Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q86TM3 (cage)
 29,987 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To examine the effect of cardiogenic gas mixing on gas exchange we measured arterial tension of O2 (PaO2) and arterial tension of CO2 (PaCO2) during 3- to 5-min breath holds (BH) before and after infusing 50 ml of saline into the pericardial space (PCF) of seven anesthetized, paralyzed, mechanically ventilated dogs. During BH the ventilator was disconnected and a bias flow of 50% O2 at 4-5 l/min was delivered through the side ports of a small catheter whose tip was positioned 1 cm cephalad of the carina. Paired runs, alternately with and without PCF, were performed in triplicate in each dog. Initial PaO2 was similar for control runs [81 +/- 3 mmHg (SE)] and PCF runs (78 +/- 3 mmHg; P greater than 0.1). After 3-min BH, PaO2 in PCF runs (33 +/- 3 mmHg) was less than that in control runs (58 +/- 4 mmHg) (P less than 0.001). In contrast, the pattern of PaCO2 during BH did not differ with PCF. After 3-min BH, PaCO2 was 49 +/- 3 mmHg with PCF and 49 +/- 2 mmHg in the control runs (P greater than 0.7). In two dogs, repeated 50-ml reductions in lung volume, produced by rib cage compression, did not alter the time course of PaO2 during BH. Although cardiac output decreased slightly with PCF, hemodynamic changes due to PCF were unlikely to account for the observed fall in PaO2. Our results indicate a substantial effect of cardiogenic gas mixing on O2 uptake when tracheal gas is O2 enriched during breath holding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of cardiogenic gas mixing on arterial O2 and CO2 tensions during breath holding. 311 Jan 19

1. Sleep-waking states of chronically implanted rats were identified polygraphically while recording the integrated electromyogram (e.m.g.) of extrinsic (scalenus medius and levator costae) and intrinsic (external and internal interosseous intercostal and parasternal) muscles of the thoracic cage. Rats breathed air, air enriched in CO2 (5%) or air deficient in O2 (10% O2 in N2) and were free to adopt any desired posture. 2. In non-rapid eye movement (non-r.e.m.) sleep, the scalenus medius and intercostal muscles of the cephalic spaces were always inspiratory; intercostal muscles of the mid-thoracic spaces were commonly expiratory while the more caudal ones were only occasionally expiratory. Expiratory activity, when present in quiet wakefulness, extended for a variable period of time into non-r.e.m. sleep and always disappeared in r.e.m. sleep regardless of the ribcage muscle under study. 3. Inspiratory activity, when present in non-r.e.m. sleep, was unaffected, partially attenuated or abolished at entry into r.e.m. sleep. The peak integrated e.m.g. activity of ribcage muscles was measured as a function of posture, gas mixture breathed and ribcage site: (a) the greater the degree of curled-up posture, the greater the respiratory activity of scalenus medius, an effect augmented by CO2 but depressed by hypoxia, and (b) the more caudally placed ribcage muscles exhibited respiratory activity which was essentially unaffected by posture and gas mixture inspired. 4. The presence or absence of tonic activity in ribcage respiratory muscles during non-r.e.m. sleep was unrelated to posture. When tonic activity was present, it always disappeared in r.e.m. sleep. When expiratory activity was present in non-r.e.m. sleep, it too always disappeared in r.e.m. sleep. Inspiratory activity present in non-r.e.m. sleep was variably affected at entry into r.e.m. sleep; it was unchanged, partially attenuated or abolished. 5. It is concluded that thoracic cage muscles exhibit marked variability in their respiratory activity depending on posture, sleep-waking states and gas mixture breathed. It is postulated that the presence of tonic and/or expiratory activity in ribcage muscles during non-r.e.m. sleep reflects an increase in functional residual capacity (F.R.C.).
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PMID:The labile respiratory activity of ribcage muscles of the rat during sleep. 311 21

The effects of stimulation of pulmonary C-fiber receptors on the distribution of motor activity to upper airway, rib cage, and abdominal muscles were studied in anesthetized, tracheotomized, spontaneously breathing dogs. Stimulation of pulmonary C-fiber receptors by injection of capsaicin (3-20 micrograms/kg) into the right atrium resulted in complete cessation of electrical activity of the upper airway dilating muscles (UADM) and the inspiratory chest wall pumping muscles. The activity of abdominal muscles was also inhibited. The duration of electrical silence was longer for the diaphragm than for the UADM. Upper airway constricting muscles and expiratory intercostal muscles, including the triangularis sterni, remained tonically active during the apneic period. The responses of these muscles were qualitatively the same when the animals breathed 100% O2, 7% CO2 in O2, or 12% O2 in N2, and without or in the presence of an expiratory threshold load. Bilateral vagotomy abolished the inhibitory effects of capsaicin on UADM, chest wall, and abdominal muscle activity, suggesting that the vagus is the major afferent pathway for the reflex. The qualitative difference in the response of intercostal expiratory muscles and abdominal muscles suggests that these two groups of synergistic muscles may be independently regulated.
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PMID:Effect of stimulation of pulmonary C-fiber receptors on canine respiratory muscles. 318 78

In the present study, antibodies directed against clathrin light (33 kDa-36 kDa) and heavy (180 kDa) chains were used to confirm, by immunocytochemistry, that coated vesicles increase in number in the exocrine cells of pancreatic lobules incubated under anoxic (N2) conditions. The same antibodies were used to check whether or not the fibrillar aggregates, which appear under the same conditions on the cis side of the Golgi stacks of these cells, contain clathrins. By immunofluorescence, clathrin light chains were localized among zymogen granules and in small masses at the periphery of the Golgi complex in acinar cells incubated under N2. By electron microscopy, antibodies for light and heavy chains reacted with numerous coated vesicles located in clusters on the trans side of the Golgi stacks, scattered individually or in small clusters among zymogen granules throughout the apical region of the cell, and associated with both the apical and basolateral plasmalemma of the exocrine cells incubated under N2. The fibrillar aggregates cis to the Golgi complex stained less intensely and much less uniformly than the coats of the coated vesicle population. These findings suggest that the fibrillar aggregates which characteristically appear on the cis side of the Golgi stacks under anoxic conditions contain only small amounts of focally distributed clathrins. Their main components are probably other proteins whose relationship (if any) to clathrins and other clathrin cage constituents remains to be investigated. The findings also indicate that pancreatic acinar cells redistribute large amounts of clathrin, presumably from preexisting pools, when the transport of secretory and other proteins into the Golgi complex is inhibited. In control cells (incubated under O2-CO2), clathrin antigens had the same structural associations as in anoxic cells but the reactive sites were considerably less numerous and the reaction less intense.
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PMID:Redistribution of clathrin heavy and light chains in anoxic pancreatic acinar cells. 355 20

The order of recruitment of single-motor units in parasternal intercostal muscles during inspiration was studied in normal human subjects during quiet breathing and voluntary hyperventilation. Electromyograms were recorded from the second and third intercostal spaces by means of bipolar fine wire electrodes. Flow at the mouth, volume, end-expired CO2, and rib cage and abdominal anterior-posterior diameters were monitored. Single-motor units were identified using criteria of amplitude and shape, and the time of first appearance of each unit in each inspiration was noted. Hyperventilation was performed with visual feedback of the display of rib cage and abdomen excursions, keeping the ratio of rib cage to abdominal expansion. Subjects were normocapnic in quiet breathing and developed hypocapnia during hyperventilation. Recruitment order was stable in quiet breathing, but in some cases was altered during voluntary hyperventilation. Some low threshold units that fired early in the breath in quiet breathing fired earlier at the beginning of a period of voluntary hyperventilation but progressively later in the breath as hyperventilation went on, whereas later firing units moved progressively toward the early part of inspiration. This suggests that different groups of motoneurons in the pool supplying parasternal intercostal muscles receive different patterns of synaptic input.
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PMID:Voluntary hyperventilation changes recruitment order of parasternal intercostal motor units. 355 79

To determine the ventilatory effectiveness of high-frequency oscillation (HFO) at different sites on the body surface, we applied HFO separately to the abdomen, the rib cage, or the whole body in eight anesthetized and paralyzed dogs. Test frequencies were 5, 7, 9, and 11 Hz with tidal volume kept constant at 2.5 ml/kg. During HFO application to the abdomen, we observed significantly higher arterial O2 partial pressure (P less than 0.05) at 5, 7, and 9 Hz and lower arterial CO2 partial pressure (P less than 0.05) at 7, 9, and 11 Hz than with rib cage or whole-body HFO. There was no significant difference in blood gases between rib cage and whole-body HFO. Thus, using blood gases as an index of ventilatory effectiveness, the present study showed that HFO applied at the abdomen was the most effective of the three kinds of body surface HFO. In comparison to rib cage or whole-body application, abdominal HFO was accompanied by substantial paradoxical movement of the diaphragm and rib cage. The associated lung distortion may result in pendelluft, which in turn may be the mechanism for increased ventilatory effectiveness with abdominal application of HFO.
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PMID:Ventilatory effectiveness of high-frequency oscillation applied to the body surface. 361 Sep 34

During active sleep, neonates exhibit asynchronous chest wall movements, which have been associated with a small but significant decrease in oxygenation. To determine the effects of maturation and residual chronic lung disease on both these phenomena, we studied 11 preterm infants with resolving bronchopulmonary dysplasia (BPD) and compared these infants to ten healthy preterm infants all at time of discharge. Synchrony of chest wall (upper rib cage and abdominal) movements, sleep state, O2 saturation, and transcutaneous CO2 (TcPCO2) were recorded during both active (AS) and quiet sleep (QS). Sleep state was determined by electroencephalographic and behavioral criteria. Normal preterm infants displayed asynchronous chest wall movements only in AS, whereas, in infants with BPD, asynchrony predominated in both sleep states, although O2 saturation and TcPCO2 did not differ between sleep states in either group. The O2 saturation during AS was lower in the BPD group than in the group of normal infants (92% vs 96%; P less than 0.02), whereas TcPCO2 was higher in the BPD group unrelated to sleep state. We conclude that infants with resolving BPD exhibit asynchronous chest wall movements in both AS and QS, and that change in sleep state from QS to AS is not associated with a detrimental fall in oxygenation in these infants.
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PMID:Effect of sleep state on chest wall movements and gas exchange in infants with resolving bronchopulmonary dysplasia. 365 32

Magnetometers measure changes in antero-posterior diameters of the rib cage and abdomen while respiratory inductance plethysmography (RIP) measures changes in chest wall cross-sectional area. We compared Konno-Mead diagrams derived from isovolume calibrated magnetometers and RIP in the DC-mode during room air and CO2 rebreathing in the sitting and supine positions. Chest wall configurations obtained during quiet tidal breathing were similar in both sitting and supine positions. During CO2 stimulated breathing, however, derived chest wall configurations were at times dissimilar. The RIP per cent rib cage contribution to tidal volume was greater than that of magnetometers during room air and CO2 rebreathing in both sitting and supine positions. Changes in end expiratory levels measured by magnetometers and RIP during CO2 rebreathing are in general proportionate to each other; however, the magnetometers usually depicted quantitatively greater decreases in abdominal end expiratory levels during rebreathing. We conclude that the qualitative and quantitative assessment of chest wall configurations and volume displacement vary depending on the method used. RIP by including lateral wall motion may more accurately reflect compartmental displacements, while magnetometers by solely measuring antero-posterior diameter may better reflect changes in abdominal volume and thus diaphragm configuration.
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PMID:Comparison of magnetometer and inductance plethysmography derived Konno-Mead diagrams during CO2 rebreathing. 392 60

Seventeen children (mean age, nine years) with chronic obstructive pulmonary disease (COPD) were studied during sleep. Electroencephalography, electrooculography, and electromyography were all recorded. Airflow was measured by nasal and oral thermistors, and abdominal and thoracic anteroposterior diameters by magnetometers. Transcutaneous partial pressure of O2 (tcPO2) and of CO2 (tcPCO2) were monitored. The average total sleep time was 283 min +/- 36 (1 SD). Breathing pauses (BP) five seconds or longer were measured. The mean time of BP expressed as a percentage of TST was 1.3 percent +/- 0.8 (1 SD). The BP occurred most frequently during REM sleep. Forty-six percent of BP were obstructive (OBP). The percentage of OBP was significantly related to the degree of lung resistance during wakefulness. Periodic breathing was observed with a mean frequency of 2.2 times per night (range: 0 to 7). Episodes with paradoxic inward rib cage motion were seen one to 29 times (mean 6.6). Drops in tcPCO2 greater than 5 mm Hg occurred one to eight times and 67 percent were observed during REM sleep. Compared to tcPCO2 during W the mean maximal decrease in tcPCO2 was 14 mm Hg (range 8 to 29). tcPCO2 rose with a mean maximal of 9.1 mm Hg (range 6 to 13). It was concluded that children with COPD had worsened gas exchange during sleep.
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PMID:Respiration during sleep in children with COPD. 396 24

The ability of the respiratory muscles to sustain ventilation against increasing inspiratory resistive loads was measured in 10 normal subjects. All subjects reached a maximum rating of perceived respiratory effort and at maximum resistance showed signs of respiratory failure (CO2 retention, O2 desaturation, and rib cage and abdominal paradox). The maximum resistance achieved varied widely (range 73-660 cmH2O X l-1 X s). The increase in O2 uptake (delta Vo2) associated with loading was linearly related to the integrated mouth pressure (IMP): delta Vo2 = 0.028 X IMP + 19 ml/min (r = 0.88, P less than 0.001). Maximum delta Vo2 was 142 ml/min +/- SD 68 ml/min. There were significant (P less than 0.05) relationships between the maximum voluntary inspiratory pressure against an occluded airway (MIP) and both maximum IMP (r = 0.80) and maximum delta Vo2 (r = 0.76). In five subjects, three imposed breathing patterns were used to examine the effect of different patterns of respiratory muscle force deployment. Increasing inspiratory duration (TI) from 1.5 to 3.0 and 6.0 s, at the same frequency of breathing (5.5 breaths/min) reduced peak inspiratory pressure and increased the maximum resistance tolerated (190, 269, and 366 cmH2O X l-1 X s, respectively) and maximum IMP (2043, 2473, and 2913 cmH2O X s X min-1, but the effect on maximum delta Vo2 was less consistent (166, 237, and 180 ml/min). The ventilatory endurance capacity and the maximum O2 uptake of the respiratory muscles are related to the strength of the inspiratory muscles, but are also modified through the pattern of force deployment.
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PMID:Inspiratory muscle forces and endurance in maximum resistive loading. 399 25


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