currents by 44 +/- 7% (large currents) and 48 +/- 13% (small currents). These results may explain, at least partly, antiasthmatic effects of ketotifen.
Acridines↗
Distribution of alpha-adrenergic bronchoconstriction in feline airways.
We studied the distribution of in vivo alpha-adrenergic bronchoconstriction roentgenographically and histologically as well as functionally, using 13 anesthetised, mechanically ventilated cats. We observed changes in airway diameter by employing tantalum bronchography and studied function by measuring pulmonary resistance (RL), static compliance (Cst), and dynamic compliance (Cdyn). alpha-adrenergic stimulation was produced by intravenous injection of norepinephrine (40 micrograms/kg) after administration of atropine (3 mg/kg, i.v.) and propranolol (2 mg/kg, i.v.). alpha-adrenergic stimulation produced a significant increase in RL (76.2 +/- 4.0 (mean +/- SE)%) and a significant decrease in Cst and Cdyn (23.7 +/- 2.2 and 27.9 +/- 4.2%, respectively). Tantalum bronchograms revealed that alpha-adrenergic stimulation produced a significant decrease in airways with bronchial diameter of 0.5-1.0 mm (9.5 +/- 3.7%). Histological study using a rapid-freezing technique with liquid nitrogen was added to ascertain the site of alpha-adrenergic bronchoconstriction, demonstrating bronchoconstriction in the airways from small bronchi to bronchioli, especially in bronchioli less than 0.5 mm in internal diameter. We conclude that alpha-adrenergic responsiveness can be observed roentgenographically and histologically as well as functionally in vivo, and that the main site of alpha-adrenergic responsiveness is bronchioli less than 1 mm in internal diameter.
Animals↗
[Rapid diagnosis of respiratory infection due to Streptococcus pneumoniae].
Explore the source record for details and available documents.
Agglutination Tests↗
Effects of qing-fei-tang (seihai-to) and baicalein, its main component flavonoid, on lucigenin-dependent chemiluminescence and leukotriene B4 synthesis of human alveolar macrophages.
A traditional Chinese remedy, Qing-Fei-Tang (Seihai-to, T90), has been used for treatment of chronic respiratory diseases with long-lasting cough and sputum, e.g. chronic bronchitis. We examined the effect of T90 and its main component flavonoid, baicalein, on the lucigenin-dependent chemiluminescence (CL) and leukotriene B4 (LTB4) synthesis of human alveolar macrophages (AM). AM were obtained by bronchoalveolar lavage from patients with various respiratory diseases, including sarcoidosis, idiopathic pulmonary fibrosis, bronchial asthma, chronic bronchitis and lung cancer. CL were observed by stimulating 1 x 10(5) AM with phorbol myristate acetate in the presence of lucigenin. LTB4 were generated by incubating 1 x 10(6)/ml AM with Ca ionophore A23187 for 30 min and determined by reverse phase high performance liquid chromatography and radioimmunoassay. T90 (0.2-2.0 mg/ml) and baicalein (0.1-100 microM) inhibited both CL and LTB4 production of AM in a dose-dependent fashion. These inhibitory effects were not due to cytotoxic effects of the procedure because neither 2 mg/ml T90 nor 100 M baicalein affected the viability of AM nor lactate dehydrogenase release from AM. These results suggest that T90 exerts its effect on inflammatory lung diseases through the anti-inflammatory action, i.e. inhibiting the oxidative and arachidonate metabolism of local inflammatory lung cells.
Acridines↗
Effects of airway anesthesia on ventilatory responses to graded dead spaces and CO2.
Ventilatory response to graded external dead space (0.5, 1.0, 2.0, and 2.5 liters) with hyperoxia and CO2 steady-state inhalation (3, 5, 7, and 8% CO2 in O2) was studied before and after 4% lidocaine aerosol inhalation in nine healthy males. The mean ventilatory response (delta VE/delta PETCO2, where VE is minute ventilation and PETCO2 is end-tidal PCO2) to graded dead space before airway anesthesia was 10.2 +/- 4.6 (SD) l.min-1.Torr-1, which was significantly greater than the steady-state CO2 response (1.4 +/- 0.6 l.min-1.Torr-1, P less than 0.001). Dead-space loading produced greater oscillation in airway PCO2 than did CO2 gas loading. After airway anesthesia, ventilatory response to graded dead space decreased significantly, to 2.1 +/- 0.6 l.min-1.Torr-1 (P less than 0.01) but was still greater than that to CO2. The response to CO2 did not significantly differ (1.3 +/- 0.5 l.min-1.Torr-1). Tidal volume, mean inspiratory flow, respiratory frequency, inspiratory time, and expiratory time during dead-space breathing were also depressed after airway anesthesia, particularly during large dead-space loading. On the other hand, during CO2 inhalation, these respiratory variables did not significantly differ before and after airway anesthesia. These results suggest that in conscious humans vagal airway receptors play a role in the ventilatory response to graded dead space and control of the breathing pattern during dead-space loading by detecting the oscillation in airway PCO2. These receptors do not appear to contribute to the ventilatory response to inhaled CO2.
Administration, Inhalation↗
VIP augments cholinergic-induced glycoconjugate secretion in tracheal submucosal glands.
Using isolated submucosal glands from feline trachea, we examined the effect of vasoactive intestinal peptide (VIP) on mucus glycoprotein secretion and glandular contraction by measuring released radiolabeled glycoconjugates and induced tension, respectively. VIP (10(-10) to 10(-6) M) produced a dose-dependent increase in [3H]glycoconjugate release of up to 300% of controls, which was inhibited by VIP antiserum and not inhibited by atropine, propranolol, or phentolamine. VIP at a low concentration (10(-9) M), which did not produce any significant increases over controls, produced a 2.4- to 5-fold augmentation of the glycoconjugate release induced by 10(-9) to 10(-7) M methacholine (MCh). Atropine or VIP antiserum abolished the augmentation. VIP did not produce any alteration in isoproterenol- or phenylephrine-evoked glycoconjugate secretion. VIP (up to 10(-5) M) did not produce any alteration in the tension, even when the gland had contracted with MCh, or any augmentation of contraction induced by MCh (10(-9) to 10(-7) M). These results indicate that VIP induces mucus glycoprotein release from secretory cells and also that it potentiates the secretion induced by cholinergic stimulation.
Animals↗
Influences of pressure surrounding the heart and intracardiac pressure on the diastolic coronary pressure-flow relation in excised canine heart.
We investigated the change in the instantaneous diastolic left coronary pressure-flow relation (DPFR) when the pressure surrounding the heart (SHP), right heart pressure (RHP), and left heart pressure (LHP) were systematically varied. Eight excised and maximally vasodilated canine hearts placed in an air-tight chamber were used. To obtain a capacitance-free DPFR, coronary perfusion pressure was slowly decreased (about 2 mm Hg/sec) during a prolonged diastole. The zero-flow pressure (Pf = 0) and the slope of the DPFR were analyzed. The mean values of the slope did not change significantly throughout the interventions. The mean value of Pf = 0 in the control state (SHP = RHP = LHP = 0 mm Hg) was 6.0 +/- 2.0 mm Hg (mean +/- SD, n = 8), significantly higher than the venous outflow pressure, RHP (p less than 0.001), and the other two pressures (p less than 0.001). When SHP was raised to 15 and 30 mm Hg, while the other pressures remained at 0 mm Hg, the mean values of Pf = 0 increased to 20.9 +/- 2.4 and 35.6 +/- 3.1 mm Hg (p less than 0.001 and p less than 0.0005, respectively, vs. control). The mean values of Pf = 0 when only RHP was elevated to 15 and 30 mm Hg were 16.0 +/- 1.5 and 29.3 +/- 1.5 mm Hg (p less than 0.001 and p less than 0.0005 vs. control). On elevation of LHP to 15 and 30 mm Hg, the mean values of Pf = 0 were 12.0 +/- 2.8 and 17.3 +/- 3.6 mm Hg (p less than 0.01 and p less than 0.01 vs. control). When both SHP and LHP were almost evenly elevated to about 15 and 30 mm Hg, the mean values of Pf = 0 were raised to 22.0 +/- 2.9 and 35.3 +/- 3.2 mm Hg, respectively. These mean values were not significantly different from those when only SHP was elevated to the comparable levels. The observation that Pf = 0 exceeded RHP in the control state and that RHP, which was elevated above the preceding Pf = 0, was identical with the present Pf = 0 supports the vascular waterfall mechanism when RHP is low. Furthermore, the evidence that the degree of DPFR shift was almost linearly dependent on the SHP level rather than on the LHP level indicates that the pressure on the epicardial side is one of the factors that determines the pressure at the top of the vascular waterfall.
Animals↗