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C Shindoh

Publications and source records attributed to C Shindoh.

At least 19 recordsLinked to original sources

Interleukin-12 prevents diaphragm muscle deterioration in a septic animal model.

The effects of an intravenous injection of Interleukin-12 (IL-12) after endotoxin administration and without endotoxin administration on diaphragm muscle were studied using Wistar rats. Three treatment groups, namely a control (Saline+endotoxin) group, an IL-12+endotoxin group and an IL-12 only group were studied. E. coli endotoxin (30 mg/kg) was injected intraperitoneally 5 min after Saline or IL-12 (0.25 microg) injection. In the control group, the force-frequency curves, twitch tension (TT) and slope during contraction time (TT/CT) were significantly lower at 4 h than those at 0 h due to endotoxin (P<0.001, P<0.01 and P<0.01, respectively), and NO production was increased at 4 h as shown by NADPH diaphorase staining. In the IL-12+endotoxin group, the decrement of the force-frequency curves, TT and TT/CT induced by endotoxin at 4 h were significantly prevented compared with those of the control group (P<0.001, P<0.05 and P<0.05, respectively), and NO production was blocked at 4 h. In the IL-12 only group, the force-frequency curves were decreased in the range of high frequency and IL-12 resulted in NO production. Furthermore, the positive muscle fibers detected by NADPH diaphorase staining were classified as type I and IIa muscle fibers by ATPase staining in the control and IL-12 only groups. It is concluded that IL-12 prevents the deterioration of diaphragm muscle contraction induced by endotoxin by reducing NO production in type I and IIa muscle fibers. These results suggest that IL-12 and endotoxin may interfere with each other.

Adenosine Triphosphatases↗

Interleukin-13 prevents diaphragm muscle deterioration in a septic animal model.

The effects of an intravenous injection of Interleukin-13 (IL-13) after endotoxin administration on diaphragm muscle were studied using Wistar rats. Two treatment groups, a control (saline+endotoxin) group and an IL-13 (IL-13+endotoxin) group were studied. E. coli endotoxin (10 mg/kg) was injected intraperitoneally 5 minutes after saline or IL-13 (0.25 microg) injection. The force-frequency curves, twitch kinetics and fatigability were measured at 0 and 4 hours after endotoxin injection. The force-frequency curves and twitch tension in the control group were significantly lower at 4 hours than those at 0 hour due to endotoxin. On the other hand, IL-13 prevented the decrement of the force-frequency curves and twitch tension induced by endotoxin. Nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase histochemistry showed positive staining at 4 hours due to endotoxin in the control group; however, IL-13 also blocked NADPH diaphorase staining at 4 hours. Furthermore, the positive muscle fibers detected by the NADPH diaphorase staining were classified as type I (slow twitch) muscle fibers by ATPase staining. We conclude that IL-13 prevents the deterioration of contraction induced by endotoxin by inhibiting nitric oxide production in the diaphragm muscle, mainly the type I muscle fibers.

Animals↗

Effects of L-NAME and L-arginine on diaphragm contraction in a septic animal model.

The effects of nitric oxide on diaphragm contraction after endotoxin administration were studied in Wistar rats. The animals were divided into seven treatments: a saline-injected group as control, three groups injected with L-NAME (0.01, 0.1, 1 mg/kg) and three groups injected with L-arginine (1, 10, 100 mg/kg). Escherichia coli endotoxin was injected into the peritoneal cavity 15 min later. Twitch kinetics and force-frequency curves were measured 0, 2, and 4 hr after endotoxin injection. In the control group, the force-frequency curves significantly decreased from 0 hr to 4 hr. In the L-NAME group, the force-frequency curves at 4 hr showed significant increases in a dose-dependent manner. In the L-arginine group, the force-frequency curve with 100 mg/kg at 4 hr showed a significant increase. There was no consistent change in the contraction time, half relaxation time, or fatiguability. NADPH diaphorase histochemistry performed on diaphragm muscle samples 4 hr after endotoxin injection showed positive in the control and L-arginine group, but was only weakly observed in L-NAME group. These data suggest that nitric oxide contributes to the endotoxin induced diaphragm contractile deterioration.

Animals↗

Protective effects of interleukin-10 on diaphragm muscle in a septic animal model.

The effects of Interleukin (IL)-10 intravenous injection after endotoxin administration on diaphragm muscle were studied using Wistar rats. The animals were divided into two treatment groups: A saline + endotoxin group as control and an IL-10 + endotoxin group. E. coli endotoxin (10 mg/kg) was injected intraperitoneally 5 minutes after saline or IL-10 (1250 U, 0.25 mg) injection. The force-frequency curves, twitch kinetics and fatigability were measured at 0 and 4 hours after endotoxin injection. In the saline + endotoxin group, the force-frequency curves and half relaxation time were significantly decreased at 4 hours (p < 0.001 and p < 0.05, respectively) compared to those at 0 hour. In the IL-10 + endotoxin group, the decrement in the force-frequency curves by endotoxin was prevented at 4 hours compared to that at 0 hour. Nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase histochemistry showed positive staining in the saline + endotoxin at 4 hours, but there was no significant staining at 0 or 4 hours in the IL-10 + endotoxin group. These data suggest that IL-10 prevents the deterioration of contraction induced by endotoxin by inhibiting nitric oxide production in the diaphragm muscle.

Animals↗

N-acetylcysteine inhibits loss of diaphragm function in streptozotocin-treated rats.

We examined whether streptozotocin (STZ)-induced diabetic rats have an impairment in diaphragm contractility, and if so, whether N-acetylcysteine (NAC), a nonspecific antioxidant, prevents this impairment. First, diaphragm contractility, assessed by tension-frequency relationships and twitch kinetics in in vitro diaphragm strip preparations of Wistar rats, was obtained on Days 3 and 7 after administration of STZ of 30 or 60 mg/kg body weight, and compared with that of the control group. Second, NAC at 500 mg/kg body weight or vehicle solution was administered orally every day in rats treated with STZ at 60 mg/kg body weight, and diaphragm function on Day 7 after starting NAC treatment was compared between vehicle control and STZ-treated groups. We found that diaphragm function in STZ-treated rats, which had hyperglycemia, decreased in a dose- and time-dependent manner. NAC inhibited the decrease in diaphragm contractility in STZ-treated rats without reducing blood glucose. These findings suggest that the loss of diaphragm function in STZ-induced diabetic rats is not directly related to hyperglycemia. The data are consistent with secondary alterations of normal cytokine signaling or changes in the redox state of the cell, both of which could be affected by NAC treatment.

Acetylcysteine↗

[Relief of dyspnea after lung volume reduction in patients with pulmonary emphysema].

We studied dyspnea and pulmonary function during treadmill exercise in 10 patients with pulmonary emphysema before and at least 3 months after thoracoscopic volume reduction. Dyspnea was significantly less after surgery. Ventilatory function, gas exchange, respiratory muscle function, and exercise performance also improved significantly. The degree of volume reduction, estimated by the decrease in FRC as measured by body plethysmography correlated with the degree to which dyspnea was relieved. Volume reduction may be appropriate as a treatment for dyspnea in patients with pulmonary emphysema.

Dyspnea↗

TNF-alpha mRNA expression in diaphragm muscle after endotoxin administration.

We studied gene expression and production of TNF-alpha in the diaphragm tissue and changes of muscle contractile properties after endotoxin injection (Escherichia coli, 20 mg/kg) in 88 rats. We assessed the muscle contractile properties by force-frequency curves and twitch kinetics using dissected diaphragm muscle strips. The peak tensions of force-frequency curves decreased from control values (2.15 +/- 0.2 kg/cm2) up to 4 h (0.81 +/- 0.17, p < 0.001), and then increased at 6 h (1.36 +/- 0.19, p < 0.05) after endotoxin injection. The cytotoxic activity on L929 cells in arterial blood samples maximally increased at 2 h (p < 0.001), then decreased to 6 h (p < 0.05). TNF-alpha mRNA in diaphragm tissue was detected by Northern blot method at 1 and 1.5 h, and the immunolocalization of TNF-alpha was evaluated at 2 and 4 h by immunohistochemistry in the muscle tissues. Furthermore, preinjection with anti-m TNF-alpha antibody prevented the decrement of force-frequency curves after endotoxin injection of 10 microliters/kg. From this evidence that TNF-alpha gene expression and production occurred in the diaphragm tissue, but anti-m TNF-alpha antibody preinjection prevented the deterioration of diaphragm muscle contractile properties, we suggest that TNF-alpha may act on muscle cells extracellularly.

Analysis of Variance↗

[Portable home monitoring system in screening for sleep-disordered breathing].

Screening for sleep-disordered breathing is often done in an interview and with a questionnaire. This method is indirect and it appears to underestimate the prevalence of sleep apnea syndrome. Recently, several devices such as the Medilog and Vitalog portable monitoring systems were developed. However, these devices are difficult for patients to operate by themselves, because they include EEG monitoring or measurement of chest and abdominal movement. Therefore, we developed a portable monitoring system that is easier to operate. This system can be used to assess three variables: oronasal airflow, tracheal sound, and electrical activity of the heart. It stores the time of the onset of apnea, apnea duration, and R-R intervals with a built-in microcomputer. Apnea episodes, total apnea time, mean apnea time, and R-R interval are analyzed with a host computer. The sensitivity an specificity of this system are 92.5% and 87.5%, respectively, with an apnea index (AI) of less than 10 episodes/h. Using this device, we found that the prevalence of sleep apnea syndrome among Japanese industrial workers who had an AI of more than 10 episodes was 7.5%. Moreover, from 1984 to 1994 we used this device to monitor 1019 outpatients who complained of sleep disturbances such as snoring, abnormal breathing during sleep, and excessive daytime sleepiness, and found sleep apnea (AI > or = 10) in about 50% of these patients. This monitoring system is useful for screening of outpatients with sleep apnea and for epidemiological studies of sleep apnea. However, it may be necessary to include a non-invasive system for monitoring oxygen saturation in the portable sleep monitor, to detect hypoventilation during sleep.

Adolescent↗

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↗

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↗

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↗

Effect of PEG-superoxide dismutase on the diaphragmatic response to endotoxin.

Although it is known that endotoxin can induce diaphragmatic dysfunction, the mechanism of this effect is not fully understood. However, because the effects of endotoxin on other tissues appear to be mediated in part by free radicals, the present study sought to determine if free radicals may also contribute to the diaphragmatic dysfunction induced by endotoxin administration. Studies were performed on four groups of hamsters. One group of animals received intraperitoneal injections of endotoxin on the first and second days of study (i.e., 10 and 20 mg/kg, respectively). The second group received saline rather than endotoxin, the third group received both endotoxin and a free radical scavenger, PEG-SOD (2,000 U/kg given intraperitoneally every 12 h on Days 1 and 2), and the fourth group received PEG-SOD alone. All groups were killed on the third study day (i.e., 48 h after the initial injections). Diaphragmatic contractile function was assessed in vitro using muscle strips excised from the costal diaphragms of freshly killed animals; diaphragm samples were also assayed for malondialdehyde (MDA), a commonly used index of free-radical-mediated lipid peroxidation. MDA levels were higher in diaphragms from endotoxin-treated animals than from saline-treated control animals, and the contractility of diaphragm strips from endotoxin-treated animals was reduced when compared with strips from saline-treated control animals. Administration of PEG-SOD prevented MDA formation and contractile dysfunction in endotoxin-treated animals. Diaphragm contractility and MDA levels for animals given PEG-SOD alone were similar to those for saline-treated control animals.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[Bronchial asthma].

In the first study, to clarify whether increased vagal afferent activity contributes to the increase in ventilatory response to CO2 in patients with asthma, we examined the effects of prostaglandin E2 (PGE2) inhalation on the respiratory response to CO2 in seven normal subjects. After PGE2 inhalation, the ventilatory and occlusion pressure responses to CO2 increased significantly compared with those after saline inhalation, with no increase in respiratory resistance. These results suggest that increase in vagal afferent activity may play a role in the increased hypercapnic response during acute exacerbations of asthma. In the second study, to clarify the reduced respiratory chemosensitivity associated with asthma-related deaths, we examined the hypercapnic and hypoxic ventilatory responses in five patients with near-fatal asthma who were given artificial ventilation and/or became unconsciousness during an acute exacerbation of asthma. Hypoxic ventilatory response was significantly lower in these subjects than in patients with uncomplicated asthma and normal subjects, suggesting that lowered hypoxic ventilatory response may be related to death from asthma.

Asthma↗

Decrease in functional residual capacity during inspiratory loading and the sensation of dyspnea.

The purposes of the present study were to determine the changes in functional residual capacity (FRC) during inspiratory loading and to examine their mechanisms. We studied seven normal subjects seated in a body plethysmograph. In both graded inspiratory elastic (35, 48, and 68 cmH2O/l) and resistive (21, 86, and 192 cmH2O.l-1.s) loading, FRC invariably decreased from control FRC and phasic expiratory activity increased. The reduction in FRC was greater with greater loads. A single inspiratory effort against an inspiratory occlusion at three different target mouth pressures (-25, -50, and -75 cmH2O) and durations (1, 2, and 5 s) also resulted in a decrease in FRC with an increase in expiratory electromyogram activity in the following expiration. The decrease in FRC was greater with greater target pressure and duration. This decrease in FRC is qualitatively similar to that during inspiratory loaded breathing, and we suspect that the same mechanisms are at work. Because neither vagal nor chemoreceptor reflex can account for these responses, we suspect conscious awareness of breathing or behavioral control to be responsible. In an additional study, the sensation of discomfort of breathing during elastic loading decreased with a decrease in FRC. These results suggest that the reduced FRC may be due to behavioral control of breathing to reduce the sensation of dyspnea during inspiratory loading.

Adult↗

Effect of acute fasting on diaphragm strength and endurance.

The effects of short periods of fasting on diaphragm contractile function remain unclear. The purpose of the present study was (1) to examine the relationship between duration of acute fasting and diaphragm contractile performance, and (2) to assess the effects of fasting on diaphragm glycogen stores and the relationship between changes in diaphragm function and alterations in muscle glycogen stores. Studies were performed on four groups of Syrian hamsters (nine animals in each group). One group served as a control and was allowed to feed normally, whereas the other three groups were fasted for either 1, 2, or 3 days. Diaphragm strips from animals were studied in vitro by measuring tension during electrically induced contractions. Two strips from each animal were studied; one strip was examined with a bath glucose equal to the prevailing blood glucose, and the second was preincubated in a high glucose solution (170 mg/dl) for 20 min. Fasting resulted in reductions in body weight, blood glucose concentrations, diaphragm strength, and diaphragm endurance in strips tested at the prevailing blood glucose levels. These effects were pronounced in animals fasted for 3 days, with little or no change in diaphragm contractility observed in animals fasted for shorter periods. Diaphragm weight, thickness, and glycogen content were unchanged in the fasted animals, as was the weight of the soleus muscle. Preincubation of strips from 3-day-fasted animals in a high glucose medium resulted in a significant increase in diaphragm strip strength and endurance.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

Effects of elastic loading and exercise on pulmonary gas exchange in dogs.

We assessed the effects of negative intrathoracic pressure induced by inspiratory elastic loading on pulmonary, gas exchange with and without electrically induced hindlimb exercise in 8 normal, anesthetized dogs. Two elastic loads (EL) were used; one of 81 and one of 140 cmH2O/liter. These are equivalent to doubling and tripling the normal elastance of the dog's respiratory system, respectively. Elastic loading decreased ventilation and caused hypoxemia and hypercapnia, but it did not affect systemic arterial pressure or heart rate. During exercise, increase in ventilation was limited, whereas increase in cardiac output was not affected by elastic loading. Alveolar-arterial O2 tension difference (A-aDO2) was not changed significantly by exercise alone. However, elastic loading accompanied by exercise increased A-aDO2. Although comparable end-inspiratory pleural pressure was achieved with large EL (-29 +/- 2 cmH2O, mean +/- SE) and small EL with exercise (-30 +/- 2 cmH2O), the latter increased A-aDO2 whereas the former did not. Large negative intrapleural pressure combined with increased cardiac output may have caused transient interstitial edema.

Animals↗

[Restrictive lung disease].

It was found that functional residual capacity (FRC) invariably decreased during inspiratory elastic loaded breathing and that its magnitude increased progressively with an increase in the intensity of the load. This response could not be explained by chemoreflexes nor neural reflexes. Because the sensation of dyspnea decreased at lowered FRC (FRC-0.5 liter) than that at FRC during elastic loading, we speculate that FRC decreased behaviorally during elastic loading to reduce the sensation of dyspnea. We found that the respiratory muscle became fatigued more easily at FRC than at lowered FRC during elastic loading. We therefore conclude that the decrease in FRC may be one of the compensatory mechanisms during elastic loaded breathing.

Functional Residual Capacity↗