Prevalence of sleep apnea syndrome in Japanese industrial workers using a home sleep monitor.
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Adolescent↗
Biomedical subjects
S Okabe
Publications and source records attributed to S Okabe.
Regulation of gastroduodenal bicarbonate secretion by capsaicin-sensitive sensory neurons in rats.
We investigated the role of capsaicin-sensitive sensory neurons in regulation of gastroduodenal HCO3- secretion in anesthetized rats. The stomach (under acid inhibition by omeprazole 60 mg/kg i.p.) or the duodenum was perfused with saline (pH 4.5) and HCO3- output was determined by pH change in the perfusate. Both the duodenum and stomach responded to prostaglandin E2 (PGE2; 300 micrograms/kg i.v.) or luminal acid by a significant increase in pH and HCO3- output. These tissues also responded to luminal application of capsaicin (0.3-6 mg/ml for 30 min), resulting in a significant increase of pH and HCO3- output in a concentration-related manner. The HCO3- stimulatory action of capsaicin was markedly attenuated by functional ablation of capsaicin-sensitive sensory neurons, significantly mitigated by indomethacin, and exhibited tachyphylaxis after repeated application at a high concentration. The acid-induced pH and HCO3- responses were also significantly mitigated by sensory deafferentation and by indomethacin, whereas those induced by PGE2 remained unaffected. In addition, defunctionalization of these sensory nerves resulted in macroscopically visible damage in the duodenum when acid secretion was concomitantly stimulated by histamine. We conclude that capsaicin-sensitive sensory neurons may be involved in the regulatory mechanism of gastroduodenal HCO3- secretion and contribute to protection of the mucosa against acid. Endogenous PGs may be involved in the HCO3- stimulatory action mediated by capsaicin-sensitive sensory neurons.
Afferent Pathways↗
Spectroscopic factors for alpha -cluster wave functions in 44Ti observed via the (6Li,d) reaction.
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Journal Article↗
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↗
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↗
Endogenous sulfhydryls in healing gastric mucosal injury induced by HCl in the rat.
The role of endogenous sulfhydryls (SH) in the healing of HCl-induced gastric injury was investigated in the rat. The animals fasted for 18 h were given 1 ml of 0.6 N HCl by gavage, and they were fed normally from 1 h later and killed various days after HCl treatment. Gastric lesions induced by HCl healed to quiescent states within 7 days both macroscopically and histologically. Mucosal SH levels were markedly reduced after induction of damage by HCl, but recovered gradually to or above normal values within 5 days. Gastric acidity was also significantly reduced after administration of 0.6 N HCl (induction of lesions), followed by a return to normal values within 5 days, although the volume of gastric contents remained unchanged before and after HCl treatment. The healing of HCl-induced gastric lesions was significantly impaired by diethylmaleate (DEM 0.3 ml/kg x 2) when this drug was given subcutaneously for 5 days. Glutathione (GSH: 100 mg/kg x 2) alone did not affect the healing of gastric lesions, but the combined administration of GSH with DEM significantly antagonized the delayed healing caused by DEM. Administration of DEM caused a marked and persistent reduction in the mucosal SH contents, while GSH by itself significantly increased the mucosal SH levels and partially reversed the reduced SH contents caused by DEM. Gastric acid secretion was not significantly altered by either DEM or GHS. These results suggest that endogenous SH may play some roles in the healing process of gastric mucosal lesions. DEM caused a deleterious effect on the healing of gastric lesions, probably by reducing the mucosal SH.
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↗
[The state of the art of gastric antisecretory drugs].
This review article describes the effect and mechanism of various antisecretory drugs. Both histamine H2-receptor antagonists and gastric proton pump inhibitors are now world-widely used as the first choice for the treatment of acid-related diseases. Because of their potential effectiveness in inhibiting gastric acid secretion, new H2-antagonists and pump inhibitors are under development with the aim of mitigating of the side effects. The local antisecretory effects of FPL-52694, NC-1300-O-3 and ME 3407, which were demonstrated in Heidenhain pouch dogs, will provide clues for the development of new types of antisecretory drugs. Antigastrin drugs are also promising.
Animals↗
Mechanism by which indomethacin delays gastric ulcer healing in the rat: inhibited contraction of the ulcer base.
Repeated administration of indomethacin delays the healing of acetic acid-induced gastric ulcers in rats, but the underlying mechanism remains unclear. We examined the effect of indomethacin on the contraction of the connective tissue isolated from the base of 1-week-old ulcers. The tissue samples, suspended in an organ bath, were contracted by serotonin, bradykinin and carbachol and also slightly contracted by prostaglandin (PG) F1 alpha. The effect of serotonin was the most potent. However, 6-keto-PGF1 alpha, PGE2 and histamine had little or no contraction inducing effect. The contractile response to serotonin of the tissue in the indomethacin-treated group was significantly less than that in the control group (without indomethacin treatment). After a 2-week treatment with indomethacin, a histological study of the ulcers showed that the length of rupturing of the muscularis mucosa was significantly greater than that observed in the control group. However, indomethacin had no effect on the length of the regenerated mucosa and the thickness of the ulcer base. We conclude that the connective tissue at the ulcer base has the ability to contract and that the prevention of the contraction of the tissue by indomethacin might be involved in the mechanism underlying delayed ulcer healing.
Acetates↗
Cytoprotective action of L-arginine against HCl-induced gastric injury in rats: involvement of nitric oxide?
We examined the cytoprotective effect of L-arginine on gastric damage induced by 0.6 N HCl in rats and investigated whether the mechanism of this action is related to the nitric oxide (NO)-mediated protection. The animals were given 0.6 N HCl by gavage and killed 1 hr later. L-Arginine (100, 300 and 750 mg/kg) given p.o. 30 min before HCl treatment prevented these lesions in a dose-dependent manner, but had no effect when given i.v. (200 mg/kg). Similar effects were observed by D-arginine but not by an equimolar dose of mannitol. This effect of L-arginine (p.o.) was attenuated significantly by prior administration of indomethacin (5 mg/kg, s.c.) but not by NG-nitro-L-arginine methyl ester (L-NAME) (5 mg/kg, i.v.), the NO synthase inhibitor. Both L- and D-arginine produced a reduction in potential difference (PD), inhibition of gastric motility, and increases of luminal pH and mucosal blood flow when they were given intragastrically. Indomethacin significantly mitigated these changes induced by L-arginine except PD reduction, while L-NAME showed significant inhibition only against the increased pH response. We conclude that L-arginine given p.o. exhibits gastric cytoprotection against HCl-induced damage in rats, probably by acting as a mild irritant. The mechanism of this action may appear through "adaptive cytoprotection" mediated by endogenous prostaglandins and does not involve the NO-mediated protective pathway.
Animals↗
Effects of indomethacin and prednisolone on the different stages of healing of acetic acid-induced gastric ulcers in the rat.
Repeated administration of indomethacin or prednisolone for 2 weeks apparently delayed the healing of initial gastric ulcers induced by acetic acid injection in rats. While indomethacin significantly interfered with the healing of partially healed 2-week-old ulcers, prednisolone did not. Indomethacin had no effect on the healing of "unhealed" 4-week-old ulcers. However, prednisolone significantly enhanced the healing of such "unhealed" ulcers, and it decreased the weight of the connective tissue at the ulcer base and the collagen content. These results suggest that prednisolone enhances the healing of "unhealed" gastric ulcers by degrading the fibroplasia that had amply developed in the connective tissue.
Acetates↗
Effect of NC-1300-O-3 on healing of acetic acid-induced gastric ulcers in rats.
We examined the effect of NC-1300-O-3 on the healing of acetic acid-induced gastric ulcers in male Donryu rats. NC-1300-O-3, administered orally once daily for 2, 4 or 8 weeks after ulceration, significantly accelerated the spontaneous healing of both fresh and unhealed ulcers (induced by pretreatment with indomethacin). The delay in ulcer healing caused by indomethacin was markedly prevented by concurrent administration of NC-1300-O-3 once daily for 4 weeks in a dose-related manner. A bolus administration of NC-1300-O-3 to rats with 5-day-old ulcers potently and persistently (> 48 hr) inhibited both the basal and histamine-stimulated gastric secretion. However, the potency and duration of the anti-secretory activity of the compound, with or without indomethacin, gradually decreased with the period of treatment. After an 8-week treatment with NC-1300-O-3 alone, the volume of the gastric contents was markedly increased, resulting in an increased acid output. Administration of the compound together with indomethacin for 8 weeks resulted in a significant increase in the volume, no change in acid output and a significant increase in the pH. The spontaneous or delayed healing of gastric ulcers induced 4 weeks after pretreatment with NC-1300-O-3 was also significantly enhanced or prevented with NC-1300-O-3, with a weakened antisecretory activity. Therefore, NC-1300-O-3 seems to promote ulcer healing or prevents delayed healing by its potential antisecretory and/or ulcer-healing activities.
2-Pyridinylmethylsulfinylbenzimidazoles↗
Capsaicin-sensitive sensory nerves in recovery of gastric mucosal integrity after damage by sodium taurocholate in rats.
We compared the recovery process of gastric mucosal integrity after damage by 20 mM sodium taurocholate (TC) in control, sensory deafferented and indomethacin-treated rats. Under anesthetized conditions, the stomach was mounted on a chamber and perfused with saline or 50 mM HCl. Application of TC (30 min) to the saline-perfused stomach produced a marked reduction in the potential difference (PD) (surface epithelial damage), followed by increases of gastric mucosal blood flow (GMBF) and luminal pH (alkalinization), but there was a rapid recovery of PD without development of gross lesions. Chemical ablation of capsaicin-sensitive sensory nerves had no influence on the PD reduction and luminal alkalinization, but significantly inhibited the rise in GMBF and the PD recovery. Indomethacin pretreatment (5 mg/kg, s.c.) significantly inhibited these changes seen after exposure to TC, except for PD reduction. In contrast, TC caused a sizable amount of H+ back-diffusion and a more pronounced and persistent rise in GMBF in the stomach perfused with 50 mM HCl, yet only minimal damage was observed in the control animals. Under these conditions, both sensory deafferentation and indomethacin inhibited such GMBF responses, leading to hemorrhagic damage without affecting the degree of H+ back-diffusion. These results suggest that capsaicin-sensitive sensory nerves contribute to the recovery of gastric mucosal integrity after damage, probably by maintaining GMBF responses associated with H+ back-diffusion and preventing the later extension to gross damage in the presence of acid.
Animals↗
Stimulation by nitric oxide synthase inhibitors of gastric and duodenal HCO3- secretion in rats.
The role of nitric oxide (NO) in the regulation of gastroduodenal HCO3- secretion was investigated in anesthetized rats using the NO biosynthesis inhibitor NG-nitro-L-arginine methyl ester (L-NAME). HCO3- secretion was measured at pH 7.0 using a pH-stat method in the chambered stomach in the presence of omeprazole or in the proximal duodenum. Intravenous administration of L-NAME (1-5 mg/kg) increased HCO3- secretion in a dose-dependent manner in both the stomach and duodenum, with a concomitant elevation of arterial blood pressure. The stimulatory effect of L-NAME on HCO3- secretion was mimicked by another NO synthase inhibitor, NG-monomethyl-L-arginine (50 mg/kg), but not by the enantiomer NG-nitro-D-arginine methyl ester, and was significantly antagonized by concurrent administration of L-arginine, but not D-arginine, at 200 mg/kg. The exogenous NO donor nitroprusside (4 mg/kg) by itself decreased the rate of HCO3- secretion and significantly antagonized the HCO3- stimulatory action of L-NAME. Furthermore, the increased HCO3- secretion caused by L-NAME was significantly attenuated by prior administration of atropine (1 mg/kg, s.c.) or indomethacin (5 mg/kg, s.c.) and by bilateral vagotomy but was not influenced by sensory deafferentation after capsaicin pretreatment, though none of the treatments had any effect on the changes in blood pressure induced by L-NAME. These results suggest that L-NAME stimulates HCO3- secretion in the gastroduodenal mucosa. This action is associated with the inhibition of NO biosynthesis and may be partly dependent on vagal-cholinergic innervation and mediated by endogenous prostaglandins.
Amino Acid Oxidoreductases↗
Anticarcinogenic activity of green tea polyphenols.
The main physiologically active polyphenol in green tea extract is (-)-epigallocatechin gallate (EGCG). Green tea extract has an advantage over EGCG as a cancer chemopreventive agent for humans, as is apparent from the Japanese custom of injesting green tea on a daily basis. Green tea extract similarly inhibited protein kinase C activation by teleocidin, a tumor promoter, as did EGCG. In addition, EGCG and green tea extract showed inhibitory effects on the growth of lung and mammary cancer cell lines with similar potencies. An experiment using the estrogen-dependent MCF-7 cell line showed the mechanisms of action of these compounds to be inhibiting the interaction of estrogen with its receptors. Considering our previous results of a single application of EGCG to mouse skin inhibiting the specific binding of 3H-12-0-tetradecanoylphorbol-13-acetate (3H-TPA) and 3H-okadaic acid, we postulated that EGCG and compounds in green tea extracts would block the interaction of tumor promoters, hormones and growth factors with their receptors: a kind of sealing effect. The sealing effect would account for reversible growth arrest, and may be induced by various kinds of compound.
Animals↗
Effect and mechanism of sucralfate on healing of acetic acid-induced gastric ulcers in rats.
We examined the effect of sucralfate on spontaneous and delayed healing of experimental gastric ulcers and the underlying mechanism of action. Gastric ulcers were produced 5 days after submucosal injection of 20% acetic acid (0.03 ml) into the antral-oxyntic border of rat stomachs. To delay the healing of ulcers, indomethacin was administered s.c. at 1 mg/kg once daily for 4 weeks from 5 days after the acid injection. Sucralfate, administered p.o. three times daily, significantly accelerated the spontaneous healing of ulcers, the healing rates being 13.7%, 43.7% and 47.1% with 100 mg/kg, 300 mg/kg and 600 mg/kg, respectively. In addition, the drug also significantly prevented the delay in ulcer healing caused by indomethacin, the preventive rates being 56.6% and 83.9% with 300 mg/kg and 600 mg/kg, respectively. Sucralfate, even at 1000 mg/kg, had no effect on the mucosal prostaglandin E2 (PGE2) level around the ulcers and did not affect the reduced PGE2 content caused by indomethacin. A single dose of sucralfate significantly increased the volume and the pH of the gastric contents in a dose-dependent manner, the effects persisting for up to 8 hr. These results suggest that the mechanism by which sucralfate accelerates the healing of gastric ulcers is unrelated to endogenous PGs but related to the acid-neutralizing activity.
Acetates↗
[Usefulness of subtotal colectomy with colorectal anastomosis for chronic ulcerative colitis].
Recently in Japan, most of surgeons have been performing restorative proctocolectomy with ileoanal anastomosis for ulcerative colitis, leaving unsolved problems with regard to postoperative complications. Analysis was made on subtotal colectomy with colorectal anastomosis with the following policies. Firstly, the inflammation of the remnant intestine could be easily and correctly controlled by medication in outpatient. Secondly, carcinomas associated with ulcerative colitis can be discovered by postoperative colonoscopic examinations. Operations were carried out to 26 cases of ulcerative colitis for the past 13 years. Subtotal colectomy with colorectal anastomosis were performed to 11 cases. Three cases of colorectal carcinomas associated with ulcerative colitis were experienced. One of the resected specimen was investigated using stereomicroscopy after alcian blue staining to formalin fixed one. As a result of this research, we have convinced that colorectal anastomosis should be favorable surgical potion to the cases of chronic ulcerative colitis because postoperative anal function and quality of life are excellent in our series, in addition, carcinomas in the remnant intestine can be probably easily found out at the early stage by annual colonoscopic examinations with dye staining.
Adolescent↗