The Experts below are selected from a list of 2418 Experts worldwide ranked by ideXlab platform

K Shirato - One of the best experts on this subject based on the ideXlab platform.

  • Effects of prostaglandin E2 inhalation on Hypercapnic Response in normal subjects.
    American journal of respiratory and critical care medicine, 1994
    Co-Authors: J Midorikawa, Y Kikuchi, O Taguchi, W Hida, S Okabe, T Takishima, K Shirato
    Abstract:

    It is known that the ventilatory Response to carbon dioxide (CO2) is increased in asthmatics with airway obstruction. Increased vagal afferent activity as well as increased airway resistance have been postulated as the causative mechanisms. However, whether increased vagal afferent activity without bronchoconstriction increases the ventilatory Response to CO2 has not been investigated in humans. We examined the effects of prostaglandin E2 (PGE2) inhalation, which is known to stimulate vagal afferent receptors in the lung without an increase in airway resistance, on the respiratory Response to CO2 in seven healthy male subjects. Either physiologic saline or PGE2 (100 micrograms/ml) was inhaled through a Bird nebulizer for 3 min. Twenty minutes after each inhalation, the Responses of minute ventilation (VE) and occlusion pressure (P0.1) to hyperoxic hypercapnia were measured. Both the relationships between VE and P0.1 to an increase in tension of end-tidal CO2 (PETCO2) were analyzed by linear regression. Although the mean value of respiratory resistance after PGE2 (3.0 cm H2O/L/s +/- 0.4) did not differ significantly from that after saline (3.1 cm H2O/L/s +/- 0.4), inhaled PGE2 significantly increased the Hypercapnic Response. This result suggests that the increased vagal afferent activity per se plays an important role in increasing the Hypercapnic ventilatory Response in humans.

  • Effects of prostaglandin E2 inhalation on Hypercapnic Response in normal subjects.
    American Journal of Respiratory and Critical Care Medicine, 1994
    Co-Authors: J Midorikawa, Y Kikuchi, O Taguchi, W Hida, S Okabe, T Takishima, K Shirato
    Abstract:

    It is known that the ventilatory Response to carbon dioxide (CO2) is increased in asthmatics with airway obstruction. Increased vagal afferent activity as well as increased airway resistance have been postulated as the causative mechanisms. However, whether increased vagal afferent activity without bronchoconstriction increases the ventilatory Response to CO2 has not been investigated in humans. We examined the effects of prostaglandin E2 (PGE2) inhalation, which is known to stimulate vagal afferent receptors in the lung without an increase in airway resistance, on the respiratory Response to CO2 in seven healthy male subjects. Either physiologic saline or PGE2 (100 micrograms/ml) was inhaled through a Bird nebulizer for 3 min. Twenty minutes after each inhalation, the Responses of minute ventilation (VE) and occlusion pressure (P0.1) to hyperoxic hypercapnia were measured. Both the relationships between VE and P0.1 to an increase in tension of end-tidal CO2 (PETCO2) were analyzed by linear regression. Al...

Merrill M. Mitler - One of the best experts on this subject based on the ideXlab platform.

  • Effect of bedtime alcohol on inspiratory resistance and respiratory drive in snoring and nonsnoring men.
    Alcoholism clinical and experimental research, 1997
    Co-Authors: Arthur Dawson, Barbara G. Bigby, J. Steven Poceta, Merrill M. Mitler
    Abstract:

    We measured inspiratory resistance (R1), inspiratory occlusion pressure (P0.1), and the ventilatory Responses to hypercapnia and isocapnic hypoxia during waking and during stage 2 non-rapid eye movement sleep in nine young men who were habitual snorers. They were studied on 2 nights during the 3 hours after receiving a bedtime drink containing either a placebo or 100-proof vodka (1.5 ml/kg) in orange juice. We compared the results with those we reported previously in 10 nonsnoring but otherwise similar men. Waking R1 was the same in nonsnorers and snorers, and it was not affected by ethanol. During sleep on the control night, R1 increased by 70% in nonsnorers and by 280% in snorers. On the ethanol night, the increase from waking to sleeping was more than doubled in both nonsnorers and snorers. P0.1 and the Responses to hypercapnia and hypoxia showed no differences between nonsnorers and snorers, therefore the results from the two groups were pooled. Minute ventilation and the Hypercapnic Response decreased from waking to sleeping and P0.1 was more negative during sleep, but there was no significant effect of ethanol. There was a significant correlation between the changes from waking to sleeping in R1 and P0.1 on the ethanol night suggesting that inspiratory effort increased in Response to the increased resistance. The Response to isocapnic hypoxia showed no effect of either sleep state or drink. Inspiratory time did not change but mean inspiratory flow (VT/T1) was significantly reduced during sleep on both control and ethanol nights. The duty cycle ratio (T1/Ttot) was significantly increased during sleep on the ethanol night. Despite its great effect on inspiratory resistance, especially in snorers, ethanol, in the dose used in our study, does not augment the depression of minute ventilation or of the Hypercapnic Response that occur normally in stage 2 non-rapid eye movement sleep. After ethanol, our subjects showed the decreased VT/T1 and the increased T1/Ttot that occur normally during sleep in Response to an inspiratory resistive load. However, they also showed increased inspiratory effort. The combination of increased inspiratory resistance and greater inspiratory effort would increase the tendency of an unstable upper airway to collapse and could account for the aggravation of obstructive sleep apnea by ethanol.

  • Effect of bedtime ethanol on total inspiratory resistance and respiratory drive in normal nonsnoring men.
    Alcoholism clinical and experimental research, 1993
    Co-Authors: Arthur Dawson, Patricia Lehr, Barbara G. Bigby, Merrill M. Mitler
    Abstract:

    We have previously reported that bedtime ethanol (2.0 ml/kg of 100 proof vodka) increases upper airway closing pressure in males who habitually snored but were otherwise healthy. We also observed that some of these snorers developed obstructive apneas. To explore this phenomenon in more detail, we measured the inspiratory resistance (R1) and respiratory drive after bedtime ethanol in 10 nonobese men (ages 23 to 33) with no history of snoring. Subjects went to bed wearing a tightly fitting valved mask over the nose and mouth that allowed measurement of inspiratory and expiratory flow, pressure in the mask, and endtidal CO2. We measured R1 by calculating the pressure difference between the mouth and a balloon positioned in the midesophagus. Respiratory drive was quantified by the inspiratory occlusion pressure (P0.1), the ventilatory Response to hyperoxic hypercapnia (ΔVE/ΔPETCO2), and the ventilatory Response to isocapnic hypoxia (ΔVE/ΔSaO2). Measurements were made during waking and during stage 2 NREM sleep on two nights: (1) when the subjects drank 1.5 ml/kg of 100 proof vodka in orange juice over a 30-min period 15-45 min before lights out and (2) when the orange juice contained less than 0.1 ml of vodka floating on the top. Eight of the nine men in whom we had technically adequate measurements showed a rise in R1 during NREM sleep above the waking level on both control and ethanol nights and the sleeping R1 was greater on the ethanol than on the control night. There was a tendency for P0.1 to be higher during sleep and greater on the ethanol night, suggesting that the neural output to the respiratory muscles was not depressed and may have been stimulated by the inspiratory “loading” secondary to the increased R1. The Hypercapnic Response was significantly depressed during sleep. Whereas the Response tended to be less on the ethanol than on the control night, the difference was not significant. The hypoxic Response showed little change from waking to sleeping and no significant change with ethanol. We speculate that inspiratory loading due to increased upper airway resistance tends to stimulate respiratory drive and thereby partially offsets the depressant effect of ethanol on the central respiratory chemoreceptors.

J Midorikawa - One of the best experts on this subject based on the ideXlab platform.

  • Effects of prostaglandin E2 inhalation on Hypercapnic Response in normal subjects.
    American journal of respiratory and critical care medicine, 1994
    Co-Authors: J Midorikawa, Y Kikuchi, O Taguchi, W Hida, S Okabe, T Takishima, K Shirato
    Abstract:

    It is known that the ventilatory Response to carbon dioxide (CO2) is increased in asthmatics with airway obstruction. Increased vagal afferent activity as well as increased airway resistance have been postulated as the causative mechanisms. However, whether increased vagal afferent activity without bronchoconstriction increases the ventilatory Response to CO2 has not been investigated in humans. We examined the effects of prostaglandin E2 (PGE2) inhalation, which is known to stimulate vagal afferent receptors in the lung without an increase in airway resistance, on the respiratory Response to CO2 in seven healthy male subjects. Either physiologic saline or PGE2 (100 micrograms/ml) was inhaled through a Bird nebulizer for 3 min. Twenty minutes after each inhalation, the Responses of minute ventilation (VE) and occlusion pressure (P0.1) to hyperoxic hypercapnia were measured. Both the relationships between VE and P0.1 to an increase in tension of end-tidal CO2 (PETCO2) were analyzed by linear regression. Although the mean value of respiratory resistance after PGE2 (3.0 cm H2O/L/s +/- 0.4) did not differ significantly from that after saline (3.1 cm H2O/L/s +/- 0.4), inhaled PGE2 significantly increased the Hypercapnic Response. This result suggests that the increased vagal afferent activity per se plays an important role in increasing the Hypercapnic ventilatory Response in humans.

  • Effects of prostaglandin E2 inhalation on Hypercapnic Response in normal subjects.
    American Journal of Respiratory and Critical Care Medicine, 1994
    Co-Authors: J Midorikawa, Y Kikuchi, O Taguchi, W Hida, S Okabe, T Takishima, K Shirato
    Abstract:

    It is known that the ventilatory Response to carbon dioxide (CO2) is increased in asthmatics with airway obstruction. Increased vagal afferent activity as well as increased airway resistance have been postulated as the causative mechanisms. However, whether increased vagal afferent activity without bronchoconstriction increases the ventilatory Response to CO2 has not been investigated in humans. We examined the effects of prostaglandin E2 (PGE2) inhalation, which is known to stimulate vagal afferent receptors in the lung without an increase in airway resistance, on the respiratory Response to CO2 in seven healthy male subjects. Either physiologic saline or PGE2 (100 micrograms/ml) was inhaled through a Bird nebulizer for 3 min. Twenty minutes after each inhalation, the Responses of minute ventilation (VE) and occlusion pressure (P0.1) to hyperoxic hypercapnia were measured. Both the relationships between VE and P0.1 to an increase in tension of end-tidal CO2 (PETCO2) were analyzed by linear regression. Al...

  • Bronchial asthma
    Nihon Kyobu Shikkan Gakkai zasshi, 1992
    Co-Authors: Y Kikuchi, J Midorikawa, W Hida, S Okabe, G Tamura, M Homma, C Shindoh, T Takishima
    Abstract:

    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.

M Cupa - One of the best experts on this subject based on the ideXlab platform.

  • effects of doxapram on Hypercapnic Response during weaning from mechanical ventilation in copd patients
    Chest, 1992
    Co-Authors: J L Pourriat, M Baud, Christine Lamberto, J P Fosse, M Cupa
    Abstract:

    Failure of weaning from mechanical ventilation in COPD patients is often related to diaphragmatic fatigue. Whether there is a central respiratory drive fatigue and a reserve of excitability is still debated. The purpose of this study was to analyze the following in 13 COPD patients weaned from mechanical ventilation: (1) ventilatory ( V ˙ e/PetCO 2 ) and neuromuscular (P0.1/PetCO 2 ) Response to hypercapnia; (2) the maximum reserve capacity measured through changes in the V ˙ e/PetCO 2 and P0.1/PetCO 2 slopes after doxapram (DXP) infusion, which, given during the test, allows measurement of the maximum Response capacity to overstimulation; and (3) analyze the influence of these changes on the outcome of weaning. The results show a variable P0.1/PetCO 2 Response and a low V ˙ e/PetCO 2 . DXP infusion does not change the slopes of these relations but increases the end-expiratory volume (ΔFRCd); (p<0.02). Since there was no change in the V ˙ e/PetCO 2 , P0.1/PetCO 2 , and ΔFRC values with or without DXP, there was no excitability reserve in patients who were successfully weaned. When weaning failed, DXP did not change V ˙ e/PetCO 2 and P0.1/ PetCO 2 slope, but ΔFRCd was greater the ΔFRC (p

  • Effects of Doxapram on Hypercapnic Response during Weaning from Mechanical Ventilation in COPD Patients
    Chest, 1992
    Co-Authors: J L Pourriat, Christine Lamberto, Baud M, M Cupa
    Abstract:

    Failure of weaning from mechanical ventilation in COPD patients is often related to diaphragmatic fatigue. Whether there is a central respiratory drive fatigue and a reserve of excitability is still debated. The purpose of this study was to analyze the following in 13 COPD patients weaned from mechanical ventilation: (1) ventilatory ( V ˙ e/PetCO 2 ) and neuromuscular (P0.1/PetCO 2 ) Response to hypercapnia; (2) the maximum reserve capacity measured through changes in the V ˙ e/PetCO 2 and P0.1/PetCO 2 slopes after doxapram (DXP) infusion, which, given during the test, allows measurement of the maximum Response capacity to overstimulation; and (3) analyze the influence of these changes on the outcome of weaning. The results show a variable P0.1/PetCO 2 Response and a low V ˙ e/PetCO 2 . DXP infusion does not change the slopes of these relations but increases the end-expiratory volume (ΔFRCd); (p

Eric Herlenius - One of the best experts on this subject based on the ideXlab platform.

  • astrocytes release prostaglandin e2 to modify respiratory network activity
    eLife, 2017
    Co-Authors: David Forsberg, Thomas Ringstedt, Eric Herlenius
    Abstract:

    : Previously (Forsberg et al., 2016), we revealed that prostaglandin E2 (PGE2), released during Hypercapnic challenge, increases calcium oscillations in the chemosensitive parafacial respiratory group (pFRG/RTN). Here, we demonstrate that pFRG/RTN astrocytes are the PGE2 source. Two distinct astrocyte subtypes were found using transgenic mice expressing GFP and MrgA1 receptors in astrocytes. Although most astrocytes appeared dormant during time-lapse calcium imaging, a subgroup displayed persistent, rhythmic oscillating calcium activity. These active astrocytes formed a subnetwork within the respiratory network distinct from the neuronal network. Activation of exogenous MrgA1Rs expressed in astrocytes tripled astrocytic calcium oscillation frequency in both the preBotzinger complex and pFRG/RTN. However, neurons in the preBotC were unaffected, whereas neuronal calcium oscillatory frequency in pFRG/RTN doubled. Notably, astrocyte activation in pFRG/RTN triggered local PGE2 release and blunted the Hypercapnic Response. Thus, astrocytes play an active role in respiratory rhythm modulation, modifying respiratory-related behavior through PGE2 release in the pFRG/RTN.

  • astrocytes release prostaglandin e2 to modify respiratory network activity
    bioRxiv, 2017
    Co-Authors: David Forsberg, Thomas Ringstedt, Eric Herlenius
    Abstract:

    Prostaglandin E2 (PGE2) released during Hypercapnic challenge increases Ca 2+ oscillation frequency in the chemosensitive parafacial respiratory group (pFRG/RTN). Here, we demonstrate that pFRG/RTN astrocytes are the PGE2 source. Two distinct astrocyte subtypes were found using transgenic mice expressing GFP and MrgA1 receptors in astrocytes. Although most astrocytes appeared dormant during time-lapse calcium imaging, a subgroup displayed persistent, rhythmic oscillating calcium activity. These active astrocytes formed a subnetwork within the respiratory network distinct from the neuronal network. Activation of exogenous MrgA1 receptors expressed in astrocytes tripled their calcium oscillation frequency activity in both the preBotzinger complex and pFRG/RTN. However, neurons in the preBotC were unaffected, whereas neuronal calcium oscillatory frequency in pFRG/RTN doubled. Notably, astrocyte activation in pFRG/RTN triggered local PGE2 release and blunted the Hypercapnic Response. Thus, astrocytes play an active role in respiratory rhythm modulation, modifying respiratory-related behavior through PGE2 release in the pFRG/RTN.