Biomedical subjects

K Shirato

Publications and source records attributed to K Shirato.

At least 235 records · Page 13Linked to original sources

PubMed1994

Oxygen consumption of respiratory muscles in patients with COPD.

We measured the oxygen consumption (VO2) of respiratory muscles in 8 COPD patients and 12 age-matched healthy subjects using a closed circuit device which allows a continuous increase in external dead space and is equipped with a 9-L Collins spirometer. Furthermore, we measured simultaneously mouth occlusion pressure at 0.1 s of inspiration (P0.1), minute ventilation (VE), and other ventilatory parameters during the measurement of total VO2 (VO2 tot). We found that the logarithm of VO2tot (logVO2tot) had a good correlation with VE in both groups. The mean slope of the regression line of logVO2tot and VE (delta logVO2tot/delta VE) of COPD patients was significantly higher than that of normal subjects (p < 0.001). However, the mean Y-intercept (metabolic VO2[VO2met]) of the regression lines did not differ between the two groups. The P0.1 in COPD patients was higher than that in normal subjects at the corresponding dead space loading. However, the VE did not differ between the two groups except for at rest and the first 1 min after dead space loading. These results suggest that the VO2 of respiratory muscles in patients with COPD is higher at given ventilation compared with that in age-matched normal subjects and that this increased VO2 partly may be due to an augmented ventilatory drive.

Aged↗

PubMed1994

Upper airway muscle activity during REM and non-REM sleep of patients with obstructive apnea.

We measured electromyograms (EMGs) of genioglossus muscle (GG) and inspiratory intercostal muscle (IIM) in both rapid eye movement (REM) sleep and non-REM sleep of 12 patients with obstructive sleep apnea (OSA) to examine the influence of different sleep stages on upper airway muscle activity during sleep apnea. Quantifications of both muscle activities were assessed by their individual peak amplitude of integrated inspiratory EMG. Genioglossus and IIM activities showed a qualitatively similar cyclic change with an alteration of apneic and ventilatory phases during both non-REM and REM sleep. Both muscle activities increased gradually in the late apneic phase and reached each peak at the opening of the upper airway and, subsequently, decreased gradually. There were no significant differences in both muscles activities in either the ventilatory or early apneic phase between non-REM sleep and REM sleep. On the other hand, GG and IIM activities in the late apneic phase during REM sleep were significantly lower than those during non-REM sleep. The relative activity of GG to IIM in the late apneic phase was significantly lower during REM sleep than that during non-REM sleep. These results indicate that upper airway and intercostal muscle activation in the later apneic phase during REM sleep were inhibited compared with those during non-REM sleep and that this inhibition was observed predominantly in upper airway muscles.

Adult↗

PubMed1994

Effects of unilateral phrenic nerve denervation on diaphragm contractility in rat.

We examined the early effects of phrenic nerve denervation on the diaphragm muscle 1, 3, 7 and 14 days after unilateral denervation in rats. In the denervated hemidiaphragms, force frequency curves at 3, 7 and 14 days decreased significantly by 51%, 50% and 38% respectively of the peak tension of the force frequency curves of the diaphragms of rats with sham operation. Twitch tensions increased significantly at 14 days, and contraction times and half relaxation times slowed significantly at 3, 7 and 14 days. The tensions of denervated diaphragms at 5 min during the fatigue runs was significantly increased at 14 days. As determined by histological staining, the mean cross sectional area of fast-twitch fibers (type II) decreased significantly from 2,742 (sham) to 1,599 microns (14 days), but that of the slow-twitch fibers (type I) did not change significantly during the same period. These findings suggest that, during the first two weeks of denervation, fast twitch fibers (type II) atrophy more rapidly than slow twitch fatigue resistant fibers (type I), as confirmed by the contractile properties and histological findings.

Adenosine Triphosphatases↗

PubMed1994

Bronchoalveolar lavage as a possible cause of acute exacerbation in idiopathic pulmonary fibrosis patients.

In the past 13 years (1980 to 1992), bronchoalveolar lavage (BAL) was performed on 124 idiopathic pulmonary fibrosis (IPF) patients (29 F and 95 M, 60 +/- 1 years, mean +/- S.E.) at Tohoku University Clinic and Hospital. Among them, three patients showed acute exacerbation immediately after BAL and died of progressive respiratory failure after 2.5 weeks, 2 months and 3.5 months, respectively, despite intensive care. They were all older patients (79, 74 and 66 years old) and we failed to find any evidence of viral, bacterial or fungus infections either before or after BAL in blood, sputum or BAL fluid samples. Further, all autopsied lungs showed interstitial pneumonia and fibrosis and no evidence of infectious diseases. In contrast, no progressive deteriorations after BAL were observed in 282 patients (122 F and 160 M, 48 +/- 1 years old) with other pulmonary diseases (sarcoidosis, bronchial asthma, collagen diseases and other interstitial lung diseases), who received BAL during the same period. This suggests that BAL itself sometimes induces a progressive degeneration in IPF patients, especially in older patients.

Aged↗

PubMed1994

[Bronchial asthma and desaturation--assessment by pulse oximetry].

In the first study, we used pulse oximetry to continuously measure SpO2 and pulse rate in inpatients with paroxysmal attacks of acute asthma. Desaturation and increases in pulse rate occurred during coughing, urination, defecation, eating, and sleeping. Desaturation was most severe and frequent when peak expiratory flow was in the red zone. When it was in the yellow zone or blue zone, desaturation was less severe and less frequent. In the second study, outpatients experiencing exacerbations of chronic asthma and inpatients experiencing acute asthmatic attacks inhaled of a beta 2-stimulant via an ultrasonic nebulizer and were monitored with pulse oximetry. In the former, SpO2 either did not change or increased, but in the latter SpO2 decreased markedly when patients were in the red zone. Therefore, when patients inhale a bronchodilator during an acute asthmatic attack they should be carefully monitored with pulse oximetry. In the third study, pulse oximetry was used to measure saturation in outpatients who were suspected of having hyperresponsive airways and had undergone an airway hyperresponsiveness test with an Astograph. Almost all of those who had desaturation of more than 4% from were markedly hyperresponsive. The degree of desaturation and the percent change in respiratory resistance were significantly correlated. In conclusion, pulse oximetry can be useful in the short-term and long-term management of asthma tic patients.

Adolescent↗

PubMed1993

The effect of an oral leukotriene antagonist, ONO-1078, on allergen-induced immediate bronchoconstriction in asthmatic subjects.

BACKGROUND: Cysteinyl leukotrienes are potent contractile agonists for airway smooth muscle. To examine the relative role of cysteinyl leukotrienes in immediate airway obstruction in human subjects with asthma after allergen challenge, we investigated the effect of ONO-1078, a potent receptor antagonist of cysteinyl leukotrienes, on the response. METHODS: ONO-1078 and an inactive placebo, in 150-mg capsule form, were administered every 12 hours for 1 week, in a double-blind, cross-over fashion. To examine the effect on the early part of the response, total respiratory resistance (Rrs) was continuously evaluated for 10 minutes after the start of a 1-minute exposure to an appropriate concentration of allergen. Rrs and FEV1.0 were estimated every 10 minutes for 60 minutes after the exposure. RESULTS: ONO-1078 significantly reduced percent changes in Rrs and FEV1.0 from 20 to 60 minutes after the exposure, as well as percent maximum changes in these indices, although the treatment did not alter the time from the start of allergen exposure to the beginning of elevation of Rrs, the time from the start to the point at which total respiratory conductance decreased by 35% from its baseline value, or percent changes in Rrs or FEV1.0 10 minutes after the exposure. CONCLUSIONS: Therefore, we conclude that cysteinyl leukotrienes primarily mediate a later part of immediate airway obstruction after allergen exposure.

Administration, Oral↗

PubMed1993

Effects of percutaneous transluminal mitral valvuloplasty on plasma catecholamine levels during exercise.

Elevation of plasma catecholamine levels during exercise in patients with mitral stenosis correlated with the severity of the disease. We investigated the plasma norepinephrine changes in six patients before and after percutaneous transluminal mitral valvuloplasty (PTMV) during continuously graded ergometer exercise. Peak exercise intensity was increased from 65.8 W to 87.5 W after PTMV. Plasma norepinephrine level at 60 W workload intensity was decreased from 2308 +/- 864 pg/ml to 841 +/- 233 pg/ml after PTMV (p < 0.05). We concluded that PTMV decreased the plasma norepinephrine level during exercise in the patients with mitral stenosis. Percutaneous transluminal mitral valvuloplasty is a novel procedure for the improvement of symptoms in patients with mitral stenosis.

Adult↗

PubMed1993

Modification of regional myocardial performance caused by blood withdrawal and infusion in acute ischaemic canine heart.

The effect of changes in preload on regional myocardial motion in acute ischaemia was examined by miniature ultrasonic gauges after left anterior descending coronary artery occlusion in eight open chest dogs with the pericardium preserved. Left ventricular end-diastolic pressure was varied by blood withdrawal and infusion. When preload changed, isovolumetric shortening in the non-ischaemic region was inversely related to that in the ischaemic region. When preload decreased, stroke volume decreased and was accompanied by a decrease in end-diastolic length and ejection shortening in the non-ischaemic region together with an increase in isovolumetric bulging in the ischaemic region. When preload increased, these variables changed in opposite directions. These results indicate that in acute ischaemia: (1) changes in isovolumetric shortening in the non-ischaemic and ischaemic regions were related with each other when the level of volume expansion varied, and suggest that; (2) stroke volume is affected by end-diastolic length, ejection shortening in the non-ischaemic region and isovolumetric bulging in the ischemic region.

Animals↗

PubMed1993

The responses of left ventricular end-systolic pressure-diameter relationship to acute pressure overload induced by aortic constriction.

The aim was to investigate the responses of the left ventricular (LV) end-systolic pressure-diameter relationship (ESPDR) to acute pressure overload. ESPDRs were made by 2-min ascending and descending aortic constrictions before and after administration of propranolol and atropine sulphate (both 0.2 mg kg-1 i.v.) in eight open-chest dogs with the pericardium preserved. LV anterior-posterior diameter was measured with ultrasonic crystals. In the ascending aortic constriction, end-diastolic pressure (EDP) and end-diastolic diameter (EDD) were unchanged and ESPDR shifted to the left. In the descending aortic constriction, EDP and EDD increased from 6.8 +/- 0.7 to 8.8 +/- 0.9 mmHg (P < 0.01) and from 32.7 +/- 1.4 to 34.5 +/- 1.6 mm (P < 0.05) and ESPDR shifted to the right. After administration of propranolol and atropine sulphate, cases having smaller changes in EDD during 2 min constriction (0.3 +/- 0.3 mm in all cases of ascending, 0.3 +/- 0.2 mm in four cases of descending aorta) showed a leftward shift of ESPDR. The remaining four cases of descending aortic constriction with larger changes in EDD (1.8 +/- 0.8 mm, P < 0.05) showed a rightward shift of ESPDR. An inverse curvilinear correlation was found between percentage changes in EDD and in the slopes. These results suggest that the responses in ESPDR to acute pressure overload were determined by not only changes in the contractile state but also the interplay between adaptation to acute pressure overload (the Anrep effect) and pre-load.

Animals↗

PubMed1993

Increased expression of PDGF A- and B-chain genes in rat lungs with hypoxic pulmonary hypertension.

To study the molecular basis of vascular remodeling in pulmonary hypertension, we developed an experimental system in which male Sprague-Dawley rats were exposed to hypoxia for up to 3 wk. Both the right ventricular systolic pressure and gravimetric index for right ventricular hypertrophy were higher in rats exposed to hypoxia for 3 wk than those of age-matched control rats (P < 0.01), indicating that pulmonary hypertension was established under conditions used. To examine the possible involvement of platelet-derived growth factor (PDGF) in the pulmonary vascular remodeling caused by hypoxia, we cloned rat PDGF A- and B-chain cDNA and prepared specific cRNA probes. Northern blot analysis revealed that PDGF B-chain mRNA levels in the lungs were increased, reached a maximum of day 1, and were sustained at day 3, whereas PDGF A-chain mRNA levels reached a maximum on day 3. Thus the increase in the PDGF B-chain mRNA level precedes that in the PDGF A-chain mRNA level. These results suggest that the PDGF A- and B-chain products may be coordinately and sequentially involved in hypoxic pulmonary vascular remodeling.

Amino Acid Sequence↗

PubMed1993

Neuropeptide Y inhibits neurogenic inflammation in guinea pig airways.

We examined the effect of neuropeptide Y (NPY) on neurogenic airway microvascular leakage. Male Dunkin-Hartley guinea pigs (250-350 g) were anesthetized with urethan (2 g/kg ip). The cervical artery and vein were cannulated for monitoring blood pressure and injecting drugs, respectively. Atropine and propranolol (each 1 mg/kg i.v.) were administered 30 min before the experiment. After pretreatment with saline (vehicle for NPY) or NPY (1-100 micrograms/kg i.v.), Evans blue dye (30 mg/kg iv) was administered. Then, bilateral vagal nerves were electrically stimulated (5 V, 7 Hz, 5-ms duration for 3 min) to induce airway plasma leakage. Airways were divided into four sections [trachea (Tr), main bronchi, central intrapulmonary airways (IPA), and peripheral IPA] and incubated in formamide (37 degrees C for 16 h). The concentration of Evans blue dye was measured by spectrophotometer. Furthermore, we examined the effect of NPY on exogenous substance P- (0.3 microgram/kg i.v.) induced plasma extravasation. Bilateral vagal stimulation significantly increased leakage of dye in Tr to peripheral IPA. NPY did not affect basal leakage but did significantly inhibit neurogenic plasma extravasation in a dose-dependent manner with maximal inhibitions of 42.3 (Tr), 67.7 (main bronchi), 38.2 (central IPA), and 26.3% (peripheral IPA) at 30 micrograms/kg. Exogenous substance P-induced plasma extravasation was not inhibited by NPY. We conclude that NPY inhibits neurogenic inflammation by prejunctional inhibition of neuropeptide release from airway sensory nerve terminals.

Adrenergic beta-Antagonists↗

PubMed1993

Upper airway muscle activity during sustained hypoxia in awake humans.

To examine the effects of sustained hypoxia on upper airway and chest wall muscle activity in humans, we measured genioglossus muscle (GG) activity, inspiratory intercostal muscle (IIM) activity, and ventilation during sustained hypoxia in 17 normal subjects and 17 patients with obstructive sleep apnea (OSA). The trial of sustained hypoxia was performed as follows: after an equilibration period of 3 min, isocapnic hypoxia (arterial O2 saturation = 80 +/- 2%) was maintained for 20 min. GG EMG was measured with a fine-wire electrode inserted percutaneously, and IIM EMG was measured with surface electrodes. Ventilatory response to sustained hypoxia was initially increased and subsequently decreased. Stable phasic GG activity during spontaneous tidal breathing was observed in 6 normal subjects and 10 patients with OSA. Responses of GG and IIM activities to sustained hypoxia showed a biphasic response qualitatively similar to the ventilatory response in these 16 subjects. The absolute value of the subsequent decline in GG activity was similar to that of the initial increase, whereas the subsequent decline in IIM activity was smaller than that of the initial increase. Percent GG activity was significantly lower than both percent IIM activity and percent minute ventilation during the decline and plateau phases. There were no significant differences in ventilatory and EMG responses between the normal subjects and the patients with OSA. We conclude that, during wakefulness, upper airway muscle activity declined to a greater extent than inspiratory pump muscle activity during sustained hypoxia.

Adult↗

PubMed1993

Prevalence of sleep apnea among Japanese industrial workers determined by a portable sleep monitoring system.

We developed a new portable sleep monitoring system and studied the prevalence of sleep apnea syndrome among Japanese industrial workers. This device assessed three kinds of parameters: nasal airflow, tracheal sound and electrocardiogram (ECG), and digitally stored the clock time of the onset of apnea, apnea duration and R-R intervals by a built-in microcomputer. After monitoring, the portable sleep monitor was connected to a host computer, and apneic episodes, the so-called 'apnea index' as apneic episodes corrected by measuring time ('AI') and R-R intervals were analyzed. In 170 inpatients referred to our sleep clinic, sleep monitoring by this device was performed simultaneously with all-night polysomnography, and the sensitivity and specificity of this device was determined under different criteria of the apnea index (AI) (AI > 5, 10, 15 and 20 episodes/h) by polysomnography. In all AI criteria, the sensitivity was more than 90%, and the specificity was also reasonably high. Using this system, successive 2-night home sleep monitoring was performed on 168 healthy workers in one Japanese industrial company, and 159 people (140 males; 19 females) who had successful monitoring were analyzed. The percentage of persons who had 'AI' of more than 10 episodes/h was 7.5%. There were no significant correlations between 'AI' and age, body weight or scores estimated by sleep questionnaires. These results suggest that even in people who are seemingly healthy significant apneic episodes could be detected by the portable home sleep monitoring system. This system may therefore be useful in evaluating the occurrence of sleep apnea syndrome in general populations.

Adolescent↗

PubMed1993

Modification of myogenic intrinsic tone and [Ca2+]i of rat isolated arterioles by ryanodine and cyclopiazonic acid.

The role of the sarcoplasmic reticulum (SR) in regulating myogenic tone and [Ca2+]i was examined with ryanodine and cyclopiazonic acid (CPA) in the rat skeletal muscle arteriole (A(sk)) and mesenteric arteriole (Ams). Arterioles were cannulated at both ends to control luminal pressure in a tissue bath. Luminal diameter was measured with a video-monitored microscopic system. Fura 2-AM was loaded to measure [Ca2+]i using the fluorescence intensity ratio at excitation wavelengths of 340 to 380 nm (F340/380). The myogenic response (luminal pressure was increased from 40 to 100 mm Hg) and the intrinsic tone at 40 mm Hg were observed in A(sk) but not in Ams. Ryanodine (10(-5) M decreased the steady-state diameter of A(sk) from 138 +/- 8 to 85 +/- 9 microns (P < .05) and increased the F340/380 ratio; these effects were reversed by nifedipine or Ca(2+)-free solution. Ryanodine shifted the [Ca2+]o-contraction response curve upward. CPA (10(-5) M) also decreased the steady-state diameter of A(sk) from 131 +/- 7 to 98 +/- 11 microns (P < .05). In contrast, Ams responded to neither ryanodine nor CPA. Caffeine-induced contractions were significantly reduced by either ryanodine or CPA in both arterioles. These results indicate that SR dysfunction increased the susceptibility of the arteriolar tone to [Ca2+]o and enhanced the tone of A(sk). In conclusion, the SR function may play a critical role in regulating [Ca2+]i and the intrinsic tone of A(sk) that was myogenically active at physiological luminal pressure.

Animals↗

PubMed1993

Involvement of superoxide in ozone-induced airway hyperresponsiveness in anesthetized cats.

To determine whether oxygen radical scavengers inhibit ozone-induced airway hyperresponsiveness, we examined the protective effect of polyethylene glycol-superoxide dismutase (PEG-SOD) and PEG-catalase (PEG-CAT) on ozone-induced airway hyperresponsiveness in cat airways. Twenty-five cats divided into five groups were anesthetized and mechanically ventilated. There was no difference between the groups in baseline airway responsiveness to inhaled acetylcholine (ACh). In the control group, AChPC, the concentration required to produce a doubling increase in baseline pulmonary resistance, was significantly reduced by ozone exposure (2.0 ppm for 2 h); the ratios of AChPC before ozone exposure to after ozone exposure (AChPC ratio) were 14.8 +/- 5.7 (p < 0.001) and 4.80 +/- 1.6 (p < 0.01) 30 and 120 min after exposure, respectively. Local administration of PEG-SOD (2,000 U/kg) into airways partially but significantly prevented ozone-induced airway hyperresponsiveness. The AChPC ratios were 6.2 +/- 1.4 and 1.5 +/- 0.2 30 and 120 min after exposure, respectively, which were significantly different from those of the control group (p < 0.05), whereas PEG-CAT pretreatment (6,000 U/kg) was without effect. Combined pretreatment with PEG-SOD and PEG-CAT had no additional protective effect compared with PEG-SOD alone. PEG-SOD had no direct effect on airway responsiveness to ACh. These results suggest that superoxide may be involved in ozone-induced airway hyperresponsiveness.

Acetylcholine↗

PubMed1993

Antiasthma drug, ibudilast, inhibits neurogenic plasma extravasation in guinea-pig airways.

We examined the effect of ibudilast, an antiasthma drug, on neurogenic microvascular leakage in guinea-pig airways by measuring extravasation of Evans blue dye. After intravenous pretreatment with atropine (1 mg/kg) and propranolol (1 mg/kg), bilateral vagal stimulation significantly increased nonadrenergic noncholinergic (NANC)-mediated leakage of dye in the trachea (Tr), the main bronchi (MB), and the central (cIPA) and peripheral (pIPA) intrapulmonary airways. Ibudilast (1.0 to 100 micrograms/kg given intravenously) did not affect basal leakage, but it significantly inhibited NANC-mediated plasma extravasation in a dose-dependent manner, with a maximal inhibition of 74.0% (Tr, p < 0.05), 89.1% (MB, p < 0.05), 91.4% (cIPA, p < 0.01), and 84.3% (pIPA, p < 0.05) at 100 micrograms/kg. Plasma extravasation induced by exogenous substance P (1 microgram/kg given intravenously) was not inhibited by ibudilast. Glibenclamide, an inhibitor of ATP-sensitive potassium channels, blocked the inhibitory effect of ibudilast. We conclude that ibudilast inhibits neurogenic leakage by prejunctional inhibition of neuropeptide release from airway sensory nerve terminals via an ATP-sensitive potassium channel.

Animals↗

PubMed1993

Morphometric analysis of airways in Sjögren's syndrome.

Sjögren's syndrome is characterized by a decrease in exocrine gland secretion and the destruction of secretory tissue and cells, that is, salivary and lacrimal glands. Although patients with Sjögren's syndrome have chronic cough and sometimes sputum, we have little knowledge concerning the morphology of their airways. We performed morphometric analysis of goblet cells and bronchial glands and compared them with intraluminal mucus volume by measuring the mucus-occupying ratio (MOR) in the airways of patients with Sjögren's syndrome. A total of 6 nonsmoking patients with Sjögren's syndrome who had no significant prolonged airway infections (Group SG) (6 women, 55 +/- 2 yr) were compared with four control patients with no pulmonary diseases (Group NL) (1 woman and 3 men, 64 +/- 2 yr) and five patients with chronic bronchitis (Group CB) (1 woman and 4 men, 52 +/- 5 yr). Autopsied lungs from 15 patients were used for morphometry by a digitalizing computer. Area proportion of bronchial glands (gland %) to bronchial wall, goblet cell-occupying ratio to total epithelial layer (goblet %), and MOR were measured in central (3-8 mm in diameter) and peripheral airways (2 mm or less in diameter). Gland % and goblet % in central and MOR in peripheral airways from Group SG were significantly larger than those from Group NL: 15 +/- 2 versus 6 +/- 1% (p < 0.01), 6 +/- 1 versus 2 +/- 1% (p < 0.05), and 9 +/- 2 versus 0.6 +/- 0.3% (p < 0.05), respectively. Further, these values from Group SG did not significantly differ from those from Group CB.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

Effects of a combination therapy of anticoagulant and vasodilator on the long-term prognosis of primary pulmonary hypertension.

A therapy consisting of a combination of an anticoagulant and a vasodilator was investigated to determine its effects on the long-term prognosis of primary pulmonary hypertension (PPH). Twenty patients with PPH who had undergone diagnostic catheterization in our hospital were studied. The mean follow-up period after the initial catheterization was 6 years, with the longest follow-up being 24.4 years. Seven patients were treated with warfarin as an anticoagulant, combined with either isoproterenol (3 patients) or nifedipine (4 patients) as a vasodilator (AV group). The remaining 13 patients were not treated (control group). Although there were no significant differences in the physical activity or hemodynamics between the groups, improvement was seen in 43% of the AV group and in only 7.6% of the controls. The 5 year survival rate was significantly higher in the AV group (57% vs 15%; P < 0.05). Hemodynamics were evaluated repeatedly in 8 patients and improvement was seen only in the AV group. These results suggest that a therapy consisting of a combination of an anticoagulant and a vasodilator may improve the long-term prognosis of PPH.

Adolescent↗