Biomedical subjects

H Edo

Publications and source records attributed to H Edo.

9 recordsLinked to original sources

PubMed1999

Manifestation of pulmonary hypertension during REM sleep in obstructive sleep apnea syndrome.

The effect of sleep stage change on pulmonary circulation has not been well documented in patients with obstructive sleep apnea syndrome (OSAS). We investigated whether or not stage-specific change can affect pulmonary artery pressure (Ppa) in patients with OSAS. Thirty-one patients with OSAS underwent right cardiac catheterization in the daytime and the following night, including 19 patients in whom Ppa could be measured throughout non-rapid eye movement (NREM) and rapid eye movement (REM) sleep. Ten of the 19 patients had daytime pulmonary hypertension (PH) defined by a mean Ppa (Ppa) >/= 20 mm Hg. Then we analyzed Ppa response to hypoxia spontaneously occurring during the period of sleep apnea. The slopes of the regression lines between arterial oxygen saturation measured by pulse oximeter (SpO2) and Ppa curves were almost the same in both NREM and REM patient groups with or without daytime PH, whereas the response curve was significantly shifted upward in REM compared with NREM patients with daytime PH. Furthermore, Ppa was elevated more markedly in association with REM burst, phasic REM, compared with tonic REM. We conclude that vascular tone of pulmonary artery could be elevated in association with REM sleep which is independent of the degree of hypoxia, and that this state-specific change is manifested in patients with daytime PH.

Adult↗

PubMed1998

Effects of chest wall vibration on breathlessness during hypercapnic ventilatory response.

Vibratory stimulation applied to the chest wall during inspiration reduces the intensity of breathlessness, whereas the same stimulation during expiration has no effect or may increase breathlessness. The purpose of the present study was to determine whether vibration reduced the intensity of breathlessness during progressive hypercapnia with and without the addition of an external resistive load. A second objective was to see whether the mouth occlusion pressure at 0.2 s (P0.2) was reduced by the vibratory stimulation. Hypercapnic ventilatory response was conducted in 10 healthy male volunteers with simultaneous measurement of visual analog scale, P0.2, and minute ventilation. Hypercapnic ventilatory response was performed and randomly combined with or without vibratory stimulation (100 Hz) as well as with or without inspiratory load. With inspiratory load, in-phase vibration did not cause any significant changes in the slopes of P0.2 and minute ventilation to CO2, whereas the slope of visual analog scale to CO2 significantly decreased from 0.47 +/- 0.15 to 0.34 +/- 0.11 (SE) cm/Torr (P < 0.05). We conclude that in-phase vibration could decrease the slope of breathlessness elicited by inspiratory load combined with hypercapnia without changing motor output.

Adult↗

PubMed1998

Compensatory excretion of prostacyclin and thromboxane metabolites in obstructive sleep apnea syndrome.

Since obstructive sleep apnea syndrome (OSAS) is often linked with systemic hypertension, we sought to clarify the characteristics of prostanoid metabolism in OSAS. In 7 OSAS patients (apnea-hypopnea index, 51.0 +/- 23.4) and 7 non-snorers as control, nocturnal urine was sampled and analyzed for stable metabolites of prostacyclin (PGI2) and thromboxane A2 (TxA2), [6-keto-PGF1alpha and thromboxane B2 (TxB2)]. The ratio of 6-keto-PGF1alpha to TxB2 was significantly higher in OSAS (2.97 +/- 1.52) than in control (1.38 +/- 0.38). Successful treatment with nasal continuous positive airway pressure (8.3 +/- 1.5 cmH2O) for 3 days caused a significant decrease in mean blood pressure in OSAS. Moreover, the 6-keto-PGF1alpha to TxB2 ratio also significantly decreased to 1.74 +/- 0.58, a level which may not significantly different from control. These results suggest that the production ratio of PGI2 to TxA2 is shifted toward vasodilatation in untreated OSAS. We conclude that the production of prostanoids plays a role in compensating for the systemic hypertension in OSAS.

6-Ketoprostaglandin F1 alpha↗

PubMed1998

Control of upper airway function in response to hypoxia in patients with obstructive sleep apnea syndrome.

To clarify the characteristics of upper airway muscles under hypoxic condition in obstructive sleep apnea syndrome (OSAS), we performed the isocapnic progressive hypoxia test during wakefulness in 8 controls and 7 OSAS patients. Electromyographic activities were recorded from the genioglossal muscle (EMG(GG)) and diaphragm (EMG(DIA)) with ventilatory variables. Minute EMG (peak integrated EMG x respiratory rate) activity against P(ET)O2 was calculated by exponential equation, and its response slope represented the hypoxic sensitivity of each muscle, slope(GG) and slope(DIA). There was no significant difference between the slopes of OSAS and control. In contrast, the ratio of the two responses, slope(GG)/slope(DIA), was significantly higher in OSAS (1.61 +/- 0.49 SD) than in control (0.98 +/- 0.43). Moreover, the slope(GG)/slope(DIA) ratio was negatively correlated with the ratio of sleep time with SpO2 lower than 90% to total sleep time. We conclude that the neuromuscular compensatory mechanism of upper airway muscles is effectively developed and plays an important role in preventing nocturnal hypoxemia in OSAS.

Adult↗

PubMed1997

[Nocturnal pulmonary hypertension in patients with obstructive sleep apnea associated with daytime pulmonary hypertension].

We investigated the effect of state-specific changes associated with REM sleep on pulmonary artery pressure in patients with obstructive sleep apnea (OSAS). Six male patients with OSAS (age; 40 +/- 12 SD yrs, BMI; 39.0 +/- 8.6 kg/m2, AHI; 51.5 +/- 28.5) were examined throughout the night by polysomnography, while monitoring pulmonary artery pressure via right cardiac catheterization. All patients had pulmonary hypertension (PH) during periods of wakefulness, and their mean pulmonary artery pressure (PAPm) was 31.1 +/- 7.4 mmHg. PAPm was analyzed at two different points in each apneic episode. PAPbase was the baseline value when inspiratory effects during apnea were not elicited, and PAPpeak was the peak value observed just after the cessation of OSA. PAPpeak was higher in REM (56.3 +/- 12.4) than in NREM (41.4 +/- 6.9 mmHg; P < 0.01), and both values were significantly higher than those observed during periods of wakefulness. The magnitude of elevation of PAP (delta PAP; PAPpeak-PAPbase) in REM and NREM were 11.6 +/- 2.0 and 6.9 +/- 2.8 mmHg, respectively. Relative ratios in the response of PAP to a decrease in O2 desaturation (delta PAP/delta SpO2) showed almost the same value for REM (-0.57 +/- 0.27) and NREM sleep (-0.57 +/- 0.26 mmHg/%). The values of PAPm at SpO2 75% were significantly higher in REM than in NREM (48.7 +/- 11.2 vs. 41.6 +/- 6.2 mmHg). We conclude that transient pulmonary hypertension could be caused not only by hypoxia, but also by state-specific responses (which are unrelated to hypoxia) that occur during REM sleep.

Adult↗

PubMed1994

Differences in the response of genioglossal muscle activity to sustained hypoxia between healthy subjects and patients with obstructive sleep apnea.

The depression of EMG activity in upper airway muscles during sleep is known to be a predisposing factor causing upper airway obstruction in patients with obstructive sleep apnea syndrome (OSAS). To clarify whether or not the selective depression of upper airway muscles could be associated with the hypoxic ventilatory depression, we performed sustained hypercapnic hypoxia tests during wakefulness in 11 control subjects and 10 patients with OSAS. Isocapnic sustained hypoxia around SaO2 80% with mild hypercapnia [PETO2: 45.8 +/- 1.6 (SD) and 46.7 +/- 2.8 mm Hg and PETCO2: 44.2 +/- 4.7 and 43.1 +/- 5.0 mm Hg in control and OSAS groups, respectively] was applied for 20 min. Electromyogram activities were recorded from the genioglossal muscle (EMGGG) and diaphragm (EMGDIA) with ventilatory variables. The magnitudes of hypoxic depression in terms of minute ventilation (VI) and minute EMGDIA (EMGDIA/min) were compared in percentage between peak value and the value at the late period. These values were not significantly different between two groups (VI: 79.2 +/- 10.7 and 66.9 +/- 12.8% and EMGDIA/min: 63.2 +/- 17.1 and 60.4 +/- 24.0% in control and OSAS, respectively). On the contrary, the depression in EMGGG was not consistently observed in control (86.1 +/- 38.6% of the peak value) whereas EMGGG was markedly depressed in OSAS (38.6 +/- 15.7% of the peak value; p < 0.01). It is concluded that sustained hypoxia attenuates the activity in genioglossal muscle in patients with OSAS, but not in control subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed1993

The effect of hypoxic depression on genioglossal muscle activity in healthy subjects and obstructive sleep apnea patients.

We investigated whether selective depression of the genioglossus muscle (GG) activity could be associated with hypoxic ventilatory depression, which is developed in the late phase of the biphasic ventilatory response during sustained hypoxia. Eleven control subjects and 10 patients with obstructive sleep apnea syndrome (OSAS) were examined by an isocapnic sustained hypoxia test for 20 minutes. Ventilatory parameters and electromyographic (EMG) activities were recorded from GG (EMGGG) and diaphragm (EMGDIA). Hypoxic depression in minute ventilation (V1) and EMGDIA occurred when compared between the peak value and the value at late period in both groups. On the contrary, depression in EMGGG was not observed in controls (86% of the peak value), whereas EMGGG was strikingly depressed in OSAS (39% of the peak value). We conclude that sustained hypoxia reduces the activity of GG in OSAS, but not in control subjects. These data suggest that the lack of a compensatory response of GG to sustained hypoxia is possibly responsible for the pathogenesis of OSA.

Electromyography↗

PubMed1992

[Hypoxic ventilatory response and hypoxic depression].

We investigated whether or not the adaptation of peripheral chemoreceptor (PCR) activity can contribute to hypoxic ventilatory depression (HVD) during sustained hypoxia for 20 min in both healthy subjects and patients with sleep apnea. Effects of HVD on diaphragm (DIA) and genioglossal muscle (GG) were also assessed. Withdrawal test, which is well established to solely represent the function of PCR, was repeatedly conducted at 5 and 20 min during sustained hypoxic condition. The results suggested that PCR did not play an important role in the development of HVD. When HVD ensued during sustained hypoxia, minute ventilation and EMGDIA were suppressed to the same extent in both groups. On the other hand, EMGGG was strongly and consistently attenuated in OSAS, whereas it was not always the case in healthy subjects. We speculate that treatment for hypoxic conditions can induce improvement of impaired regulation of breathing via central mechanisms, and it can be an important factor reducing the incidence and the severity of upper airway occlusion or collapse.

Adult↗

PubMed1984

Effect of an anti-ulcer agent, 2'-carboxymethoxy-4, 4'-bis (3-methyl-2-butenyloxy) chalcone (SU-88), on the biosynthesis of gastric sulfated mucosubstances in restrained and water-immersed rats.

2'-Carboxymethoxy-4,4'-bis(3-methyl-2-butenyloxy) chalcone (SU-88) has an anti-ulcer effect which is considered to increase the resistant factors of the gastric mucosa. In order to clarify the mechanism of the action of SU-88, the biosynthesis of gastric sulfated mucosubstances (SMS) in vivo and in vitro was investigated in rats with gastric erosion induced by restraint and water-immersion. The incorporation of 35S-sulfate into gastric SMS was significantly reduced 18 hr after the onset of stress. Pretreatment with SU-88 (500 mg/kg, p.o., X 10 days) prevented a reduction in the incorporation of 35S-sulfate due to stress when 35S-sulfate was administered in vivo. On the contrary, the incorporating activity of 35S-sulfate into the SMS in the isolated rat gastric mucosa with erosion was significantly increased 12 hr after the onset of stress, as compared with that of the control group in vitro. The incorporation of 35S-sulfate into the SMS was still further increased by the oral administration of SU-88. The mode of action of SU-88 on the biosynthesis of SMS was discussed.

Animals↗