Search PubMed⌕ Search

Biomedical subjects

T Chonan

Publications and source records attributed to T Chonan.

At least 37 records · Page 2Linked to original sources
PubMed1991

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↗
PubMed1990

Effects of focal cooling in the ventrolateral medulla on chemoresponsiveness in dogs.

Studies in cats and dogs have shown that the ventrolateral region of the medulla participates significantly in the shaping of the respiratory rhythm. The purpose of this study was to examine the effects of unilateral focal cooling (15-20 degrees C) in the ventrolateral medullary region on respiratory responses to hypercapnia and hypoxia in dogs. A cryoprobe was used to cool selected locations in the ventrolateral medulla in 9 anesthetized and vagotomized dogs. Diaphragmatic electromyogram (EMG) was measured with implanted electrodes. The animals were ventilated artificially at a constant rate with 100% O2 and the inspired gas was switched to 7% CO2 in O2 or 10% O2 in N2 to determine the response to hypercapnia or hypoxia. The sites cooled ranged 4.0-8.0 mm rostral to obex, 3.0-5.5 mm lateral to midline, and within 1.5 mm deep from the ventral surface of the medulla. Unilateral focal cooling in this region significantly decreased the responses of both the amplitude and the rate of rise of diaphragmatic EMG to hypercapnia and hypoxia. These results support the hypothesis that neural structures in the ventrolateral medulla are important in the respiratory responses to hypoxia and hypercapnia as well as for the setting of respiratory drive and timing.

Animals↗
PubMed1990

Sensation of dyspnea during hypercapnia, exercise, and voluntary hyperventilation.

To determine whether the intensity of dyspnea at a given level of respiratory motor output depends on the nature of the stimulus to ventilation, we compared the sensation of difficulty in breathing during progressive hypercapnia (HC) induced by rebreathing, during incremental exercise (E) on a cycle ergometer, and during isocapnic voluntary hyperventilation (IVH) in 16 normal subjects. The sensation of difficulty in breathing was rated at 30-s intervals by use of a visual analog scale. There were no differences in the level of ventilation or the base-line intensity of dyspnea before any of the interventions. The intensity of dyspnea grew linearly with increases in ventilation during HC [r = 0.98 +/- 0.02 (SD)], E (0.95 +/- 0.03), and IVH (0.95 +/- 0.06). The change in intensity of dyspnea produced by a given change in ventilation was significantly greater during HC [0.27 +/- 0.04 (SE)] than during E (0.12 +/- 0.02, P less than 0.01) and during HC (0.30 +/- 0.04) than during IVH (0.16 +/- 0.03, P less than 0.01). The difference in intensity of dyspnea between HC and E or HC and IVH increased as the difference in end-tidal PCO2 widened, even though the time course of the increase in ventilation was similar. No significant differences were measured in the intensity of dyspnea that occurred with changes in ventilation between E and IVH. These results indicate that under nearisocapnic conditions the sensation of dyspnea produced by a given level of ventilation seems not to depend on the method used to produce that level of ventilation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Effects of expiratory resistive loading on the sensation of dyspnea.

To determine whether an increase in expiratory motor output accentuates the sensation of dyspnea (difficulty in breathing), the following experiments were undertaken. Ten normal subjects, in a series of 2-min trials, breathed freely (level I) or maintained a target tidal volume equal to (level II) or twice the control (level III) at a breathing frequency of 15/min (similar to the control frequency) with an inspiratory load, an expiratory load, and without loads under hyperoxic normocapnia. In tests at levels II and III, end-expiratory lung volume was maintained at functional residual capacity. A linear resistance of 25 cmH2O.1(-1).s was used for both inspiratory and expiratory loading; peak mouth pressure (Pm) was measured, and the intensity of dyspnea (psi) was assessed with a visual analog scale. The sensation of dyspnea increased significantly with the magnitude of expiratory Pm during expiratory loading (level II: Pm = 9.4 +/- 1.5 (SE) cmH2O, psi = 1.26 +/- 0.35; level III: Pm = 20.3 +/- 2.8 cmH2O, psi = 2.22 +/- 0.48) and with inspiratory Pm during inspiratory loading (level II: Pm = 9.7 +/- 1.2 cmH2O, psi = 1.35 +/- 0.38; level III: Pm = 23.9 +/- 3.0 cmH2O, psi = 2.69 +/- 0.60). However, at each level of breathing, neither the intensity of dyspnea nor the magnitude of peak Pm during loading was different between inspiratory and expiratory loading. The augmentation of dyspnea during expiratory loading was not explained simply by increases in inspiratory activity. The results indicate that heightened expiratory as well as inspiratory motor output causes comparable increases in the sensation of difficulty in breathing.

Adult↗
PubMed1990

Effects of changes in level and pattern of breathing on the sensation of dyspnea.

Breathing during hypercapnia is determined by reflex mechanisms but may also be influenced by respiratory sensations. The present study examined the effects of voluntary changes in level and pattern of breathing on the sensation of dyspnea at a constant level of chemical drive. Studies were carried out in 15 normal male subjects during steady-state hypercapnia at an end-tidal PCO2 of 50 Torr. The intensity of dyspnea was rated on a Borg category scale. In one experiment (n = 8), the level of ventilation was increased or decreased from the spontaneously adopted level (Vspont). In another experiment (n = 9), the minute ventilation was maintained at the level spontaneously adopted at PCO2 of 50 Torr and breathing frequency was increased or decreased from the spontaneously adopted level (fspont) with reciprocal changes in tidal volume. The intensity of dyspnea (expressed as percentage of the spontaneous breathing level) correlated with ventilation (% Vspont) negatively at levels below Vspont (r = -0.70, P less than 0.001) and positively above Vspont (r = 0.80, P less than 0.001). At a constant level of ventilation, the intensity of dyspnea correlated with breathing frequency (% fspont) negatively at levels below fspont (r = -0.69, P less than 0.001) and positively at levels above fspont (r = 0.75, P less than 0.001). These results indicate that dyspnea intensifies when the level or pattern of breathing is voluntarily changed from the spontaneously adopted level. This is consistent with the possibility that ventilatory responses to changes in chemical drive may be regulated in part to minimize the sensations of respiratory effort and discomfort.

Adult↗
PubMed1989

Effects of electrical stimulation of the genioglossus on upper airway resistance in anesthetized dogs.

We examined the relationship between the frequency of stimulation of the genioglossus and upper airway resistance in six anesthetized dogs in the supine position. The upper airway was isolated from the lower airway by transecting the cervical trachea, and the pressure flow relationship of the upper airway was obtained by applying constant negative pressure (5, 10, and 20 cm H2O) to the proximal cut end of the trachea. Electrical stimulation of the genioglossus was performed at a constant voltage (10 to 20 V) and at various frequencies (as high as 100 Hz). Upper airway resistance (Rua) during both inspiration and expiration increased with an increase in tracheal negative pressure, and at each tracheal negative pressure Rua was significantly reduced by stimulation of the genioglossus. The effects of genioglossal muscle stimulation were nonlinearly dependent on the stimulating frequency. Below 50 Hz, Rua decreased markedly as the stimulating frequency was increased, but above 50 Hz, Rua plateaued at a minimum value. These findings suggest that at a stimulating frequency of more than 50 Hz, upper airway patency is stably maintained in anesthetized dogs.

Airway Resistance↗
PubMed1989

Effects of submental electrical stimulation during sleep on upper airway patency in patients with obstructive sleep apnea.

We examined the effects of percutaneous electrical stimulation of the genioglossus in six patients with obstructive sleep apnea syndrome (OSAS) during sleep and investigated the possible applicability of this procedure as a treatment of OSAS. Six patients with OSAS were polysomnographically studied in the supine position during all-night sessions with and without electrical stimulation of the genioglossus. Using an apnea demand-type stimulator that we developed, electrical pulses of 0.5 ms (repetition rate, 50 Hz) and 15 to 40 V were delivered through bipolar electrodes (10 mm in diameter) attached to the skin of the submental region when apnea lasted more than 5 s, and was stopped immediately after breathing resumed or after 10 s at the longest. With submental stimulation, the apnea index, apnea time/total sleep time, longest apnea duration, and the number of times per hour that oxygen saturation dropped below 85% decreased significantly compared with those on control nights. The lowest arterial oxygen saturation and the duration of sleep stages III and IV increased significantly. The stimulation employed did not cause arousal, and it did not affect blood pressure or heart rate significantly. These findings show that submental stimulation decreases the incidence of apnea episodes and promotes deeper sleep without accompanying serious side effects, suggesting that the apnea demand-type stimulator may be a noninvasive and effective treatment for OSAS.

Electric Stimulation↗
PubMed1989

Change in P wave height during progressive exercise in patients with chronic obstructive pulmonary disease.

We examined changes in P wave height in lead II of electrocardiogram during progressive exercise in patients with chronic obstructive pulmonary disease (COPD), and obtained the slope (delta P/delta VO2, %/ml/min) of the regression line calculated from the relationship between percent change of P wave height and oxygen consumption (VO2). Four COPD patients, who had a decrease over 5 mmHg in arterial oxygen tension (PaO2) at maximal exercise (group A), had significantly greater slope (0.45 +/- 0.14%/ml/min, mean +/- S.E.) than in five COPD patients (group B, 0.14 +/- 0.05), who did not have a decrease over 5 mmHg in PaO2 at maximal exercise. The increase in P wave height during exercise was inhibited by oxygen inhalation at the given VO2 in group A. These findings suggest that increase in P wave height during exercise in COPD patients may be correlated with hypoxemia during exercise.

Adult↗
PubMed1989

[Pulmonary hemodynamics during exercise in anesthetized dogs with inspiratory loading and in patients with chronic obstructive pulmonary disease].

We studied 1) the effects of inspiratory elastic loading on pulmonary hemodynamics and pulmonary gas exchange with and without electrically induced hindlimb exercise in 8 anesthetized dogs, 2) pulmonary hemodynamics at rest and during single stage exercise on a supine cycle ergometer in 6 patients with chronic obstructive pulmonary disease (COPD) and 3) changes in P wave height in lead II of electrocardiogram during progressive exercise on a treadmill in 9 COPD patients. The pulmonary arterial pressure-flow relationship from resting to exercise was not affected by inspiratory elastic loading, but elastic loading accompanied by exercise increased alveolar-arterial O2 tension difference (AaDO2). The pulmonary arterial pressure-flow relationship in COPD from rest to exercise showed higher pulmonary vascular resistance than that in control group. Moreover, we found a greater increase in P wave height during exercise in COPD with decrease in PaO2 during exercise than in COPD without decrease in PaO2 during exercise. This increase in P wave height during exercise was inhibited by oxygen inhalation. We speculated that 1) increased AaDO2 during exercise with elastic loading may be due to increased shunt effects with low ventilation-perfusion ratio and 2) increased P wave height during exercise in COPD may be correlated with hypoxia during exercise and may be useful to detect latent cor pulmonale in COPD.

Aged↗
PubMed1988

Rate of elimination of excess CO2 in humans.

This study examined the ability of the respiratory system of awake normal subjects to correct an acute disturbance in body CO2 stores produced by rebreathing. Thirteen subjects, after 10 min of O2 breathing, rebreathed CO2 for 4 min in order to increase CO2 stores. The rate of CO2 elimination (VelCO2) after rebreathing was measured breath by breath for the next 10 min. The VelCO2 was highest immediately after the end of rebreathing and then decreased non-linearly toward the pre-rebreathing level as stored CO2 decreased. The time for 90% of this change in VelCO2 to occur (T90) was measured as an index of the rate of correction of body CO2 imbalance. The T90 was independent of the peak PCO2 obtained by rebreathing, and changes in CO2 storage did not produce significant changes in T90. The value of T90 was 120 +/- 48 sec (mean +/- SD) and there was a significant negative correlation between T90 and the slope of the ventilatory response to CO2 among subjects (r = -0.864, P less than 0.001). These results suggest that the capacity to eliminate the acutely stored CO2 in awake normal subjects is dependent on the ventilatory response to CO2. The data were further analyzed by using a mathematical model. Mathematical analysis confirmed the inverse relationship between CO2 sensitivity and T90. Model simulations also suggested that the restoration speed of CO2 balance under hyperoxic conditions is affected by brain blood flow but mainly determined by the sensitivity of central chemoreceptors.

Adult↗
PubMed1988

Effects of airway anesthesia on ventilatory responses to graded dead spaces and CO2.

Ventilatory response to graded external dead space (0.5, 1.0, 2.0, and 2.5 liters) with hyperoxia and CO2 steady-state inhalation (3, 5, 7, and 8% CO2 in O2) was studied before and after 4% lidocaine aerosol inhalation in nine healthy males. The mean ventilatory response (delta VE/delta PETCO2, where VE is minute ventilation and PETCO2 is end-tidal PCO2) to graded dead space before airway anesthesia was 10.2 +/- 4.6 (SD) l.min-1.Torr-1, which was significantly greater than the steady-state CO2 response (1.4 +/- 0.6 l.min-1.Torr-1, P less than 0.001). Dead-space loading produced greater oscillation in airway PCO2 than did CO2 gas loading. After airway anesthesia, ventilatory response to graded dead space decreased significantly, to 2.1 +/- 0.6 l.min-1.Torr-1 (P less than 0.01) but was still greater than that to CO2. The response to CO2 did not significantly differ (1.3 +/- 0.5 l.min-1.Torr-1). Tidal volume, mean inspiratory flow, respiratory frequency, inspiratory time, and expiratory time during dead-space breathing were also depressed after airway anesthesia, particularly during large dead-space loading. On the other hand, during CO2 inhalation, these respiratory variables did not significantly differ before and after airway anesthesia. These results suggest that in conscious humans vagal airway receptors play a role in the ventilatory response to graded dead space and control of the breathing pattern during dead-space loading by detecting the oscillation in airway PCO2. These receptors do not appear to contribute to the ventilatory response to inhaled CO2.

Administration, Inhalation↗
PubMed1988

Effects on respiratory pattern of focal cooling in the medulla of the dog.

Studies in cats have shown that, in addition to respiratory neuron groups in the dorsomedial (DRG) and ventrolateral (VRG) medulla, neural structures in the most ventral medullary regions are important for the maintenance of respiratory rhythm. The purpose of this study was to determine whether a similar superficially located ventral region was present in the dog and to assess the role of each of the other regions in the canine medulla important in the control of breathing, in 20 anesthetized, vagotomized, and artificially ventilated dogs, a cryoprobe was used to cool selected regions of the medulla to 15-20 degrees C. Respiratory output was determined from phrenic nerve or diaphragm electrical activity. Cooling in or near the nucleus of the solitary tract altered timing and produced little change in the amplitude or rate of rise of inspiratory activity; lengthening of inspiratory time was the most common timing effect observed. Cooling in ventrolateral regions affected the amplitude and rate of rise of respiratory activity. Depression of neural tidal volume and apnea could be produced by unilateral cooling in two ventrolateral regions: 1) near the nucleus ambiguus and nucleus para-ambiguus and 2) just beneath the ventral medullary surface. These findings indicate that in the dog dorsomedial neural structures influence respiratory timing, whereas more ventral structures are important to respiratory drive.

Animals↗
PubMed1988

Role of CO2 responsiveness and breathing efficiency in determining exercise capacity of patients with chronic airway obstruction.

We examined the role of CO2 responsiveness and breathing efficiency in limiting exercise capacity in 15 patients with chronic airway obstruction (FEV1 = 0.88 +/- 0.25 L, mean +/- SD). Responses of minute ventilation and P0.1 (mouth pressure 0.1 s after the onset of occluded inspiration) to hypercapnia (delta VE/delta PCO2, delta P0.1/delta PCO2) were measured by rebreathing, and the ratio of the two (delta VE/delta P0.1) was defined as an index of breathing efficiency during hyperventilation. Exercise capacity was measured as symptom-limited, maximal oxygen consumption (VO2max/BW) in an incremental treadmill test and also as the 12-min walking distance (TMD). All patients discontinued the treadmill test because of dyspnea, and the exercise capacity correlated with the degree of airway obstruction, although there was a wide variability among patients with comparable FEV1. There were no significant correlations between the responses to CO2 and exercise capacity. However, there was a significant correlation between delta VE/delta P0.1 and VO2max/BW (r = 0.87, p less than 0.001) or TMD (r = 0.78, p less than 0.001), and these correlations remained significant even when the relational effects of FEV1 were taken out. These results support the hypothesis that airway obstruction and breathing efficiency are important, but that CO2 responsiveness is not a major factor in determining the exercise capacity of patients with chronic airway obstruction.

Aged↗
PubMed1987

Effect of digitalis on the diaphragm in anesthetized dogs.

We examined the effect of digitalis on diaphragmatic contractility and fatigability in 19 anesthetized mechanically ventilated dogs. The diaphragmatic force was assessed from transdiaphragmatic pressure (Pdi) developed at functional residual capacity against an occluded airway during cervical phrenic nerve stimulation. In a first group of five dogs, Pdi-stimulus frequency relationships were compared before and after administration of ouabain in doses of 0.01, 0.02, and 0.04 mg/kg. In a second group, diaphragmatic fatigue was produced by bilateral phrenic nerve stimulation at 30 Hz. Ten seconds of stimulation and 15 s of mechanical ventilation were repeated for 30 min. The rates of decrease in Pdi were compared between two groups, one of 0.05 mg/kg deslanoside-treated dogs (n = 7) and one of nontreated dogs (n = 7). After ouabain administration Pdi was significantly greater at each frequency in a dose-dependent manner. On the other hand, the rate of decrease in Pdi in the deslanoside group was significantly smaller than that in the nontreated group, whereas deslanoside did not greatly change the Pdi-frequency curves in fresh diaphragm. We conclude that ouabain improves contractility of the fresh diaphragm and that deslanoside has a protective effect against fatigability.

Animals↗
PubMed1987

Effects of voluntary constraining of thoracic displacement during hypercapnia.

The study evaluated the interrelationships between the extent of thoracic movements and respiratory chemical drive in shaping the intensity of the sensation of dyspnea. Normal subjects rated their sensations of dyspnea as PCO2 increased during free rebreathing and during rebreathing while ventilation was voluntarily maintained at a constant base-line level. Another trial evaluated the effects on the intensity of dyspnea, of voluntary reduction in the level of ventilation while PCO2 was held constant. During rebreathing, there was a power function relationship between changes in PCO2 and the intensity of dyspnea. At a given PCO2, constraining tidal volume and breathing frequency to the prerebreathing base-line level resulted in an increase in dyspnea. The fractional differences in the intensity of dyspnea between free and constrained rebreathing were independent of PCO2. However, the absolute difference in the intensity of dyspnea between free and constrained rebreathing enlarged with increasing hypercapnia. At PCO2 of 50 Torr, this difference correlated significantly with the increase in both minute ventilation (r = 0.675) and tidal volume (r = 0.757) above the base line during free rebreathing. Similarly, during steady-state hypercapnia at 50 Torr PCO2, the intensity of dyspnea increased progressively as ventilation was voluntarily reduced from the spontaneously adopted free-breathing level. These results indicate that dyspnea increases with the level of respiratory chemical drive but that the intensity of the sensation is further accentuated when ventilation is constrained below that demanded by the level of chemical drive. This may be explained by a loss of inhibitory feedback from lung or chest wall mechanoreceptors acting on brain stem and/or cortical centers.

Adult↗
PubMed1986

Ventilatory response to phasic contraction and passive movement in graded anesthesia.

The ventilatory response to electrically induced contraction (EIC) and passive movement (PM) of hindlimb muscles at different levels of anesthesia was studied in 11 chloralose-urethan anesthetized dogs with and without rhizotomy. The level of anesthesia was assessed by corneal reflexes and measurements of the ventilatory response to hypercapnia. Muscle contraction was induced by electrically stimulating the peripheral cut ends of the sciatic and femoral nerves for 4-5 min, and PM was induced manually at the same frequency and amplitude as during EIC. In spinal intact dogs (n = 7), initial rapid increases in minute ventilation (VE) during EIC and PM were found in both light and deep anesthesia. Further increases in VE above the initial rise were seen during EIC but not PM. The initial rapid increases in VE did not differ between the two anesthetic levels. The steady-state ventilatory response during EIC decreased as anesthesia deepened but did not do so during PM. Rhizotomy (n = 4) abolished the initial rapid increase in VE during EIC and PM and the steady-state VE response to PM at both anesthetic levels. These results suggest that the transitional ventilatory response is neurally mediated from the muscles and not affected by the level of general anesthesia. Additionally, the anesthesia-induced reduction of ventilatory response may be due to depression of responsiveness to CO2 rather than to the inspiratory motoneuron pathway.

Anesthesia, General↗
PubMed1985

Effect of clenbuterol on peripheral airway obstruction in bronchial asthma.

A study was carried out in 6 patients with bronchial asthma to investigate the effects of clenbuterol, a beta 2-sympathomimetic bronchodilator, on peripheral airway obstruction. The basal lung functions of the patients were almost within normal range in both vital capacity (VC) and forced expiratory volume in 1 second (FEV1), but their maximal flow rates were lower in effort-independent phase of both maximal expiratory flow volume (MEFV) curve and partial expiratory flow volume (PEFV) curve. Furthermore, they demonstrated marked basal frequency dependence of dynamic compliance [CL,dyn]. Oral administration of clenbuterol (40 micrograms) produced a significant increase in the maximal flow in effort-independent phase of both MEFV and PEFV curves, and markedly decreased frequency dependence of CL,dyn in comparison with the baseline values, while it improved both VC and FEV1 to a lesser extent. These results suggest that clenbuterol preferentially reduced the peripheral airway obstruction in bronchial asthma.

Adolescent↗