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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of non-rapid-eye-movement (NREM) sleep on total pulmonary resistance (RL) and respiratory muscle function was determined in four snorers and four nonsnorers. RL at peak flow increased progressively from wakefulness through the stages of NREM sleep in all snorers (3.7 +/- 0.4 vs. 13.0 +/- 4.0 cmH2O X 0.1(-1) X s) and nonsnorers (4.8 +/- 0.4 vs. 7.5 +/- 1.1 cmH2O X 1(-1) X s). Snorers developed inspiratory flow limitation and progressive increase in RL within a breath. The increased RL placed an increased resistive load on the inspiratory muscles, increasing the pressure-time product for the diaphragm between wakefulness and NREM sleep. Tidal volume and minute ventilation decreased in all subjects. The three snorers who showed the greatest increase in within-breath RL demonstrated an increase in the contribution of the lateral rib cage to tidal volume, a contraction of the abdominal muscles during a substantial part of expiration, and an abrupt relaxation of abdominal muscles at the onset of inspiration. We concluded that the magnitude of increase in RL leads to dynamic compression of the upper airway during inspiration, marked distortion of the rib cage, recruitment of the intercostal muscles, and an increased contribution of expiratory muscles to inspiration. This increased RL acts as an internal resistive load that probably contributes to hypoventilation and CO2 retention in NREM sleep.
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PMID:Airway resistance and respiratory muscle function in snorers during NREM sleep. 403 May 85

We examined the respiratory activity of the genioglossus, sternothyroid, and sternohyoid muscles of the rat during nonrapid eye movement (non-REM) and REM sleep. Each animal carried implanted electrodes for recording the integrated EMG activity of respiratory muscles, the postural tone (EMG), and electrocortical activity (polygraphic identification of sleep-waking states). The three upper airway muscles exhibited inspiratory activity during non-REM sleep while rats breathed ambient air. Curled up postures promoted inspiratory activity of genioglossus and sternothyroid muscles, an effect enhanced by CO2 breathing but reduced by hypoxic breathing. During REM sleep, genioglossus and sternothyroid muscles lost their activity but the sternohyoid muscles retained their inspiratory activity. We conclude that the genioglossus and sternothyroid muscles contribute to upper airway patency during non-REM sleep, an effect CO2 augments but hypoxia reduces. The sternohyoid muscles have at least two functions during both sleep states: they contribute to maintenance of upper airway patency and to rib cage fixation, thereby optimizing the ventilatory action of the diaphragm.
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PMID:Respiratory roles of genioglossus, sternothyroid, and sternohyoid muscles during sleep. 404 87

This study compared the respiratory responses to ventilatory loading in 8 normal subjects and 11 quadriplegic patients with low cervical spinal cord transection. Progressive hypercapnia was produced by rebreathing. Rebreathing trials were carried out with no added load and with inspiratory resistive loads of 5 and 16 cmH2O. l-1 X s. Measurements were made of ventilation and of diaphragmatic electromyographic activity. Base-line hypercapnic ventilatory responses were significantly lower than normal in the quadriplegic patients, but the effects of resistive loading on the ventilatory responses were comparable in the two groups. The change in peak moving-average diaphragmatic electrical activity (DI peak) for a given change in CO2 partial pressure (PCO2) and DI peak at PCO2 55 Torr increased significantly with resistive loading both in the normal subjects and the quadriplegic patients. In the normal subjects, but not in the quadriplegic patients, inspiratory duration increased progressively with increasing resistance. The increase in DI peak during ventilatory loading in the normal subjects was a consequence of inspiratory prolongation. In contrast, in the quadriplegic patients during breathing against the larger resistive load, there was a significant increase in the average rate of rise (DI peak divided by the time from onset to peak) of diaphragmatic activity. The change in DI rate of rise for a given change in PCO2 increased to 137 +/- 13% (SE), and the DI rate of rise at PCO2 55 Torr increased to 128 +/- 8% (SE) of control values. These results indicate that compensatory increases in diaphragmatic activation during ventilatory loading occur in quadriplegic patients in whom afferent feedback from rib cage receptors is disrupted.
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PMID:Respiratory responses to ventilatory loading following low cervical spinal cord injury. 407 83

We investigated the respiratory muscle contribution to inspiratory load compensation by measuring diaphragmatic and intercostal electromyograms (EMGdi and EMGic), transdiaphragmatic pressure (Pdi), and thoracoabdominal motion during CO2 rebreathing with and without 15 cmH2O X l-1 X s inspiratory flow resistance (IRL) in normal sitting volunteers. During IRL compared with control, Pdi measured during airflow and during airway occlusion increased for a given change in CO2 partial pressure and EMGdi, and there was a greater decrease in abdominal (AB) end expiratory anteroposterior dimensions with increased expiratory gastric pressure (Pga), this leading to an inspiratory decline in Pga with outward AB movement, indicating a passive component to the descent of the abdomen-diaphragm. The response of EMGic to IRL was similar to that of EMGdi, though rib cage (RC)-Pga plots did infer intercostal muscle contribution. We conclude that during CO2 rebreathing with IRL there is improved diaphragmatic neuromuscular coupling, the prolongation of inspiration promoting a force-velocity advantage, and increased AB action serving to optimize diaphragm length and configuration, as well as to provide its own passive inspiratory action. Intercostal action provides increased assistance also. Therefore, compensation for inspiratory resistive loads results from the combined and integrated effort of all respiratory muscle groups.
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PMID:Respiratory muscle function during CO2 rebreathing with inspiratory flow-resistive loading. 621 76

To determine whether the rib cage and abdomen-diaphragm contributions to tidal volume (VT) during CO2 rebreathing are affected by postural change, using respiratory inductive plethysmography, we measured in eight healthy volunteers the compartmental VT responses to progressive hypercapnia in both seated and supine postures. The ventilatory, frequency, and VT responses to CO2 of the total respiratory system were not significantly different between postures. VT responses, corrected for body size, ranged from 1.67 to 3.71% vital capacity (VC) X Torr-1 (mean 2.27) in seated subjects and from 1.08 to 3.79% VC X Torr-1 (mean 2.06), in supine subjects. In both postures, the VT response of the abdominal compartment was nearly uniform among subjects and independent of the total respiratory system VT response (slope = 0.091, r = 0.210 P greater than 0.3 seated; slope = 0.043, r = 0.077, P greater than 0.3 supine), whereas the VT response of the rib cage varied among subjects and was significantly correlated to the total VT response (slope = 0.815, r = 0.84, P less than 0.01, seated; slope = 1.125, r = 0.859, P less than 0.01, supine). Thus high tidal volume responses to CO2 rebreathing are determined largely by recruitment of the rib cage compartment in both seated and supine postures.
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PMID:Effect of posture on thoracoabdominal movements during CO2 rebreathing. 622 9

We have measured the ventilatory response to inhaled CO2 of six newborn infants in rapid-eye-movement (REM) and non-REM (NREM) sleep. Ventilatory responses were measured using the Read rebreathing technique. The response was further partitioned into the volume contributions of the rib cage and abdominal compartment using the respiratory inductance plethysmograph. Sleep state was defined by electroencephalogram, electrooculogram, and behavioral criteria. In NREM sleep, there was a highly significant linear correlation between both tidal volume (VT) and instantaneous minute ventilation (VI) with CO2. Among infants, the slope of VT varied from 1.0 to 0.34 ml X Torr-1 X kg-1. However, these differences were largely due to differences in rib cage contribution, which varied from 0.56 to -0.08 ml X Torr-1 X kg-1. The abdominal contribution was similar among infants (0.41-0.56 ml X Torr-1 X kg-1). In REM, the slopes of VI were less steep than in NREM, with greater breath-to-breath variability. Slopes of VT also tended to be lower. The abdominal responses were similar to those in NREM, whereas the rib cage response was low and negative in three studies. We conclude that the slope of the CO2 response curve is primarily determined by the extent of rib cage recruitment.
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PMID:Rib cage and abdominal contributions to ventilatory response to CO2 in infants. 623 43

To examine the mechanical effects of the fall in abdominal pressure (Pab) that occurs during inspiration in diaphragmatic paralysis, we studied lung inflation and rib cage expansion before and after the abdomen was opened in nine spontaneously breathing dogs with bilateral phrenicotomy . We measured Pab, tidal volume, and parasternal electromyographic (EMG) activity during quiet breathing and CO2-induced hyperpnea. In six dogs, we also measured changes in anteroposterior and transverse rib cage diameters, the resting length of the parasternal intercostal muscles, and the amount of shortening of these muscles during inspiration. Opening the abdomen caused a marked reduction in the fall in Pab during inspiration and invariably resulted in a decrease in tidal volume (mean decrease, 13%), which contrasted with marked increases in inspiratory rib cage expansion and in the amount of parasternal intercostal shortening. The procedure, however, did not affect the resting length or inspiratory EMG activity of the parasternals . These findings indicate that although the fall in Pab, which occurs during inspiration in diaphragmatic paralysis, causes paradoxical inward displacement of the ventral abdominal wall, it has a salutary effect on tidal volume. This phenomenon is probably due to the fact that the diaphragm is part of the abdominal wall.
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PMID:Salutary effect of fall in abdominal pressure during diaphragm paralysis. 623 45

The aim of the present study was to determine whether acute changes in blood gases and pH alter sulfamethazine (SMZ) kinetics. Groups of conscious rabbits were exposed for 270 min either to air or to a high CO2 and (or) low O2 atmosphere to produce hypercapnia, hypoxemia, or both. Another group of rabbits received 47 mL/kg of 0.3 M HCl by gavage tube to induce metabolic acidosis. Once the blood gases were stabilized, the rabbits received 20 mg/kg SMZ i.v. Multiple blood samples were drawn for 180 min to assess SMZ kinetic parameters, SMZ protein binding, and blood gases. Fifteen minutes after the administration of SMZ, a suboccipital puncture was performed to determine the concentration of SMZ in the cerebrospinal fluid (CSF). Urine was collected for the first 180 min through a sterile catheter and for the next 21 h in a metabolic cage. Hypercapnia alone did not significantly influence SMZ kinetics. Hypoxemia, hypoxemia combined with hypercapnia, and metabolic acidosis increased the SMZ apparent volume of distribution (V) and total body clearance (CL). This increase in the SMZ V correlated positively (p less than 0.01) to the ratio of SMZ concentration in CSF to SMZ concentration in plasma. The increase in SMZ CL was mainly due to an increase in nonrenal clearance, although a slight increase in SMZ renal clearance was also observed.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of hypercapnia and (or) hypoxemia and metabolic acidosis on sulfamethazine kinetics in the conscious rabbit. 649 28

The present study examined the possibility that mechanoreceptors in the chest wall structures (rib cage and diaphragm) contribute to the increase in the neuromuscular drive to breathe (occlusion pressure) when the load on the respiratory muscles is increased in conscious animals and humans. Studies were carried out in 4 awake dogs in which external resistive loads (12 cmH2O/L/s) were applied during inspiration to increase the load on the respiratory muscles. Loads were applied via a tracheostomy during complete vagal blockade performed by cooling exteriorized cervical vagal loops. The ventilatory and occlusion pressure responses to the load were compared over the same range of chemical drive by applying loads during CO2 rebreathing. During vagal blockade, inspiratory resistive loads had no consistent effect on the duration of inspiration or expiration and decreased the ventilatory response to hypercapnia by decreasing average inspiratory flow rate. In all animals, however, inspiratory loading increased the occlusion pressure (P100) response to hypercapnia. The P100 at PCO2 = 55 mmHg increased during flow loading in all 4 animals, and the slope of the change in P100 produced for a given change in PCO2 (delta P100/delta PCO2) increased in 3 of the 4. Flow loading had no effect on end-expiratory lung volume at rest and did not influence the decrease in lung volume observed during hypercapnia. The present study indicated that the neuromuscular drive to breathe, as assessed from the occlusion pressure, is increased in conscious animals subjected to ventilatory loads during vagal blockade.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Respiratory responses to external resistive loads during vagal blockade in awake dogs. 672 Dec 79

We examined the effects of different levels of inspired CO2 on ventilation and the pattern of breathing in healthy adults during the awake and the stage II quiet-sleep states. During both states, subjects were studied supine with their heads enclosed in a canopy. Tidal volume (VT) was determined from quantitative measurements of abdominal and rib cage excursions with magnetometers. Inspired CO2 was raised by blending CO2-enriched gas into the airflow, which continuously flushed the canopy. During sleep, while room air was breathed, VT decreased significantly from 410 to 360 ml, and respiratory rate also fell from 17 to 16 breaths/min. As a consequence, ventilation was significantly reduced from 6.5 to 5.8 l/min, and end-tidal CO2 partial pressure (PCO2) rose from 39.1 to 42.5 Torr. Ventilatory responses to CO2 were reduced, on the average, during sleep to 79% of waking levels. The change in average inspiratory flow produced by CO2 was also less during sleep. Waking and sleeping ventilatory responses to CO2 correlated inversely with the rise in end-tidal PCO2 when room air was breathed during sleep. At all levels of VT, the rib cage contribution to VT was greater during quiet sleep than during wakefulness. These findings suggest that quiet sleep, in addition to depressing ventilation and the response to CO2 alters the manner in which VT is attained by rib cage and abdominal displacements.
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PMID:Effect of quiet sleep on resting and CO2-stimulated breathing in humans. 679 Apr 87


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