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

The effects of diaphragm paralysis on respiratory activity were assessed in 13 anesthetized, spontaneously breathing dogs studied in the supine position. Transient diaphragmatic paralysis was induced by bilateral phrenic nerve cooling. Respiratory activity was assessed from measurements of ventilation and from the moving time averages of electrical activity recorded from the intercostal muscles and the central end of the fifth cervical root of the phrenic nerve. The degree of diaphragm paralysis was evaluated from changes in transdiaphragmatic pressure and reflected in rib cage and abdominal displacements. Animals were studied both before and after vagotomy breathing O2, 3.5% CO2 in O2, or 7% CO2 in O2. In dogs with intact vagi, both peak and rate of rise of phrenic and inspiratory intercostal electrical activity increased progressively as transdiaphragmatic pressure fell. Tidal volume decreased and breathing frequency increased as a result of a shortening in expiratory time. Inspiratory time and ventilation were unchanged by diaphragm paralysis. These findings were the same whether O2 or CO2 in O2 was breathed. After vagotomy, no significant change in phrenic or inspiratory intercostal activity occurred with diaphragm paralysis in spite of increased arterial CO2 partial pressure. Ventilation and tidal volume decreased significantly, and respiratory timing was unchanged. These results suggest that mechanisms mediated by the vagus nerves account for the compensatory increase in respiratory electrical activity during transient diaphragm paralysis. That inspiratory time is unchanged by diaphragm paralysis whereas the rate or rise of phrenic nerve activity increases suggest that reflexes other than the Hering-Breuer reflex contribute to the increased respiratory response.
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PMID:Respiratory responses in reversible diaphragm paralysis. 679 66

Although there has been extensive research into the control of breathing in adults with chronic obstructive lung diseases, there is little information in this area in children with cystic fibrosis (CF). The purpose of this study was to investigate the respiratory response of children with CF to CO2 under hyperoxic conditions. Using a standard CO2 rebreathing technique, we studied 14 children with CF. We evaluated their response to CO2 in terms of ventilation (VE), mean inspiratory flow rate (VT/TI), and the pressure generated at the mouth after 0.1 s of an inspiratory effort against an occlusion (P0.1). In order to understand the contributions of the rib cage and abdominal components to ventilation, we assessed the volume change in each compartment by attaching magnetometers to the chest and abdomen. Overall changes in lung volume were assessed in a volume displacement plethysmograph. We found that, when corrected for the height of the child, the slope of VE versus end tidal CO2 (PETCO2), as well as the slope of VT/TI versus PETCO2 correlated significantly with the degree of airway obstruction as expressed by the forced expiratory flow between 25 and 75% of vital capacity. The values for P0.1 were all within the normal range and showed no correlation with the degree of airway obstruction. The contribution of the rib cage and abdomen to ventilation during rebreathing was similar to that previously reported for adults. No changes were observed in functional residual capacity during rebreathing. We showed that tests involving a mechanical response to CO2 correlated with the degree of airway obstruction, but there was no evidence that the neuromuscular drive was abnormal.
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PMID:Ventilation, respiratory center output, and contribution of the rib cage and abdominal components to ventilation during CO2 rebreathing in children with cystic fibrosis. 679 78

Phenomena associated with a deformation of short-time occurrence and noticed on concentration curves of tidal O2 and CO2 were examined in adult hens sitting quietly in a cage or suspended in prone position. During the episode of deformation, a decrease in arterial oxygen-gas tension was apparent. It was associated with a slight increase in arterial carbon-dioxide-gas tension and a slight acidic shift of arterial blood pH. The episode was associated with increases in intrapressure of the interclavicular and bilateral abdominal air sacs. The tracheal expiratory-gas flow changed in pattern. Hypoventilation due to reduction in tidal volume or respiratory rate could not be detected during the episode. The episode was suddenly terminated at the hen's body movement induced spontaneously or by pinching the comb, at coughlike activity or at no obvious change in behavior in a quietly resting position. Deformation similar to the spontaneous one could be induced by 3 ml-water flushing into the trachea or 0.1% methacholine aerosol inhalation. The mechanism responsible for the genesis of deformation was discussed. It was presumed to be based upon some mechanism, such as mucous accumulation in the lung, rather than upon the pulmonary smooth-muscle contraction.
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PMID:An analysis on the mechanism responsible for genesis of deformation of expiratory-gas-concentration curves in chickens. 680 76

After describing the clinical and functional effects of pathological changes in the thoracic cage ("mechanical syndrome" and "neuromuscular syndrome"), the authors discuss the disorders of respiratory function observed in a group of patients with poliomyelitic scoliosis. The aim was to establish the type and nature of these changes with a view to clarifying certain pathogenetic aspects. Two factors suggest that the altered geometry of the thoracic cage in scoliosis is responsible for the mechanical inefficiency of the thoracopulmonary apparatus, namely: 1. changes in respiratory function, since there was a strict correlation between the severity of the scoliosis and the degree of change in certain indices of respiratory function (vital capacity, maximum expiratory volume per second, maximum ventilation per minute); 2. changes in the regulation of ventilation, indicated by: a) good correlation between the ventilatory response to CO2 and the severity of the anatomical lesion; b) a reduction in the occlusion pressure, which is regarded as the pressure available to produce ventilation.
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PMID:Changes in respiratory function in disorders of the thoracic cage. With special reference to the ventilatory mechanism and the regulation in scoliosis. 688 93

To evaluate the role of phrenic and sternocleidomastoid afferents as alternate sources of inhibitory feedback during mechanical ventilation, we studied five C2-C3 quadriplegics with sensory denervation of the rib cage and diaphragm, six C1-C2 quadriplegics with additional loss of sensory feedback from the neck muscles, and seven normal subjects. We compared the return of inspiratory muscle activity [the recruitment threshold (PCO2RT)] during mechanical ventilation between subject groups after stepwise increases in end-tidal PCO2 (PETCO2) either by increasing the inspired fraction of CO2 (FICO2), decreasing tidal volume (VT; 50 ml/min), or decreasing frequency (f; 1 breath/2 min). Normal subjects were mechanically hyperventilated via a nasal mask until inspiratory activity was undetectable. Efferent input to the sternocleidomastoid was intact at both levels of spinal cord injury, but phasic activity was not evident at the quadriplegics' baseline resting ventilation. The PCO2RT was defined as the level of PETCO2 at which phasic activity of the diaphragm in normal subjects and of the sternocleidomastoid in C1-C2 and C2-C3 quadriplegics recurred. The mean PCO2RT (in response to raising PETCO2 via increased FICO2 while maintaining a high VT and f) was not significantly different (P = 0.6) between normal subjects (43 +/- 3 Torr) and C2-C3 quadriplegics (38 +/- 5 Torr). Both subject groups demonstrated a frequency- and volume-related inhibition, as evidenced by a substantially lower PCO2RT when PETCO2 was raised by reducing either VT or f. In contrast to the C2-C3 quadriplegics, the C1-C2 quadriplegics responded with a similar PCO2RT among the three different mechanical ventilation trials, independent of whether PETCO2 was raised with high VT and f, with reduced VT, or with reduced f. We conclude that feedback from at least some part of the chest wall is required to produce a volume- and frequency-dependent inhibition of inspiratory muscle activity observed during mechanical ventilation.
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PMID:Neuromechanical regulation of respiratory motor output in ventilator-dependent C1-C3 quadriplegics. 755 37

The effectiveness of positive end-expiratory pressure (PEEP) relates directly to alveolar recruitment. We tested the hypothesis that active use of expiratory muscles during labored breathing impairs the ability of PEEP to increase end-expiratory lung volume. Eight healthy volunteers naive to the purposes of our study were exposed to targeted end-expiratory pressures of 0, 5, and 10 cm H2O during mechanical ventilation applied by mouthpiece and noseclips at three levels of ventilation: resting and two levels (moderate and high) of CO2 stimulation (10.9 +/- 0.4, 19.9 +/- 0.5 and 27.5 +/- 0.5 L/min, respectively). Inductive plethysmography demonstrated that end-expiratory lung volume rose by an average of 98 +/- 5 ml/cm H2O PEEP during quiet breathing but by much less during the two levels (moderate and high) of CO2 stimulation: 78 +/- 6 ml/cm H2O and 47 +/- 5 ml/cm H2O (p < 0.05). Hyperpnea also shifted the distribution of the recruited volume toward regions sampled by the rib cage band of the plethysmograph. Whatever advantage expiratory muscle activity may have for minimizing the workload of the inspiratory muscles, the cost may be reduced effectiveness of PEEP in increasing lung volume and improving oxygen exchange.
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PMID:Hyperpnea limits the volume recruited by positive end-expiratory pressure. 792 62

Patients with cystic fibrosis (CF) often hypoventilate during sleep with marked falls in oxygen saturation (SaO2%). This occurs most commonly during REM sleep, when there is a reduction in rib cage excursion and a fall in end-expiratory lung volume (EELV). The aim of this study was to examine the effect of nocturnal nasal continuous positive airway pressure (nCPAP) on SaO2 and the respiratory disturbance index (RDI) during sleep in patients with CF and severe lung disease. Seven patients (FEV1% pred, 23 +/- 5; range, 14 to 28%) were evaluated during sleep on two nights, control and nCPAP (11 +/- 2 cm H2O; range, 8 to 16 cm H2O), with four patients breathing room air and three patients breathing supplemental oxygen on both nights. Mean awake SaO2 was 91 +/- 1% (range, 89 to 93%). All patients showed significant oxyhemoglobin desaturation and respiratory disturbance in the control study. The maximal falls in SaO2 (15 +/- 10%) were most often associated with phasic eye movements, and a decline in rib cage excursion and the sum signal (Respitrace) during REM sleep. Nasal CPAP resulted in a significant improvement in the mean minimum oxygen saturation (MMOS) during both NREM (nCPAP 91 +/- 3% vs control 88 +/- 2%, p < 0.05) and REM sleep (nCPAP 89 +/- 6% vs control 83 +/- 6%, p < 0.05). Transcutaneous CO2 measurements were not significantly different between the control and the nCPAP studies. The RDI was also significantly reduced with nCPAP especially during REM sleep (9 +/- 7 events per hour vs control 25 +/- 11 events per hour, p < 0.05). Nasal CPAP caused no change in total sleep time or sleep efficiency yet significantly reduced the RDI and improved baseline SaO2 during both NREM and REM sleep.
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PMID:Benefits of nocturnal nasal CPAP in patients with cystic fibrosis. 798 90

In a four-row cowshed adapted for rabbit housing, air temperatures and humidity were recorded ambulantly and instrumentally, air flow rate, cooling variable, gas content in the air, microbial contamination of air and dust deposition were determined ambulantly in the years 1991-1992 and in January to April 1993. The values of ambulant measurings show that at the outside temperature -0.5 degrees C to -5.0 degrees C the microclimate quality decreases particularly with respect to the drop of air temperature in the cowshed below 10.0 degrees C, to the increase in cooling variable up to the value 53.17 mW/cm2 and to the increase in NH3 and CO2 content to 50 ppm and/or 0.45 vol.% in absolute maximum values. In these circumstances, the average determined values of both gases are higher than the standard prescription. At outside temperatures above 27.0 degrees C the average relative air humidity in the cowshed made 69.20% for the average temperature of 25.0 degrees C. To avoid the water vapor tension exceeding the limit in the cowshed air above the value 14.1 mm Hg, when sultry atmosphere sets in, the average relative air humidity should be maximally 59.0%. Hence the cowshed was found to be insufficiently ventilated at high outside temperatures above 27.0 degrees C, and it is recommended to increase the ventilator performance and at the same time to reduce water evaporation from catchpit surfaces when urine output of rabbits is excessive as a result of the increased water intake. Temperature and air humidity readings confirmed the need of heating source installation when the outside temperatures drop below 0.0 degrees C. Evaluation of air microbial contamination showed high counts of molds and particularly of micrococci in comparison with the ambience of a cage facility for piglet raising at a repopulation station with strict hygienic regime. Microbial picture of dust deposition was positively influenced by longitudinal aerosol disinfection of the air in the cowshed.
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PMID:[Hygienic aspects of the microclimate in intensive management of rabbits]. 807 89

We studied the influence of diaphragmatic fatigue on the control of ventilation and respiratory muscle contribution to pressure swings in six normal seated subjects. CO2 was rebreathed before and after diaphragmatic fatigue induced by breathing against an inspiratory resistance requiring 60% maximal transdiaphragmatic pressure with each breath until exhaustion. After diaphragmatic fatigue for a given level of end-tidal PCO2, we found that tidal volume, breathing frequency, minute ventilation, duty cycle, and mean inspiratory flow did not change; esophageal pressure swings were the same, but gastric and transdiaphragmatic pressure swings were decreased; and the slope of the transpulmonary pressure-gastric pressure relationship determined at zero flow points at end expiration and end inspiration was increased. End-expiratory transpulmonary pressure progressively decreased and end-expiratory gastric pressure progressively increased with increasing end-tidal PCO2 by the same magnitude before and after diaphragmatic fatigue. We conclude that diaphragmatic fatigue induces proportionately greater contributions of inspiratory rib cage muscles than of the diaphragm, which results in the preservation of ventilatory response to CO2 despite impaired diaphragmatic contractility.
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PMID:Effect of diaphragmatic fatigue on control of respiratory muscles and ventilation during CO2 rebreathing. 822 52

We evaluated the effect of global inspiratory muscle fatigue on ventilation and respiratory muscle control during CO2 rebreathing in normal subjects. Fatigue was induced by breathing against a high inspiratory resistance until exhaustion. CO2 response curves were measured before and after fatigue. During CO2 rebreathing, global fatigue caused a decreased tidal volume (VT) and an increased breathing frequency but did not change minute ventilation, duty cycle, or mean inspiratory flow. Both esophageal and transdiaphragmatic pressure swings were significantly reduced after global fatigue, suggesting decreased contribution of both rib cage muscles and diaphragm to breathing. End-expiratory transpulmonary pressure for a given CO2 was lower after fatigue, indicating an additional decrease in end-expiratory lung volume due to expiratory muscle recruitment, which leads to a greater initial portion of inspiration being passive. This, combined with the reduction in VT, decreased the fraction of VT attributable to inspiratory muscle contribution; therefore the inspiratory muscle elastic work and power per breath were significantly reduced. We conclude that respiratory control mechanisms are plastic and that the respiratory centers alter their output in a manner appropriate to the contractile state of the respiratory muscles to conserve the ventilatory response to CO2.
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PMID:Effect of global inspiratory muscle fatigue on ventilatory and respiratory muscle responses to CO2. 822 53


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