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Biomedical subjects

K Shirato

Publications and source records attributed to K Shirato.

At least 253 records · Page 14Linked to original sources
PubMed1993

Decrease in beta-adrenergic receptors of lymphocytes in spontaneously occurring acute asthma.

To clarify changes in beta-adrenergic receptor (BAR) density in spontaneously occurring acute asthma, BAR binding studies were performed on peripheral blood lymphocytes in eight asthmatic and ten normal subjects. Spirometry also was performed. Maximum binding capacity (Bmax) of BAR in acute asthma was significantly lower by 44.2 percent compared with that in stable asthma; FEV1/FVC ratio decreased by 23.9 percent. The Bmax for acute asthma also was significantly lower than that in normal subjects. The Bmax of BAR in all subjects was significantly correlated with FEV1/FVC ratio and percent FEV1. The percentage decrease in the FEV1/FVC ratio and FEV1 from the stable to acute state for each asthmatic subject did not correlate with corresponding percentage decrease in Bmax. These data demonstrate that BAR density of lymphocytes decreases substantially in acute asthma and, simultaneously, suggest that some factors other than the BAR mechanism contribute to the airway obstruction during acute asthma.

Acute Disease↗
PubMed1993

Effects of changes in afterload on regional wall motion in acute ischemic canine heart.

The aim of the present study was to examine effects of changes in afterload on regional myocardial motion in acute ischemia. Ischemic and non-ischemic segment lengths of the left ventricular free wall were measured by miniature ultrasonic gauges in eleven open chest dogs with the pericardium preserved. In a stable state after left anterior descending coronary artery occlusion, peak left ventricular pressure was varied by the infusion of angiotensin II (n = 8) and sodium nitroprusside (n = 8). To exclude effects of preload on the responses, end-diastolic lengths of the non-ischemic region before and during infusion of each drug were matched with vena caval occlusion. When peak left ventricular pressure elevated from 113 +/- 2 (mean +/- S.E.)mmHg to 145 +/- 6, in isovolumetric contraction phase, degree of active shortening in the non-ischemic region and that of paradoxical expansion of the ischemic region did not change. In ejection phase, active shortening of the non-ischemic region decreased from 1.38 +/- 0.11 mm to 1.06 +/- 0.10 but that of the ischemic region remained unchanged. Stroke volume decreased from 14.5 +/- 1.3 ml to 10.8 +/- 1.0. When peak left ventricular pressure decreased from 111 +/- 4 mmHg to 101 +/- 6, in isovolumetric contraction phase, active shortening of the non-ischemic region decreased from 0.90 +/- 0.13 mm to 0.76 +/- 0.15 and paradoxical expansion of the ischemic region reduced from -0.95 +/- 0.11 mm to -0.80 +/- 0.11. In ejection phase, shortening of the non-ischemic region increased from 1.05 +/- 0.13 mm to 1.31 +/- 0.15 but that of the ischemic region did not change. Stroke volume increased from 11.5 +/- 1.3 ml to 14.0 +/- 1.4. These results indicate that in acute ischemia, changes in isovolumetric shortening of the non-ischemic region and paradoxical expansion of ischemic region are related with each other in isovolumetric contraction phase when afterload is altered and suggest that stroke volume is affected by the shortening of ejection phase in the non-ischemic region.

Angiotensin II↗
PubMed1993

Small airway involvement in mixed connective tissue disease.

We studied pulmonary functions in 17 female patients with mixed connective tissue disease (MCTD) to detect early pulmonary involvement in this disease; in 8 of the 17 patients follow-up studies were also performed at 1.2- to 5.9-year intervals. In the first pulmonary function tests, decreases in vital capacity (VC) and diffusing capacity (DLCO) were observed in 6 (35%) and 8 (47%) patients, respectively. The ratio of forced expiratory volume in one second to VC was normal in all the patients, but pulmonary resistance and static compliance were abnormal in 6 (35%) and 10 (59%) patients, respectively. However, frequency dependence of dynamic compliance was found in all 16 patients tested. Moreover, 4 (24%) of the 17 patients had normal DLCO and DLCO-to-alveolar volume ratio (DLCO/VA). Reductions in DLCO and DLCO/VA were significantly correlated with the disease duration. These results suggest that small airway obstruction is an early and frequent indication of functional pulmonary impairment, and that impairment of alveolar gas exchange is progressive in patients with MCTD.

Adolescent↗
PubMed1993

[Neurogenic inflammation].

Airway neurogenic inflammation is caused by neuropeptides released from airway sensory nerves, and may be involved in the pathogenesis of asthma. Airway sensory nerves are stimulated by chemical mediators such as bradykinin and leukotrienes, hyperventilation and cigarette smoke. Presynaptic modulation of airway sensory nerves by opioids, histamine H3-agonists, NPY, and potassium channel openers is effective in the control of neurogenic inflammation. Tachykinin receptor antagonists also inhibit airway neurogenic inflammation. Recently, we have demonstrated that pretreatment with a tachykinin receptor antagonist can protect against bradykinin-induced airway narrowing in asthmatic patients. This evidence indicates that endogenously released tachykinins have a functional role in the airways of asthmatics.

Asthma↗
PubMed1993

[Induction of granule release by intracellular application of Ca and GTP gamma S in human eosinophils].

The roles of Ca and G proteins in granule release from human eosinophils were examined using a patch-clamp technique in single cells. The morphological changes and the release of eosinophil peroxidase (EPO) from single cells were simultaneously observed. The intracellular application of Ca, and GTP-gamma-S induced fusion of EPO containing granules with the surface membrane which was associated with a marked increase in membrane capacitance. Ca alone caused a rapid granule release at an early stage of cell dialysis, but most granules still remained in a cluster. GTP-gamma-S alone caused a gradual degranulation. Northern blot analysis revealed the definite expression of smg p21 mRNA with no appreciable expression of smg p25A in human eosinophils.

Calcium↗
PubMed1992

Differences in myocardial fluoro-18 2-deoxyglucose uptake in young versus older patients with hypertrophic cardiomyopathy.

The purpose of this study was to determine whether regional myocardial glucose use in patients diagnosed as having hypertrophic cardiomyopathy (HC) at a younger age differs from that in those diagnosed at middle to old age. Sixteen patients with HC (group 1 aged less than 40 years (n = 8); group 2 aged greater than 40 (n = 8) were studied using positron emission tomography and fluoro-18 2-deoxyglucose (FDG). All patients were diagnosed as having HC within 6 years of the study. Contiguous regions of interest were selected circumferentially on each cross-sectional image of the left ventricular wall. In each region of interest, % FDG fractional uptake was calculated. In each patient, % left ventricular FDG fractional uptake was determined as a mean value of % FDG fractional uptake in each region of interest. Moreover, as a measure of nonhomogeneity, the % interregional coefficient of variation in FDG fractional uptake was calculated in each patient. Whereas % left ventricular FDG fractional uptake did not differ between the 2 groups, the % interregional coefficient of variation in FDG fractional uptake was increased in group 1 compared with that in group 2 (11.5 +/- 3.6 vs 7.4 +/- 1.6%; p less than 0.02). Interventricular septum/left ventricular posterior wall thickness ratio and total counts in cross-sectional image did not differ between the 2 groups. These data suggest that patients diagnosed as having HC at a younger age have more nonhomogeneous myocardial metabolic characteristics than do patients diagnosed at middle or old age, and support the notion that HC in the young may be different from that in the middle-aged or elderly.

Adolescent↗
PubMed1992

Maximum stress-volume index ratio of the left ventricle in hypertrophic cardiomyopathy.

To evaluate the left ventricular contractile state in patients with nonobstructive hypertrophic cardiomyopathy (HCM), we analyzed the maximum stress-volume index ratio (MSVR) using catheter-tip cineangiography in 11 patients with HCM and 16 normal subjects. The value of the MSVR in normal subjects was 6.48 +/- 1.25 kdyn/cm5/m2 (mean +/- SD) and we defined the range of the mean +/- 2 SD as the normal MSVR range. Six patients with HCM placed inside the normal MSVR range (IN), but the other 5 patients placed outside and to the right of the normal range (RIGHT). This suggests that the contractile states of the patients of the RIGHT group were depressed. Compared with IN, the end-diastolic and end-systolic volume indices of RIGHT were larger (EDVI; 69.3 +/- 6.9 vs. 96.1 +/- 11.1 ml/m2, p less than 0.01, ESVI; 18.2 +/- 3.2 vs. 29.1 +/- 8.3 ml/m2, p less than 0.05), but the ejection fraction did not differ (IN 73.5 +/- 5.7 vs. RIGHT 69.6 +/- 8.3%, NS). End-diastolic pressure of IN and RIGHT was higher than that of normal subjects (IN 16.5 +/- 4.5, RIGHT 16.7 +/- 4.6 vs. 8.3 +/- 2.5 mm Hg, both p less than 0.05), but there was no difference between the two groups in HCM. End-systolic pressure did not differ among the three groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

P wave height during incremental exercise in patients with chronic airway obstruction.

We examined changes in P wave height in lead 2 of an ECG obtained during progressive exercise in 23 patients with COPD, and measured both P wave changes and pulmonary hemodynamics during exercise at a constant workload corresponding to approximately 50 to 60 percent of VO2 max in nine patients. The P wave response to exercise (delta P/delta VO2, %/ml/min), estimated by the relationship between percentage of change in P wave height and VO2, was significantly greater (p less than 0.01) in 15 patients who had a decrease in PaO2 with exercise (group A) than eight patients who did not have a fall in PaO2 with exercise (group B). There was a significant negative correlation between change in PaO2 and change in P wave height from rest to maximal exercise (r = -0.68, p less than 0.001). Oxygen therapy in nine patients in group A reduced the increase in P wave height during exercise. Furthermore, change in P wave height from rest to exercise correlated significantly with that of mean pulmonary artery pressure (r = 0.75, p less than 0.01). These results suggest that increase in P wave height during exercise in COPD patients is related partly to oxygen desaturation during exercise, and continuous measurement of P wave change may be useful for noninvasively predicting the pulmonary vascular pressure response to exercise.

Aged↗
PubMed1991

Influence of reduced presynaptic myocardial norepinephrine stores on left ventricular contractility.

Many investigators have reported that myocardial norepinephrine content is decreased in congestive heart failure. However there have been no studies of how decrease in myocardial norepinephrine might influence myocardial contraction. To clarify whether decreased myocardial norepinephrine per se affects myocardial contraction, we observed the change in left ventricular contractility during 30 min of left stellate ganglion stimulation in control and acutely reserpinized dogs. We obtained left ventricular max dp/dt and left ventricular end-systolic pressure-segment length relationships as indicators of left ventricular contractility. Both parameters decreased after left stellate ganglion stimulation in reserpinized dogs (left ventricular max dp/dt: 2064 +/- 200 to 1608 +/- 168 mmHg/s, left ventricular end-systolic pressure-segment length slope 117 +/- 22 to 79 +/- 14 mmHg/mm, n = 8, P less than 0.05), while they did not change in controls. In reserpinized dogs, left ventricular norepinephrine content decreased to one-third that of controls before the stimulation, and further decreased after stimulation. These data indicate that lowered myocardial norepinephrine itself may be responsible for the negative effect on left ventricular contractility in congestive heart failure.

Animals↗
PubMed1991

Responses of atrium and ventricle to sustained sympathetic nerve stimulation.

To determine whether chronotropic and atrial inotropic responses to sympathetic nerve stimulation are maintained longer than ventricular inotropic response, the present study was performed with control and acute reserpinized dogs. We stimulated the right stellate ganglion of both groups supramaximally for 60 min and compared right atrial responses (chronotropism and inotropism) with left ventricular (LV) dP/dtmax. In the control group, heart rate (HR) immediately increased and was only slightly attenuated with 60 min of stimulation, and right atrial (RA) inotropic response was less attenuated than was LV response (7% in HR, 33% in RA dP/dtmax, 50% in LV dP/dtmax, P less than 0.01, from the peak value of each response). RA and LV norepinephrine (NE) content was decreased by the stimulation but remained higher than the LV control value. In the reserpinized group, NE content in the RA was low before the stimulation and was further decreased by the stimulation. In this group, HR response was attenuated (27% in HR, P less than 0.01) as was LV dP/dtmax, and the difference in contractile responsiveness between atrium and ventricle disappeared (58% in RA dP/dtmax vs. 61% in LV dP/dtmax, NS). The results indicate that the chronotropic response was only slightly attenuated and that the atrial contractile response was attenuated less than the ventricular response, with sustained sympathetic nerve stimulation in the normal heart. This can be ascribed to the much higher NE content in the RA than that in the LV.

Animals↗
PubMed1991

Vibration analysis of the human left ventricular posterobasal wall at the moment of the first heart sound emission.

We examined whether human left ventricular (LV) wall vibration at the first heart sound emission (LVvibr) could be a potential source of information about the left ventricular physical properties, as has been demonstrated by experimental forced vibration studies. LV posterobasal wall vibration in 51 subjects characterized by functional murmur (n = 13), mitral stenosis (n = 8), hypertrophic cardiomyopathy (HCM, n = 8), ischemic heart disease with old myocardial infarction (n = 12) and without prior infarction (n = 10), was detected with a miniature intraesophageal vibration sensor. Peak frequency, sharpness and peak power of LVvibr in patients with functional murmur and mitral stenosis were linearly related to the Q-vibration interval. HCM patients showed a higher peak frequency and sharper configuration in the power spectrum. However, differing from previous reports, we found no characteristic difference in configuration of power spectrum in patients with ischemic heart disease. These results suggest that human LVvibr possibly includes information demonstrated by experimental forced vibration analysis.

Adolescent↗
PubMed1991

Effect of pericardium on regional myocardial systolic function in acute ischemia.

To know whether or not the pericardium affects regional myocardial systolic function in acute ischemia, we measured ischemic and non-ischemic segment lengths of the left ventricle using ultrasonic crystals in 10 open-chest dogs with the pericardium preserved. When the left ventricular pressure and segment lengths were stable after left circumflex coronary occlusion, we opened the pericardium widely. After coronary occlusion, end-diastolic length (EDL) in ischemic and non-ischemic segments increased, and the ischemic segment showed paradoxical systolic expansion while the non-ischemic segment increased its active shortening. After pericardiectomy, heart rate, left ventricular systolic pressure, and peak positive and negative dP/dt did not change. EDL in ischemic and non-ischemic segments further increased from 12.02 +/- 0.18 to 12.50 +/- 0.16 mm (mean +/- S.E., p less than 0.01) and from 11.12 +/- 0.20 to 11.45 +/- 0.18 mm (p less than 0.05), respectively, despite the concomitant fall in left ventricular end-diastolic pressure (LVEDP) from 12.4 +/- 0.6 to 10.6 +/- 0.8 mmHg (p less than 0.01). End-systolic length in ischemic and non-ischemic segments also increased from 12.37 +/- 0.25 to 12.70 +/- 0.20 mm (p less than 0.05) and from 8.50 +/- 0.13 to 8.74 +/- 0.13 mm (p less than 0.01), respectively, although the left ventricular end-systolic pressure did not change. Maximum expanded systolic length of the ischemic segment also increased from 12.99 +/- 0.20 to 13.42 +/- 0.16 mm (p less than 0.01). These results indicate that, in acute ischemia, the pericardium inhibits paradoxical systolic expansion of the ischemic region and increase in end-systolic length of non-ischemic segment. Thus, it is concluded that the pericardium modifies the regional myocardial systolic function in acute ischemia, perhaps through the mechanical restraint of the pericardium.

Animals↗
PubMed1990

Left ventricular end-systolic stress-volume index ratio in aortic and mitral regurgitation with normal ejection fraction.

To evaluate the left ventricular contractile state in regurgitant valvular disease with normal ejection fraction, we analyzed the end-systolic stress-volume index relationship (ESSVR) by means of cineangiography in 15 normal subjects, 11 patients with aortic regurgitation (AR), and 10 patients with mitral regurgitation (MR) whose ejection fraction (EF) was 60% or more. The end-systolic stress-volume index ratio in normal subjects was 5.57 +/- 0.60 kdyne/cm5/m2 (mean +/- standard deviation), and we defined the range including +/- 2 standard deviations of the ratio as the normal ESSVR range. Six patients with AR and five patients with MR placed inside the normal ESSVR range, termed AR IN and MR IN, but the remaining five patients with AR and MR placed to the right of the normal range, termed AR OUT and MR OUT. EF did not differ between patients with AR IN and AR OUT (69.4 +/- 5.4 verus 70.7 +/- 6.1%) and between MR IN and MR OUT (71.6 +/- 3.6 versus 71.1 +/- 7.9%). The EF of the subdivided groups with AR and MR also did not differ from that of normal subjects (70.7 +/- 7.3%). This finding showed that the left ventricular contractile state was depressed in patients with AR OUT and MR OUT despite a normal EF. In AR and MR the end-systolic stress and end-systolic volume index of OUT did not differ from those of IN, but the end-diastolic volume index of OUT was larger than that of IN (AR OUT 156.8 +/- 27.9 versus AR IN 110.8 +/- 24.1 ml/m2, MR OUT 160.5 +/- 44.7 versus MR IN 101.0 +/ 16.6 ml/m2; both p less than 0.05), and the regurgitant fraction of OUT was higher than that of IN (AR OUT 52.6 +/- 13.6 versus AR IN 29.7 +/- 13.3%, MR OUT 52.9 +/- 10.2 versus MR IN 30.2 +/- 11.4%; both p less than 0.05). In addition, there was a linear inverse correlation between the end-systolic stress-volume index ratio and the end-diastolic volume index in all subjects (r = -0.82, n = 36). In normal subjects there was a linear inverse correlation between end-systolic stress and the EF (r = -0.91, n = 15), but this relationship failed to separate patients with OUT from those with IN. Results of the present study suggest that some patients with AR and MR whose EF was normal had a depressed contractile state, and these patients had a large end-diastolic volume index and a high regurgitant fraction.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1990

Three-dimensional quantitative coronary angiography.

A method for reconstructing the three-dimensional coronary arterial tree structure from biplane two-dimensional angiographic images is presented. This method exploits the geometrical mathematics of X-ray imaging and the tracking of leading edges of injected contrast material into each vessel for identification of corresponding points on two images taken from orthogonal views. Accurate spatial position and dimension of each vessel in three-dimensional space can be obtained by this reconstruction procedure. The reconstructed arterial configuration is displayed as a shaded surface model, which can be viewed from various angles. Such three-dimensional vascular information provides accurate and reproducible measurements of vascular morphology and function. Flow measurements are obtained by tracking the leading edge of contrast material down the three-dimensional arterial tree. A quantitative analysis of coronary stenosis based on transverse area narrowing and regional blood flow, including the effect of vasoactive drugs, is described. Reconstruction experiments on actual angiographic images of the human coronary artery yield encouraging results toward a realization of computer-assisted three-dimensional quantitative angiography.

Algorithms↗
PubMed1989

Change in P wave height during progressive exercise in patients with chronic obstructive pulmonary disease.

We examined changes in P wave height in lead II of electrocardiogram during progressive exercise in patients with chronic obstructive pulmonary disease (COPD), and obtained the slope (delta P/delta VO2, %/ml/min) of the regression line calculated from the relationship between percent change of P wave height and oxygen consumption (VO2). Four COPD patients, who had a decrease over 5 mmHg in arterial oxygen tension (PaO2) at maximal exercise (group A), had significantly greater slope (0.45 +/- 0.14%/ml/min, mean +/- S.E.) than in five COPD patients (group B, 0.14 +/- 0.05), who did not have a decrease over 5 mmHg in PaO2 at maximal exercise. The increase in P wave height during exercise was inhibited by oxygen inhalation at the given VO2 in group A. These findings suggest that increase in P wave height during exercise in COPD patients may be correlated with hypoxemia during exercise.

Adult↗
PubMed1989

Effects of verapamil and BAY K 8644 on the hypoxic contraction of the isolated human pulmonary artery.

To examine the effect of hypoxia on the human pulmonary artery (HPA), HPA segments (2 mm, o.d.) were suspended and changes in isometric force with hypoxia (PO2 = 44 +/- 3 mmHg, mean +/- S.E.) were measured. HPA contracted with hypoxia and the tension developed with 15 min of hypoxia was 127 +/- 36 (mean +/- S.E.) mg. Verapamil at 47 +/- 10% 10(-6) M inhibited and 10(-6) M BAY K 8644 enhanced the hypoxic response by (p less than 0.01) and 396 +/- 106% (p less than 0.05), respectively, compared with preceding values. These results show that activation of voltage-dependent Ca2+ channels also plays an important role in the mechanism of hypoxic pulmonary vasoconstriction in man.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1989

[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↗