Prevalence of sleep apnea syndrome in Japanese industrial workers using a home sleep monitor.
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Adolescent↗
Biomedical subjects
T Takishima
Publications and source records attributed to T Takishima.
The effect of submental electrical stimulation on sleep disordered breathing in patients with obstructive apnea.
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Electric Stimulation↗
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↗
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↗
Effects of posture on carbon dioxide responsiveness in patients with obstructive sleep apnoea.
BACKGROUND: It is well known that upper airway resistance increases with postural change from a sitting to supine position in patients with obstructive sleep apnoea (OSA). It is not known, however, how the postural change affects the ventilatory and occlusion pressure response to hypercapnia in patients with OSA when awake. METHODS: The responses of minute ventilation (VE) and mouth pressure 0.1 seconds after the onset of occluded inspiration (P0.1) to progressive hypercapnia (delta VE/delta PCO2, delta P0.1/delta PCO2) both in sitting and supine positions were measured in 20 patients with OSA. The ratio of the two (delta VE/delta P0.1) was obtained as an index of breathing efficiency. The postural changes in response to carbon dioxide (CO2) after uvulopalatopharyngoplasty (UPPP) were also compared in seven patients with OSA. RESULTS: There were no significant changes in the resting values of end tidal PCO2, P0.1, or VE between the two positions. During CO2 rebreathing, delta VE/delta PCO2 did not differ between the two positions, but delta P0.1/delta PCO2 was significantly higher in the supine than in the sitting position (supine, mean 0.67 (SE 0.09) cm H2O/mm Hg; sitting, mean 0.57 (SE 0.08) cm H2O/mm Hg), and delta VE/delta P0.1 decreased significantly from the sitting to the supine position (sitting, 4.6 (0.4) l/min/cm H2O; supine, 3.9 (0.4) l/min/cm H2O). In seven patients with OSA who underwent UPPP, delta VE/delta P0.1 improved significantly in the supine position and postural change in delta VE/delta P0.1 was eliminated. CONCLUSIONS: These results suggest that in patients with OSA the inspiratory drive in the supine position increases to maintain the same level of ventilation as in the sitting position, and that the postural change from sitting to supine reduces breathing efficiency. Load compensation mechanisms of patients with OSA appear to be intact while awake in response to the rise in upper airway resistance.
Female↗
alpha-Adrenergic augmentation of myogenic response in rat arterioles: role of protein kinase C.
We tested the hypothesis that protein kinase C (PKC) activation plays a major role in alpha-adrenergic augmentation of the myogenic response in rat isolated arterioles. Lumen diameter measured was with a video-monitored microscopic system. Lumen diameter did not change (131 +/- 5 vs. 126 +/- 6 microns) despite an increase in lumen pressure from 40 to 100 mmHg. Phenylephrine (Phe; 3 x 10(-7) M) augmented the myogenic response, since lumen diameter decreased significantly from 117 +/- 8 to 101 +/- 8 microns. High potassium (40 mM) failed to augment the myogenic response, while constricting the vessels to nearly the same extent as did Phe. PKC inhibitors 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine dihydrochloride (H-7, 5 x 10(-5) M, n = 7) and staurosporine (3 x 10(-9) M, n = 7) abolished the Phe-induced augmentation. H-7 and staurosporine depressed the myogenic response even without Phe. PKC activators phorbol 12,13-dibutyrate (3 x 10(-9) M; n = 7) and 4 beta-phorbol 12-myristate 13-acetate (6 x 10(-8) M; n = 6) constricted the vessels by 11 +/- 2 and 18 +/- 3%, respectively. However, PKC activators failed to augment the myogenic response. These results suggest that PKC activation does not play a major role in alpha-adrenergic augmentation of the myogenic response in rat skeletal arterioles.
Animals↗
Spatial features of calcium transients during early and delayed afterdepolarizations.
Although changes in intracellular Ca2+ concentration ([Ca2+]i) are spatially heterogeneous during spontaneous contraction in mammalian cardiac muscle, it has not yet been observed how [Ca2+]i changes spatially within cardiac myocytes during delayed (DADs) and early (EADs) afterdepolarizations. The aim of this study is to characterize the spatial features of the increase in [Ca2+]i during such afterdepolarizations and to understand the ionic mechanisms responsible for them. Myocytes were enzymatically isolated from guinea pig ventricles and loaded with fura 2-acetoxymethylester, the Ca2+ fluorescence indicator dye. Membrane potential was recorded with a conventional microelectrode technique, and spatiotemporal changes in fura 2 fluorescence and cell length were recorded using a digital television system. After superfusion with potassium-free Tyrode solution, DADs and EADs were induced. During DADs, fluorescence transients were heterogeneous within myocytes (n = 11). Furthermore, they often propagated within myocytes as if they were "waves." In contrast, during EADs, fluorescence transients showed no waves within myocytes but rather showed synchronous changes throughout the myocytes (n = 15). The results of this study suggest that the spatial features of the increase in [Ca2+]i differ between the DADs and EADs. We concluded from these differing features that the ionic mechanisms responsible for the two triggered activities are different.
Animals↗
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↗
Dexamethasone modulation of ion transport and fluid movement across airway epithelium.
Electrolyte or fluid is secreted across airway mucosa by both superficial epithelium and submucosal glands. To understand the effect of glucocorticoid on fluid movement across airway mucosa, we examined the effects of dexamethasone (Dex) on bioelectric properties of canine and feline tracheal epithelium and on 22Na efflux from isolated feline tracheal submucosal glands. Potential difference (PD) and short-circuit current (SCC) across tracheal epithelium were measured using an Ussing chamber, and conductance (G) was calculated as the ratio SCC/PD. Isolated glands were loaded with 22Na, and the rate constant (RC) of Na2+ efflux was calculated by measuring the radioactivity of each effluent sample. After treatment with 10(-9) to 10(-5) M Dex for up to 6 h, the epithelium and isolated glands were stimulated with isoproterenol (ISP) and methacholine (MCh), respectively. Dex treatment did not alter significantly baseline values of PD, SCC, or RC. However, Dex treatment produced a dose-dependent attenuation of ISP-evoked epithelial PD and SCC and of MCh-evoked glandular RC. In canine epithelium, pretreatment with 10(-5) M Dex for 6 h reduced by 40% the ISP (10(-6) M)-evoked rise in PD and SCC, whereas G remained unchanged. After 10(-5) M Dex treatment for 6 h, MCh (10(-5) M)-evoked RC in isolated glands was significantly less than in control glands (MCh alone) by 23%. These findings suggest that glucocorticoid decreases the fluid secretion across the airway mucosa, especially when the mucosa are stimulated.
Animals↗
Effects of beta-adrenergic receptor activation on alveolar macrophage cytoplasmic motility.
We studied the effects of fenoterol, a beta-adrenoceptor agonist, on the cytoplasmic motility of alveolar macrophages (AM) from dog lungs in vitro. Four days after the instillation of Fe3O4 particles (3 mg/kg) into the lower lobe bronchus, AM were harvested by bronchoalveolar lavage. Remanent field strength (RFS) from the AM containing Fe3O4 particles (5 x 10(6) cells) was measured immediately after magnetization. RFS decreased with time due to particle rotation (relaxation), which is related to cytoplasmic motility of AM. Fenoterol (10(-9) M to 10(-5) M) decreased the relaxation rate (lambda 0; min-1) in a concentration-dependent fashion with the maximum effect at 10(-6) M. Both forskolin (10(-6) M to 10(-4) M) and dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP) (10(-3) M) mimicked fenoterol-induced inhibitory effects on lambda 0. Fenoterol and forskolin concentration-dependently increased intracellular levels of cAMP, which were parallel to decreases in lambda 0 induced by these drugs. KT 5720 (10(-5) M), a specific inhibitor of protein kinase A, significantly inhibited fenoterol (10(-6) M)-induced inhibitory effects on lambda 0 (P < 0.01). These results imply that beta-adrenergic receptor activation inhibits cytoplasmic motility of AM via increases in intracellular levels of cAMP, which may be coupled with activation of a cAMP-dependent protein kinase.
Animals↗
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↗
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↗
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↗
Pulmonary emphysema followed by pulmonary fibrosis of undetermined cause.
Idiopathic pulmonary fibrosis (IPF) and pulmonary emphysema (PE) have distinct clinical and pathological characteristics, and have been considered to be separate disorders. However, recent animal experiments have suggested that, with regard to their pathogenesis, the diseases have some features in common. However, there are no clinical data supporting this hypothesis. We report here 9 patients (all male, 67 +/- 2 years, mean +/- SE) who had PE followed by IPF. They were found among 152 PE patients who came to Tohoku University Hospital during the past 15 years (1976-1991). All patients were male and heavy smokers and 2 patients also had prostate cancer and gastric cancer, respectively. Three patients were alive during this study and had been diagnosed as having IPF and PE by the combination of transbronchial biopsy, selective alveolobronchogram, CT examination and lung function tests. The diagnosis of IPF and PE in the other patients was based on the pathological findings of autopsied lungs in addition to clinical findings. All patients showed PE mainly in the upper lobes and IPF in the lower lobes. In all patients, in addition to all known causes of pulmonary fibrosis, the possibilities that chronic or recurrent infections in PE induced pulmonary fibrosis and that IPF produced emphysematous changes were carefully excluded by medical records and pathological findings. It is not clear whether the occurrence of emphysema and pulmonary fibrosis in these cases is coincidental, or whether the two diseases are linked by a common pathogenetic pathway.
Aged↗
Adjuvant effect of interleukin-1 on the development of late asthmatic response in guinea pigs.
The adjuvant effect of silica and IL-1 in the development of late asthmatic responses (LARs) in guinea pigs was studied. Different doses of silica or recombinant human (rh) IL-1 (1 microgram) with Ascaris suum were used for the immunization. The serum IL-1 concentration was measured after the immunization. One week after the immunization, antigen was challenged and respiratory resistance (Rrs) was measured. Rrs increased silica dose dependently in the late phase, and the increment of Rrs in the late phase was significantly correlated with the serum IL-1 concentration (p < 0.05). In addition, rhIL-1 administration showed an increase in Rrs at the late phase. Antigen-specific IgE and IgG1 were also measured and were increased in guinea pigs immunized both with silica and rhIL-1.
Adjuvants, Immunologic↗
Mechanisms of bronchoconstriction after allergen ingestion in sensitized guinea pigs.
We examined whether oral administration of allergen induced bronchoconstriction in sensitized guinea pigs and investigated the mechanisms of bronchoconstriction. The animals had been immunized intraperitoneally with a mixture of Ascaris suum extract and silica gel, and exposed to ozone. They were then challenged with an oral dose of A. suum extract (6 mg/kg), and respiratory resistance (Rrs) was measured up to 7 h. After oral administration of the allergen, an increase in Rrs was observed. The mean values at 1, 3, 5 and 7 h after oral allergen challenge were 150 +/- 21, 149 +/- 11, 151 +/- 12 and 134 +/- 10% of the baseline value, respectively. When saline instead of the allergen was orally administered, almost no significant increase in Rrs was observed up to 7 h. Moreover, in nonsensitized guinea pigs, oral administration of allergen produced no significant increase in Rrs for up to 7 h. When atropine was administered as an aerosol, the increase in Rrs induced by an oral allergen challenge was attenuated. Three of the five atropine-treated guinea pigs showed temporary increases in Rrs immediately after the oral allergen challenge. The mean values of Rrs in the atropine-treated animals challenged with oral allergen at 1, 3, 5 and 7 h were 106 +/- 3, 106 +/- 5, 115 +/- 5 and 102 +/- 4% of baseline value, respectively. In the animals which received oral allergen, the number of neutrophils in bronchoalveolar lavage fluid (BALF) significantly increased 2.0-fold (p < 0.05), while no significant increase in the number of eosinophils, macrophages, or lymphocytes in BALF was observed.(ABSTRACT TRUNCATED AT 250 WORDS)
Administration, Oral↗
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↗
Role of chemical drive in recruiting upper airway and inspiratory intercostal muscles in patients with obstructive sleep apnea.
Upper airway dilating muscle activity increases during apneic episodes in patients with obstructive sleep apnea (OSA). To elucidate the relative contribution of chemical and nonchemical stimuli to augmentation of the upper airway dilating muscle, we measured the response of genioglossus muscle (GG) and inspiratory intercostal muscle (IIM) activities to obstructive apnea during non-REM sleep and compared them with the response to progressive hypoxia and hypercapnia during awake periods in seven male patients with OSA. GG EMG was measured with a wire electrode inserted percutaneously, and IIM EMG was measured with surface electrodes placed in the second intercostal space parasternally. Responses to hypoxia and to hypercapnia were assessed by rebreathing methods in the supine position while awake. Following these measurements, a sleep study was conducted with the EMG electrodes placed in the same locations. The relationship between GG and IIM activities during the cycle of apnea and postapneic ventilation in non-REM sleep was quasi-linear, and the slope of the regression line was significantly greater than those during progressive hypoxia and progressive hypercapnia. The amplitude of GG activity at 70% of maximum IIM activities in the hypoxic test was 140 +/- 20% (mean +/- SEM) during non-REM sleep, which was also significantly greater than that during hypoxia (51 +/- 10%) and that during hypercapnia (59 +/- 15%). These results suggest that nonchemical factors contribute considerably to augmentation of GG activity during obstructive apneic episodes. The nonchemical stimuli may arise from mechanoreceptors activated by upper airway obstruction and behavioral factors associated with change in sleep states.
Adult↗