[Ultrastructural observations on human bronchial mucosa associated with chronic respiratory infections].
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Biomedical subjects
Publications and source records attributed to S Yasui.
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Smooth pursuit and saccadic components of foveal visual tracking as well as more involuntary ocular movements of optokinetic (o.k.n.) and vestibular nystagmus slow phase components were investigated in man, with particular attention given to their possible input-adaptive or predictive behaviour. Each component in question was isolated from the eye movement records through a computer-aided procedure. The frequency response method was used with sinusoidal (predictable) and pseudo-random (unpredictable) stimuli. When the target motion was pseudo-random, the frequency response of pursuit eye movements revealed a large phase lead (up to about 90 degrees) at low stimulus frequencies. It is possible to interpret this result as a predictive effect, even though the stimulation was pseudo-random and thus 'unpredictable'. The pseudo-random-input frequency response intrinsic to the saccadic system was estimated in an indirect way from the pursuit and composite (pursuit + saccade) frequency response data. The result was fitted well by a servo-mechanism model, which has a simple anticipatory mechanism to compensate for the inherent neuromuscular saccadic delay by utilizing the retinal slip velocity signal. The o.k.n. slow phase also exhibited a predictive effect with sinusoidal inputs; however, pseudo-random stimuli did not produce such phase lead as found in the pursuit case. The vestibular nystagmus slow phase showed no noticeable sign of prediction in the frequency range examined (0 approximately 0.7 Hz), in contrast to the results of the visually driven eye movements (i.e. saccade, pursuit and o.k.n. slow phase) at comparable stimulus frequencies.
We administered 1 mg of purified porcine elastase per 100 g body weight intraperitoneally twice weekly to male rats during the first 4 wk of life. This altered the structure of the lungs so that the proportion of alveolar duct air (the "core" of air internal to the mouths of alveoli in alveolar ducts) increased and the proportion of alveolar air decreased. The alveolar surface-to-volume ratio was decreased, and the lungs had too few alveoli. The lungs were also hyperexpandable, containing more air and saline per gram of lung tissue. No biochemical alterations were noted in elastin or collagen content in elastase-treated animals. In a separate experiment, we showed that elastaselike activity appears in the blood 1 h after intraperitoneal injection of elastase and, although low, was still significantly raised 24 h after injection. We feel that elastase has interfered with lung growth and alveolar development by altering mainly the elastin in the collagen-elastin network. Intraperitoneal elastase injection at the time of active elastin synthesis and alveolar multiplication may be a suitable model to test the hypothesis that lungs injured in infancy may be more susceptible to damage in later life.
QRST isointegral maps were made from 87 body surface ECGs in 41 patients with prior myocardial infarction. To evaluate the abnormalities of QRST isointegral maps, a deviation map was constructed from a deviation index, which expressed the deviation of the QRST time-integral value from the normal value at each lead point. Patients were divided into 3 groups according to the asynergic site on left ventriculograms: patients with anterior wall asynergy (n = 13), those with inferior wall asynergy (n = 13) and those with both anterior and inferior asynergies (n = 15). A consistent deviation map pattern was obtained in each group regardless of the QRS duration. Consequently, the deviation map was considered to be a practical method of identifying the asynergic site in patients with myocardial infarction, especially in those with intraventricular conduction disturbances. It is suggested that the deviation map can reveal abnormally altered intrinsic ventricular recovery properties resulting from a loss of the electromotive force of the infarcted myocardium.
In order to investigate the electrocardiographic changes in patients with chronic pulmonary emphysema (CPE), 87 unipolar electrocardiograms were simultaneously recorded in 20 normal subjects and 22 patients with CPE. The voltages and the sites of Max. R (most positive R) and Max. S (most negative S) in these 87 leads were investigated. Further, the voltages and the sites of the maximum and the minimum on isopotential maps during the QRS period were examined. In patients with CPE, the sites of Max. R, Max. S, the maximum and the minimum were all positioned lower than in normal subjects. However, the voltages of Max. R and Max. S in CPE were not significantly different from those in normal subjects. It was considered that the most prominent change in the body surface maps in CPE was the downward shift of potential distribution. This change seems to be due mainly to the downward displacement of the diaphragm and the heart resulting from the overinflation of the lung.
Body surface mapping was used to study the effects of diltiazem on exercise-induced QRS amplitude changes in 7 patients with stable effort angina pectoris. Body surface areas showing R or S amplitude changes (greater than 0.2 mV) after treadmill exercise were calculated. After the administration of 90 mg of diltiazem, the R increased area was significantly smaller than that without diltiazem (p less than 0.02), although the same workload was performed. It was suggested that diltiazem diminished the exercise-induced myocardial ischemia and this improvement of ischemia resulted in the reduction of the R increased area after exercise.
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Trapidil (Rocornal) is clinically used as a coronary vasodilator and inhibitor of coagulation of the platelet. Recently trapidil has been reported to have a bronchodilatory action in excised dog's tracheal smooth muscle. In the present study the bronchodilatory effects of trapidil were investigated in man. For 21 patients with asthma, 6 patients with emphysema and 2 patients with chronic bronchitis, 100 mg of trapidil was infused intravenously. Subjects were divided into two groups. Group I was infused for about 30 min and Group II for about 10 min. After administration of trapidil, forced vital capacity increased in both groups (p less than 0.01), forced expiratory volume at 1.0 s (p less than 0.01) and peak expiratory flow rate (p less than 0.05) increased in Group II. Respiratory resistance decreased (p less than 0.01) in Group II. From these results, it was confirmed that trapidil has bronchodilatory effect. We think trapidil is useful for the treatment of the patients not only with ischemic heart disease but with chronic obstructive lung disease.
To estimate the location and size of myocardial infarction (MI), an isointegral mapping technique was adopted from among various body surface electrocardiographic mapping techniques. QRS isointegral and departure maps were made in 35 patients with MI. These patients were separated into 3 groups, based on the location of MI: anterior, inferior, and anterior plus inferior. The severity and location of MI were estimated by thallium-201 myocardial perfusion imaging and the degree of scintigraphic defect was represented by a defect score. The extent of MI was expected to be reflected on the QRS isointegral maps as a distribution of negative QRS complex time-integral values. However, the extent and the location of MI were hardly detectable by the original maps. A departure mapping technique was then devised to observe the distribution of departure index on the body surface. Particular attention was given to the area where the departure index was less than -2, and this area was expected to reflect the location and size of specific abnormality of isointegral map due to MI. There were strong correlations between departure area and defect score in the anterior and inferior MI cases (r = 0.88 and r = 0.79, respectively). However, patients with anterior MI plus inferior MI showed no such correlation. Q-wave mapping was compared with QRS isointegral mapping, and QRS isointegral mapping was found to be more accurate in the estimation of the location and size of MI than Q wave mapping. Thus, QRS isointegral mapping, especially departure mapping, is more useful and convenient for detecting the location and size of MI than methods such as isopotential and Q wave mapping.
To ascertain whether the long cardiac pauses on the Holter ECGs of patients with the sick sinus syndrome were related to the spontaneously occurring overdrive suppression, the heart rates for the 12 seconds preceding the cardiac pauses longer than 5 seconds were compared with that averaged for 24 hours. Even in six out of seven patients with bradycardia-tachycardia syndrome the former rate was not significantly greater than the latter, indicating that episodes of such long cardiac pauses may not result from spontaneously occurring overdrive suppression. This observation was also consistent with the result that no statistically significant correlation was obtained between the maximum pauses measured from Holter ECGs of sick sinus syndrome and those obtained by the overdrive suppression test. In conclusion, many episodes of long life-threatening cardiac pauses observed in sick sinus syndrome may be attributed to accidental depression of the sinus nodal and subsidiary pacemaker activity rather than to spontaneously occurring overdrive suppression; therefore, Holter monitoring may be useful as an additional tool for diagnosis of sick sinus syndrome.
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In 38 patients with angina pectoris, 87 unipolar lead electrocardiograms were recorded from different sites over the entire thoracic surface both before and after submaximal treadmill exercise. The site of exercise-induced ST depression on the body surface was correlated with the findings of the coronary arteriography. The number of leads which showed exercise-induced ST depression was 7.2 +/- 1.8 in one vessel disease, 15.6 +/- 2.1 in two vessel disease, and 23.6 +/- 2.0 in three vessel disease (values are mean +/- SEM). Thus, the number of leads showing ST depression was proportional to the severity of the coronary artery disease. Exercise-induced ST depression was most often seen in left anterior chest leads, especially in V5 of the standard 12-ECG. However, it was not possible to identify the obstructed coronary artery from the body surface distribution of ST depression.
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