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)

We assessed respiratory muscle response patterns to chemoreceptor stimuli (hypercapnia, hypoxia, normocapnic hypoxia, almitrine, and almitrine + CO2) in six awake dogs. Mean electromyogram (EMG) activities were measured in the crural (CR) diaphragm, triangularis sterni (TS), and transversus abdominis (TA). Hypercapnia and normocapnic hypoxia caused mild to marked hyperpnea [2-5 times control inspiratory flow (VI)] and increased activity in CR diaphragm, TS, and TA. When hypocapnia was permitted to develop during hypoxia and almitrine-induced moderate hyperpnea, CR diaphragm activity increased, whereas TS and TA activities usually did not change or were reduced below control. Over time in hypercapnia, CR diaphragm, TS, and TA were augmented and maintained at these levels over many minutes; with hypoxic hyperventilation CR diaphragm, TS, and TA were first augmented but then CR diaphragm remained augmented while TS and, less consistently, TA were inhibited over time. Marked hyperpnea (4-5 times control) due to carotid body stimulation increased TA and TS EMG activity despite an accompanying hypocapnia. We conclude that in the intact awake dog 1) carotid body stimulation augments the activity of both inspiratory and expiratory muscles; 2) hypocapnia overrides the augmenting effect of carotid body stimulation on expiratory muscles during moderate hyperpnea, usually resulting in either no change or inhibition; 3) at higher levels of hyperpnea both chemoreceptor stimulation and stimulatory effects secondary to a high ventilatory output favor expiratory muscle activation; these effects override any inhibitory effects of a coincident hypocapnia; and 4) expiratory muscles of the rib cage/abdomen may be augmented/inhibited independently of one another.
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PMID:Differential responses of expiratory muscles to chemical stimuli in awake dogs. 249 85

Like other simian primates, the New World monkey Callithrix jacchus, marmoset, and Saguinus fuscicollis, tamarin, require ascorbic acid as an essential nutrient. For adult marmosets, a daily intake of 15 mg/kg metabolic body weight was found to be necessary to obtain a serum level above the kidney threshold. A survey of the serum ascorbic acid level of marmosets and tamarins in a breeding colony resulted in a vast divergence between the two species, indicating a higher ascorbic acid requirement for tamarins. Unaccustomed trial conditions or additional stressors resulted in a higher catabolism of ascorbic acid to CO2 in both species, measured with 14C labeled material, compared to a higher rate of renal excretion when the animals were accustomed to the metabolic cage. These isotope excretion studies suggest a different metabolic behavior of ascorbic acid in the two species. This is supposedly caused by a higher sensitivity of the tamarins when subjected to the same conditions as marmosets.
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PMID:Ascorbic acid in a New World monkey family: species difference and influence of stressors on ascorbic acid metabolism. 249 92

Coordination of activity of inspiratory intercostal muscles in conscious human subjects was studied by means of an array of electromyograph (EMG) electrodes. Bipolar fine wire electrodes were placed in the second and fourth parasternal intercostal muscles and in two or three external intercostal muscles in the midaxillary line from the fourth to eighth intercostal spaces. Subjects breathed quietly or rebreathed from a bag containing 8% CO2 in O2 in both supine and upright postures. Respiration was monitored by means of flow, volume, and separate rib cage and abdominal volumes. Onset of EMG activity in each breath was found near the beginning of inspiration in the uppermost intercostal spaces but progressively later in inspiration in lower spaces, indicating that activity spreads downward across the rib cage through inspiration. At higher ventilation stimulated by CO2, activity spread further and faster downward. In voluntary deep breathing, external intercostal muscles tended to be recruited earlier in inspiration than in CO2-stimulated breathing. The change from supine to sitting resulted in small and inconsistent changes. There was no lung volume or rib cage volume threshold for appearance of EMG activity in any of the spaces.
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PMID:Patterns of intercostal muscle activity in humans. 251 14

The electrical activity of the respiratory skeletal muscles is altered in response to reflexes originating in the gastrointestinal tract. The present study evaluated the reflex effects of esophageal distension (ED) on the distribution of motor activity to both inspiratory and expiratory muscles of the rib cage and abdomen and the resultant changes in thoracic and abdominal pressure during breathing. Studies were performed in 21 anesthetized spontaneously breathing dogs. ED was produced by inflating a balloon in the distal esophagus. ED decreased the activity of the costal and crural diaphragm and external intercostals and abolished all preexisting electrical activity in the expiratory muscles of the abdominal wall. On the other hand, ED increased the activity of the parasternal intercostals and expiratory muscles located in the rib cage (i.e., triangularis sterni and internal intercostal). All effects of ED were graded, with increasing distension exerting greater effects, and were eliminated by vagotomy. The effect of increases in chemical drive and lung inflation reflex activity on the response to ED was examined by performing ED while animals breathed either 6.5% CO2 or against graded levels of positive end-expiratory pressure (PEEP), respectively. Changes in respiratory muscle electrical activity induced by ED were similar (during 6.5% CO2 and PEEP) to those observed under control conditions. We conclude that activation of mechanoreceptors in the esophagus reflexly alters the distribution of motor activity to the respiratory muscles, inhibiting the muscles surrounding the abdominal cavity and augmenting the parasternals and expiratory muscles of the chest wall.
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PMID:Reflex effect of esophageal distension on respiratory muscle activity and pressure. 265 82

To determine whether the rib cage muscles actively contribute to tidal volume change in infancy, we measured tidal volume (VT), using a pneumotachograph, respiratory gastric pressure swings (Pga), using a liquid-filled gastric catheter, and rib cage and abdominal volume, using respiratory inductive plethysmography in 15 newborns, both before and during 2% CO2-induced hyperventilation. Active rib cage expansion produced by phasic contraction of the inspiratory muscles of the rib cage should reduce respiratory abdominal pressure fluctuations by moving the anterior abdominal wall outward and cephalad, thereby having an expanding influence on the abdominal cavity. During quiet sleep (n = 13), CO2-induced hyperventilation was associated with significant increases in VT, Pga, rib cage volume (Vrc), and abdominal volume (Vab). Increments in Pga were small relative to VT, as shown by an increase in the slope of the VT versus Pga respiratory loop (VT/Pga) in all subjects (p less than 0.001, paired t test). CO2 breathing was associated with an increase in the contribution of the rib cage compartment to total volume change (Vrc/Vrc + Vab) in all infants studied (p less than 0.001, paired t test), and the total volume response to hyperventilation was more strongly related to changes in rib cage volume (slope = 0.62, r = 0.90) than to abdominal volume (slope = 0.31, r = 0.60). During REM sleep (n = 6), mean VT/Pga did not change significantly, and the rib cage contribution to tidal breathing decreased in three of six infants.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Action of the inspiratory muscles of the rib cage during breathing in newborns. 271 47

The blood flow to the diaphragm, external and internal intercostal muscles, abdominal oblique muscles, and other rib-cage and abdominal muscles was measured, using radio-labelled microspheres, in 6 newborn lambs quietly breathing in air and during 3 different levels of CO2 induced hypercapnic hyperpnoea (inspired gas containing 4%, 5.5%, or 7% CO2). We also calculated the oxygen uptake of the diaphragm (VO2di). While the lambs were breathing air diaphragmatic blood flow (Qdi, 38.2 +/- 4.0 SEM ml.min-1.100 g-1) was similar to external intercostal muscle blood flow (Qei, 37.1 +/- 8.1 ml.min-1.100 g-1), and both were greater than internal intercostal muscle blood flow (Qii, 24.8 +/- 6.1 ml.min-1.100 g-1; P less than 0.05). During hyperpnoea Qdi, Qei, and Qii were augmented with Qdi equal to 200.1 +/- 12.2 ml.min-1.100 g-1 in 7% CO2 and Qei equal to 88.4 +/- 14.1 ml.min-1.100 g-1 in 7% CO2 (Qdi was greater than Qei, P less than 0.01). Qii was 40.7 +/- 5.6 ml.min-1.100 g-1 in 7% CO2 being less than Qdi (P less than 0.01) and Qei (P less than 0.05). The abdominal oblique muscles also had augmented flow in response to hyperpnoea. The level of hypercapnia that resulted in an augmentation of Qdi (5.5% inspired CO2) was lower than that which augmented Qei and Qii (7% inspired CO2). VO2di was linearly related to Qdi (r = 0.98). Our results suggest that in the newborn lamb the diaphragm is the dominant respiratory muscle in response to hypercapnia.
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PMID:Blood flow to the respiratory muscles during hypercapnic hyperpnoea in the newborn lamb. 272 19

Paralysis of the diaphragm promotes an increase in the activation of the rib cage inspiratory muscles, and previous studies have suggested that this compensation is primarily due to vagal mechanisms (6). To test this hypothesis, we have assessed the effect of diaphragmatic paralysis on the electrical response of 19 parasternal intercostal muscles in eight anesthetized, vagotomized, spontaneously breathing dogs in the supine posture. Complete diaphragmatic paralysis was induced by section of the C5, C6, and C7 phrenic nerve roots in the neck. With the animals breathing room air, diaphragmatic paralysis resulted in a mean 94% increase in the peak height of integrated parasternal activity (p less than 0.001) associated with a 14 mm Hg decrease in arterial PO2 (p less than 0.05) and an 8 mm Hg increase in arterial PCO2 (p less than 0.001). The augmented parasternal activity was unrelated to the duration of inspiration and persisted when the animals were given a hyperoxic gas mixture. Thus the rib cage inspiratory muscles still compensate for diaphragmatic paralysis in the absence of vagal signals and of hypoxemia. This compensation probably results from the considerably augmented CO2 load placed on the extradiaphragmatic muscles.
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PMID:Mechanism of rib cage inspiratory muscle recruitment in diaphragmatic paralysis. 291 34

Inspiratory mechanical loads were applied to the airway continuously for 5 min in healthy young adult volunteers maintained in a near steady-state of halothane anesthesia 1.1 MAC. The loads, both flow resistive and elastic in nature, had been selected to reduce the first loaded tidal volume approximately 10, 30 or 50%--these being designated "small," "medium," and "large" loads, respectively. The actual magnitudes of resistive load were 8 +/- 1, 21 +/- 3, and 48 +/- 6 cmH2O X l-1 X s, and of elastic load 6 +/- 1, 18 +/- 1, and 41 +/- 5 cmH2O X l-1 (mean +/- SEM). All loads caused an immediate reduction of ventilation proportional to the size of the load. This was followed by a gradual recovery of ventilation toward control values over approximately 2 min and then nearly stable ventilation for the rest of the loading period. Respiratory frequency was unchanged throughout. At 5 min of loading, ventilation and PaCO2 had been nearly steady for 3 min and O2 uptake and CO2 output at the airway were unchanged from control, suggesting the establishment of a near steady respiratory state. With the small and medium loads of both types, ventilation and PaCO2 in this near steady-state were not detectably different from control. With the large loads, however, ventilation was significantly reduced and PaCO2 slightly increased. The end-expiratory position of the chest wall and the relative contributions of the rib cage and abdomen-diaphragm to ventilation, as estimated by anteroposterior chest wall magnetometers, were not consistently altered by any load.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Ventilatory compensation for continuous inspiratory resistive and elastic loads during halothane anesthesia in humans. 293 23

The present study compared the responses of rib cage and abdominal expiratory muscles to chemical and mechanical stimuli. In pentobarbital-anesthetized spontaneously breathing dogs, electromyograms (EMG) were recorded from the triangularis sterni (TS) and transverse abdominis (TA) muscles using bipolar intramuscular wire electrodes. During resting oxygen breathing, both muscles were electrically active during expiration. Progressive hyperoxic hypercapnia significantly augmented the expiratory activity of both the TA and the TS. However, the mean percent increases in electrical activity in response to CO2 were substantially greater for the TA than for the TS at all PCO2 levels greater than 50 Torr (P less than 0.01). Occlusion of the airway at end inspiration significantly delayed the onset of TS EMG (from 0.35 +/- 0.07 to 3.35 +/- 0.67 sec; P less than 0.002) and decreased TS EMG rate of rise (P less than 0.002), but did not significantly alter these parameters for the TA. Esophageal distension increased TS EMG in all dogs (by mean of 220 +/- 64%; P less than 0.01), but in contrast decreased TA EMG in all dogs (by a mean of 63 +/- 12%; P less than 0.001). The response to esophageal distention occurred in a graded manner and appeared to be mediated predominantly via vagal afferents. We concluded that expiratory muscles of the rib cage and abdomen manifest substantial differences in their electrical responses to chemoreceptor, pulmonary stretch receptor, and esophageal mechanoreceptor stimuli.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Rib cage and abdominal expiratory muscle responses to CO2 and esophageal distension. 296 76

Chest wall distortion (inward motion of the rib cage on inspiration) has been found recently to reduce the tidal volume during active sleep in the neonatal period. To determine some of the factors that relate to the chest wall distortion and the decreased tidal volume seen in active sleep, a quantification of the phase differences between the movements of the chest wall and those of the abdominal wall, and of the relation of their phase differences to tidal volume was performed on data obtained before and during carbon dioxide stimulation in 15 newborn infants sleeping in the prone position. In quiet sleep, the breathing movements were congruent and regular, and the tidal volume and the mean inspiratory flow increased during carbon dioxide stimulation. In active sleep during exposure to carbon dioxide, the chest wall distortion decreased, the breathing movements were incongruent and the degree of the chest wall distortion was negatively correlated with the tidal volume, while the tidal volume and the mean inspiratory flow was increased. Chest wall distortion did not appear in quiet sleep and was decreased in active sleep in spite of increased ventilation during CO2 stimulation. This study favours the idea that chest wall distortion is caused by a well regulated change in neuromuscular activity and not by the strength of diaphragmatic movements overcoming the mechanical stability of the rib cage.
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PMID:The effect of carbon dioxide inhalation on phase characteristics of breathing movements in healthy newborn infants. 309 74


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